sort by

106 publications mentioning hsa-mir-301a (showing top 100)

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-301a. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 360
miR-301a mimics and inhibitors were used to up-regulate and down-regulate miR-301a in CRC cells, respectively; lentivirus was used to construct miR-301a stably up- and down-regulated CRC cell lines. [score:12]
In consistent with this, we found knockdown of miR-301a in CRC cells upregulated the protein level of TGFBR2 while ectopically overexpression of miR-301a suppressed its expression. [score:11]
Interestingly, we found miR-301a regulated TGFBR2 expression by some translational suppression mechanisms: the mRNA level of TGFBR2 did not change significantly upon transfection with miR-301a inhibitor or mimics while the protein level showed remarkable differences. [score:10]
Downregulation of miR-301a significantly inhibited the migration and invasion both in vitro and in vivo while forced up-regulation of miR-301a promoted migration and invasion. [score:9]
However, western blot demonstrated that expression of TGFBR2 protein was markedly increased in miR-301a downregulated SW620 cells and significantly reduced in miR-301a overexpressed SW480 cells (Figure  4B). [score:8]
Thus we suggest that miR-301a imperfectly bind with the 3’-UTR of TGFBR2 and regulate the expression of TGFBR2 via translational suppression. [score:8]
Unlike its expressions in the cancers mentioned above, there is no statistical difference of miR-301a expression between CRC tissues and their adjacent non-tumor tissues, nevertheless, increased miR-301a expression was observed in tumors with lymph node metastasis. [score:7]
These data demonstrated unambiguously that miR-301a suppressed TGFBR2 protein expression via targeting its specific RNA binding site. [score:7]
Functionally, we found TGFBR2 acted as a metastasis suppressor and also the effector of miR-301a in CRC cells: knockdown of TGFBR2 induced a significant increase in motility and invasiveness of SW480 cells whereas downregulation of TGFBR2 also elevated the previously abrogated migration and invasion ability initiated by LV-anti-miR-301a in SW620 cells. [score:7]
Moreover, downregulation of miR-301a in hepatocellular carcinoma (HCC) cells suppressed invasion and migration of HCC cells in vitro [21]. [score:6]
This suggested that miR-301a suppressed TGFBR2 by post-transcriptional mechanism rather than directly inhibiting the transcription. [score:6]
In line with these findings, we demonstrated that overexpression of miR-301a in less aggressive SW480 cells led to a significant increase of cell migration whereas downregulation of miR-301a in more aggressive SW620 cells resulted in decreased migratic ability, indicating the metastasis promoter role of miR-301a in CRC. [score:6]
In gastric cancer cells, ectopic expression of miR-301a led to significantly enhanced cell migration and invasion, whereas knockdown of miR-301a also inhibited cell metastasis [22]. [score:6]
Conclusively, these results suggest that downregulation of TGFBR2 is involved in miR-301a -induced metastasis and invasion; TGFBR2 is a functional target of miR-301a. [score:6]
Thus, we used the online TargetScan and PicTar algorithms systems to search for potential targets of miR-301a. [score:5]
By searching the online TargetScan and PicTar algorithms systems, we identified transforming growth factor receptor 2 (TGFBR2) as the target of miR-301a with the highest possibility. [score:5]
In supporting this, we found CRC cell lines with high metastasis capacity expressed higher miR-301a than those with low metastasis capacity and we went a step further by showing that miR-301a expression was correlated positively with the cell migratory ability in these CRC cells. [score:5]
Shi et al first reported the expression of miR-301a in human cancer: miR-301a overexpression has been implicated as a negative prognostic indicator in lymph node negative invasive ductal breast cancer and strongly associated with tumor recurrence. [score:5]
Expression of TGFBR2 was significantly and inversely associated with the expression of miR-301a (r = -0.72, P < 0.001). [score:5]
Transient transfection of anti-miR-301a in SW620 cells significantly suppressed the expression of miR-301a in SW620/anti-miR-301a cells (Figure  2A, P < 0.01). [score:5]
To this end, we focused on whether artificial expression or suppression of TGFBR2 protein could offset the effects caused by miR-301a mimics or anti-miR-301a, respectively. [score:5]
The results presented above confirmed TGFBR2 as one downstream target of miR-301a; however, it remained unclear whether miR-301a regulated metastasis and invasion in CRC cells through modulating TGFBR2. [score:4]
For CRCs, a miRNA array which analyzed the miRNA expression profiles of 44 pairs of CRCs revealed that the expression of miR-301a was elevated in tumor tissues of stage II patients compared to paired normal tissues [23]. [score:4]
Figure 4 TGFBR2 was a direct target gene of miR-301a. [score:4]
The target of miR-301a was predicted by TargetScan software and validated by qRT-PCR, immunohistochemistry, western blot and luciferase reporter gene assay. [score:4]
miR-301a is up-regulated in lymph node metastatic CRC tissues and CRC cells lines. [score:4]
Figure 1 miR-301a was upregulated in lymph node metastatic CRC tissues and highly metastatic CRC cells. [score:4]
TGFBR2 is a functional target through which miR-301a regulated metastasis and invasion in CRC cells. [score:4]
To this end, we constructed miR-301a stably down-regulated and negative control SW620 cells with lentivirus particles LV-anti-miR-301a and LV-anti-miR-301a-NC, respectively. [score:4]
Figure 5 miR-301a regulated metastasis and invasion through suppressing TGFBR2 in CRC cells. [score:4]
Upregulation of miR-301a in SW480 cells led to a marked increase of both migratory and invasive abilities in contrast with the control cells (Figure  2D, P < 0.01). [score:4]
Furthermore, we identified TGFBR2 to be one downstream target of miR-301a and also the effector of miR-301a in the regulation of metastasis in CRC cells. [score:4]
Cao G, Huang B, Liu Z, Zhang J, Xu H, Xia W, Li J, Li S, Chen L, Ding H, Zhao Q, Fan M, Shen B, Shao N: Intronic miR-301 feedback regulates its host gene, ska2, in A549 cells by targeting MEOX2 to affect ERK/CREB pathways. [score:4]
In the current study, we reported for the first time that miR-301a was up-regulated in lymph node metastatic CRC tissues and promoted CRC metastasis both in vitro and in vivo. [score:4]
miR-301a has been discovered up-regulated in various types of human cancers and proved to be an oncogene in gastric cancer [22], pancreatic cancer [32], hepatocellular cancer [21], and esophageal cancer [33]. [score:4]
Knockdown of TGFBR2 in cells treated by miR-301a inhibitor elevated the previously abrogated migration and invasion. [score:4]
In this study, though we found miR-301a indeed bound with TGFBR2, they might not perfectly match in sequence since we observed marked downregulation of TGFBR2 protein while the mRNA of TGFBR2 remained unchanged. [score:4]
As shown in Figure  6, higher TGFBR2 staining positivity was seen in tumors with low miR-301a expression; furthermore, we quantified the TGFBR2 staining intensity and made a correlation analysis between TGFBR2 and miR-301a. [score:3]
Subsequently, we evaluated the expression of miR-301a in these cells and as shown in Figure  1D, the expression of miR-301a was much higher in SW620 and HCT116 than that of LOVO, HT29, and SW480. [score:3]
Thus we wanted to know the target through which miR-301a exerted its function in CRC cells. [score:3]
Figure 3 Downregualtion of miR-301a suppressed CRC cell invasion and lung metastases in vivo. [score:3]
miR-301a binding sites were predicted using TargetScan software (http://www. [score:3]
Higher expression of TGFBR2 was observed mainly in CRCs with low miR-301a level (r = -0.72, P < 0.001). [score:3]
miR-301a represses TGFBR2 protein expression by binding to 3’-UTR. [score:3]
To understand the role of miR-301a in CRC progression, we examined the expression of miR-301a in 48 CRC tissues and their paired adjacent non-tumor tissues. [score:3]
Our data indicated that miR-301a correlated with the metastatic and invasive ability in human colorectal cancers and miR-301a exerted its role as oncogene by targeting TGFBR2. [score:3]
TGFBR2 was identified to be the downstream target of miR-301a. [score:3]
The gene encoding miR-301a is located in the human chromosome 17q22-17q23 and it has been previously reported to be overexpressed in many kinds of human cancers, including gastric cancer, liver cancer, breast cancer, etc. [score:3]
miR-301a promotes CRC cell migration and invasion in vitroTo further determine whether miR-301a could affect CRC cell migration, we transfected SW620 cells, which showed a high level of miR-301a, with the anti-miR-301a in order to suppress miR-301a (i. e. SW620/anti-miR-301a cells). [score:3]
To further determine whether miR-301a could affect CRC cell migration, we transfected SW620 cells, which showed a high level of miR-301a, with the anti-miR-301a in order to suppress miR-301a (i. e. SW620/anti-miR-301a cells). [score:3]
As shown in Figure  2B, exogenous expression of miR-301a in SW480 cells resulted in a significant increase of miR-301a by qRT-PCR (P < 0.01). [score:3]
Thus, we attempted to figure out whether TGFBR2 was a downstream target of miR-301a or not. [score:3]
miRNAs microRNAs miR-301a microRNA-301a CRC Colorectal cancer TGFBR2 Transforming growth factor receptor 2 3’-UTR 3’ un-translated regions qRT-PCR Quantitative real-time polymerase chain reaction GAPDH Glyceraldehyde-3-phosphate dehydrogenase ATCC American Type Culture Collection cDNA Complementary DNA nt Nucleotide FBS Fetal Bovine Serum NC Negative control HE Hematoxylin-eosin FBS Fetal bovine serum DMEM Dulbecco’s modified Eagle’s medium RNU6B U6 small nuclear RNA HCC Hepatocellular carcinoma PTEN Phosphatase and tensin homologue on chromosome 10 This work was supported by grants from the Scientific Research Foundation of science and Technology Commission of Shanghai Municipality (No. [score:3]
For this reason, we used bioinformatics method to predict the potential targets of miR-301a. [score:3]
However, the expression of miR-301a in CRCs and its role in CRC metastasis remain unclear. [score:3]
48 hours after transfection, cells were harvested and miR-301a expression level was monitored by qRT-PCR (U6 RNA was endogenous control), and the siRNA transfection efficiency was assessed by western blot using GAPDH as loading control. [score:3]
Besides, a series of recent functional studies demonstrated that miR-301a promoted cancer cell metastasis in breast, hepatocellular and gastric tumors through different target genes [17, 21, 22]. [score:3]
qRT-PCR demonstrated that there was no significant difference of miR-301a expression between CRC and the adjacent non-tumor mucosa (Figure  1A, P > 0.05). [score:3]
Supporting this, we observed an inverse correlation between miR-301a and TGFBR2 protein expression in CRC tumor tissues. [score:3]
Importantly, the expression of miR-301a did not differ among patients with different gender, age, tumor differentiation, tumor location, tumor histopathology, tumor local invasion or distant metastasis (Table  3). [score:3]
Additionally, overexpression of miR-301a in breast cancer cell lines could promote cell migration and invasion in vitro and lung metastases in mice mo dels. [score:3]
The procedures to establish LV-anti-miR-301a stably expressing clones and the control clones in SW620 cells (SW620/LV-anti-miR-301a and SW620/LV-anti-miR-NC) were performed as previously described [25]. [score:3]
However, the expression of miR-301a in tumors with lymph node metastases was significantly higher than that in tumors without metastases (Figure  1B, P < 0.05), which indicated that miR-301a might be involved in the metastasis of CRC. [score:3]
miR-301a, one micro -RNA reported to be expressed at different levels in a variety of cancers, has been demonstrated to be important in promoting cancer metastasis [17, 21, 22]. [score:3]
MicroRNA-301a (miR-301a) is overexpressed and displays oncogenic activity in many cancers. [score:3]
In summary, our study presented convincing evidences to show that miR-301a exerted its role as oncogene in CRC metastasis, and for the first time we identified TGFBR2 as a functional target involved in miR-301a modulated CRC cell metastasis. [score:3]
Combined together, these results suggested that miR-301a suppressed TGFBR2 in CRC cells. [score:3]
Specifically, expression of miR-301a seemed to be correlated with the metastatic ability of CRC cells by spearman correlation analysis (r = 0.96, P < 0.01). [score:3]
miR-301a could be regarded as a new target for CRC prevention and therapy. [score:3]
There was no significant difference in miR-301a expression between CRC tissues and their adjacent non-tumor tissues. [score:3]
Additionally, the gain-of-function assay with miR-301a mimics transfected in miR-301a low-expressed SW480 cells was performed to further consolidate the role of miR-301a in cell migration and invasion. [score:2]
Besides knockdown of miR-301a reduced migration and invasion of both MCF-7 and MDA-MB-231 breast cancer cell lines in vitro [17]. [score:2]
Besides, suppression of TGBFR2 by miR-301a was also validated in vivo: in the xenograft tumors from SW620/LV-anti-miR-301a nude mice, staining intensity of TGFBR2 elevated remarkably compared to that of the SW620/LV-anti-miR-NC tumors (Figure  4C). [score:2]
These data led us to ask whether miR-301a could regulate metastasis in CRCs or not. [score:2]
In line with the in vitro results, fewer metastatic lesions in the lung of nude mice injected with SW620/LV-anti-miR-301a were seen compared with that of SW620/LV-anti-miR-NC group (Figure  3B; P < 0.05), indicating the suppression of metastatic ability in SW620/LV-anti-miR-301a cells in vivo. [score:2]
We then wanted to know the mechanism through which miR-301a regulated TGFBR2. [score:2]
Indeed we found TGFBR2 was one target of miR-301a and the luciferase reporter gene assay successfully identified the binding site for miR-301a on the 3’-UTR of TGFBR2 gene. [score:2]
Furthermore, this effect was also prominent in vivo: knockdown of miR-301a significantly reduced xenograft tumor invasion and lung metastases in nude mice. [score:2]
The expression of miR-301a was significantly higher in lymph node metastasis positive compared with negative ones. [score:2]
Likewise, a recent study described that the expression level of miR-301a was significantly elevated in the primary tumors of 10 breast cancer patients with distant metastasis, as compared with that in primary tumors from 10 patients without detectable distant metastasis [34]. [score:2]
H&E staining of tumor acquied from nude mice bearing the SW620/LV-anti-miR-301a or SW620/LV-anti-miR-NC cells (indicated by arrows), 4 weeks post implantation. [score:1]
However, until now, functional evidence of miR-301a in CRCs has not been documented and its role in CRC metastasis remains unclear. [score:1]
miR-301a promotes tumor metastasis and cell invasion in vivoThe above mentioned results further led us to ask whether miR-301a functioned as a promoter of migration and invasion of CRC cells in vivo as well. [score:1]
CRC miRNA-301a Metastasis Invasion TGFBR2 Colorectal cancer (CRC) is one of the most prevalent causes of cancer-related mortalities worldwide, with 610.000 deaths each year. [score:1]
These results indicated that miR-301a is a metastatic promoter in CRC. [score:1]
However, little is known about the potential roles of miR-301a in colorectal cancer (CRC). [score:1]
As shown in Figure  5C, the enhanced TGFBR2 level by LV-anti-miR-301a was depleted upon TGFBR2 siRNA transfection. [score:1]
In the 3’-UTR of TGRBR2 mRNA there existed two putative binding sites for miR-301a: a highly conserved 7mer-m8 at nt 266-272 and a poorly conserved 7mer-m8 at position 566-572 (Figure  4D). [score:1]
Figure 2 miR-301a promoted CRC cell migration and invasion in vitro. [score:1]
Conclusively, miR-301a promotes the migration and invasion ability of CRC cells in vitro. [score:1]
qRT-PCR and western blot analysis were first employed and somehow unexpectedly, there was no significant difference of TGFBR2 mRNA levels between SW620/anti-miR-301a and SW620/anti-miR-NC cells or SW480/miR-301a and SW480/miR-NC cells (Figure  4A). [score:1]
The relative expression of miR-301a in tissues and cell lines were calculated by the 2 [-Δct] method. [score:1]
The above mentioned results further led us to ask whether miR-301a functioned as a promoter of migration and invasion of CRC cells in vivo as well. [score:1]
Actually, previous studies have shown that miR-301a acted as a metastatic promoter in different kinds of human cancers. [score:1]
Hence, miR-301a could promote tumor metastasis and invasion in vivo. [score:1]
Taken together, TGFBR2 played an important role in miR-301a mediated tumor migration and invasion in CRC. [score:1]
The expression levels of miR-301a and U6 small nuclear RNA (RNU6B, Applied Biosystems, United States) were assayed in triplicates by the TaqMan stem-loop RT-PCR method with a mirVana miRNA detection Kit and gene-specific primers (Applied Biosystems, United States). [score:1]
Wild type and two mutant fragments of 3’-UTR were co -transfected with miR-301a mimics or NC, respectively. [score:1]
Then the full length of miR-301a TGFBR2 3’-UTR including two wild-type binding sites and the two mutant fragments (mut-266, mut-566) were designed by and purchased from Sangon (Shanghai, China). [score:1]
SW620/LV-anti-miR-301a and SW620/LV-anti-miR-NC cells (5 × 10 [6] cells per mice) were implanted subcutaneously into the left flanks of 5-week-old male nude mice (10 mice per group). [score:1]
Bioinformatics analysis revealed two putative binding sites for miR-301a: a conserved 7mer-m8 at nt 266-272 of TGFBR2 3’-UTR and a poorly conserved 7mer-m8 at position 566-572 of TGFBR2 3’-UTR. [score:1]
miR-301a promotes tumor metastasis and cell invasion in vivo. [score:1]
Taqman probe stem-loop real-time PCR was used to quantitatively measure the expression level of miR-301a in 48 cases of CRC tissues and the matched adjacent non-tumor mucosa as well as in CRC cell lines. [score:1]
This was in consistent with its role as an oncogene in aforementioned cancers and might indicate a metastasis promotion role rather than a tumor initiation role of miR-301a in CRCs. [score:1]
To further determine whether TGFBR2 is responsible for the migration and invasion caused by miR-301a, we transfected TGFBR2 siRNA into SW620/LV-anti-miR-301a cells transiently. [score:1]
In this study, we investigated the expression of miR-301a in CRC specimens for the first time. [score:1]
As shown in Figure  2C, SW620/anti-miR-301a cells showed a significant (P < 0.01) reduction of migratory ability, while, unexpectedly, the invasive capacity was also significantly (P < 0.01) decreased. [score:1]
However, miR-301a did not affect the relative luciferase activity of the pMIR/TGFBR2-mut266, suggesting that miR-301a specifically bind to the conserved 7mer-m8 at nt 266-272 on 3’-UTR of TGFBR2. [score:1]
Expression of TGFBR2 was evaluated in tumors formed by SW620/LV-anti-miR-301a cells. [score:1]
SW620/LV-anti-miR-301a cells and SW620/LV-anti-miR-NC cells were separately injected into nude mice subcutaneously and mice were sacrificed four weeks later. [score:1]
As shown in Figure  3A, tumors grown of SW620/LV-anti-miR-301a cells were less-invasive as most tumors (4/5) confined within the fibrous capsules without breaking into the stromal (Figure  3A, right panel). [score:1]
Altogether, these data indicated that miR-301a may contribute to the metastasis of CRC. [score:1]
miR-301a promotes CRC cell migration and invasion in vitro. [score:1]
[1 to 20 of 113 sentences]
2
[+] score: 243
Our studies showed PlGF coordinately induced the expression of pre- miR-301a, pre- miR-454 and SKA2 mRNA, which was maximal at 4 h followed by complete return to basal level by 8 h. These expression kinetics would be expected for normal expression of this locus from a common promoter. [score:7]
Figure 1PlGF up-regulates the expression of miR-301a and miR-454 located in an intron of host gene SKA2 by activation of HIF-1α and PPAR-α(A) Schematic of 5′ end of SKA2 gene showing locations of miR-301a and miR-454 in the first intron of SKA2 and positions of cis -binding elements for HIF-1α and PPAR-α. [score:6]
The importance of this level of post-transcriptional regulation is consistent with our previous demonstration that PlGF leads to a reduction in miR-301a and miR-454 expression, thus providing a permissive cell state enhancing the PlGF induction of ET-1 and PAI-1 expression in SCD [6, 23]. [score:6]
miR-301a and miR-454, located in the first intron of host gene SKA2, are co-transcriptionally regulated by PPAR-α and HIF-1αOur previous studies show PlGF treatment of HPMVECs attenuates expression of miR-30c and miR-301a, which target the 3′-UTR of PAI-1 mRNA and thus affect its turnover [24]. [score:6]
PlGF up-regulates the expression of miR-301a and miR-454 located in an intron of host gene SKA2 by activation of HIF-1α and PPAR-α. [score:6]
We next examined the role of the ET-1 3′-UTR as the sole determinant of miR-301a and miR-454 targeting in a luciferase translation reporter, in response to PlGF. [score:5]
Further analysis predicted that miR-454 also could interact with the 3′-UTRs of ET-1 and PAI-1. We began by examining the time course of expression of SKA2, pre- miR-301a and pre- miR-454 mRNA by qRT PCR, in response to PlGF in HMEC-1. We observed that PlGF treatment of HMEC resulted in a time -dependent increase in SKA2 mRNA expression with maximal increase of ∼10-fold at 4 h (Figure 1B). [score:5]
These results extended our previous observation that plasma from SCD patients showed decreased expression of miR-301a with correspondingly higher levels of PAI-1. Furthermore, these results demonstrated that miR-301a and miR-454 are indeed co-regulated in SCD and undergo down regulation by an as yet unidentified process. [score:5]
These studies also revealed that fenofibrate, a PPAR-α agonist, approved by the Food and Drug Administration for the treatment of dyslipidemia [34] may increase the expression of both miR-301a and miR-454 leading to decreased ET-1 and PAI-1. In fact, fenofibrate has a secondary effect of reducing HIF-1α levels by inducing transcription of miR-199a2, which post-transcriptionally suppresses HIF-1α synthesis [25]. [score:5]
Our studies also show PlGF attenuates the expression of miR-30c and miR-301a in cultured endothelial cells, both of which target the 3′-UTR of PAI-1 under basal conditions [24]. [score:5]
Our previous studies show PlGF treatment of HPMVECs attenuates expression of miR-30c and miR-301a, which target the 3′-UTR of PAI-1 mRNA and thus affect its turnover [24]. [score:5]
These data showed that both miR-301a and miR-454 target the 3′-UTR of PAI-1 mRNA to attenuate PAI-1 translation. [score:5]
The fenofibrate induction of SKA2 and miR-301a/ miR-454, leading to attenuation of ET-1 expression in HMEC, may in fact also be assisted by fenofibrate -dependent reduction in HIF-1α expression. [score:5]
Figure 5Expression of miR-301a and miR-454 in lung tissues of BK-SS and SCD human subjects(A and B) Frozen lung tissue samples (−80°C storage) from BK-SS mice (n=6) and control C57BL/6NJ mice (n=6) were sliced and homogenized directly in RNA extraction buffer or protein cell lysate buffer. [score:4]
Moreover, the knockdown of PPAR-α and HIF-1α also reduced >90% the expression of pre- miR-301a and pre- miR-454 (Figure 1D). [score:4]
In conclusion, our studies provided further mechanistic insight into the co-regulation of miR-301a and miR-454 and their relationship to ET-1 mRNA and its translation. [score:4]
Mutation of the miR-301a- and miR-454 -binding sites in the luciferase translation reporter confirmed the functional interaction between these miRNAs and the 3′-UTR of ET-1 mRNA. [score:4]
However, mutation of the MRE site denoted M1 (nt +60/+63) of the ET-1 3′-UTR (shown in Figure 3A), prevented the inhibitory effects of exogenous miR-301a and miR-454 on luciferase activity. [score:4]
In the present study, we examined the role of miRNAs in the post-transcriptional regulation of ET-1 and PAI-1. Our studies showed that miR-301a and miR-454, target the 3′-UTRs of ET-1 and PAI-1 mRNAs. [score:4]
miR-301a and miR-454 target the 3′-UTR of ET-1 mRNA. [score:3]
miR-301a and miR-454 target 3′-UTR of ET-1 and attenuate ET-1 mRNA and protein levels. [score:3]
These data showed that both MRE sites were effective functional targets in the 3′-UTR of PAI-1 mRNA for miR-301a and miR-454. [score:3]
Taken together these data showed that increased levels of miR-301a and miR-454 decreased expression of ET-1, induced by PlGF. [score:3]
Expression of miR-301a and miR-454 in lung tissues of BK-SS and SCD human subjects. [score:3]
As shown above, fenofibrate increased the expression of miR-301a and miR-454 by inducing transcription of SKA2, accordingly we examined its effect on ET-1 secretion. [score:3]
Indeed, SCD patients exhibit abnormally high plasma levels of PlGF and were observed to express lower plasma levels of miR-301a and miR-454. [score:3]
We extended our study of miRNA effects on PAI-1 synthesis to determine whether miR-301a and miR-454 affected PlGF -induced PAI-1 protein expression, as reflected by changes in PAI-1 secretion from HMEC. [score:3]
We extended this observation by examining the expression of PAI-1 and miR-301a in mouse lung. [score:3]
miR-301a and miR-454 target the 3′-UTR of PAI-1 and effect a decrease in PAI-1 mRNA and protein levels. [score:3]
miR-301a and miR-454 target the 3′-UTR of PAI-1 and effect a decrease in PAI-1 mRNA and protein levels In silico analysis of the 3′-UTR of PAI-1 mRNA showed the presence of miR-301a/ miR-454 recognition elements at nt +1351/+1373 and at nt +1641/+1663 as depicted in the schematic of Figure 4(A). [score:3]
Figure 4 miR-301a and miR-454 target the 3′-UTR of PAI-1 mRNA(A) Schematic of 3′-UTR of PAI-1 mRNA showing locations of MRE for miR-301a and miR-454. [score:3]
miR-301a and miR-454 target the 3′-UTR of PAI-1 mRNA. [score:3]
PlGF transiently induced miR-301a and miR-454 in HMEC after 4 h, however expression quickly returned to basal levels by 6 h. In other words, SKA2 transcription became refractory to PlGF induction after 6 h by an unknown process preventing sustained transcription of the SKA2 gene. [score:3]
We examined miR-301a expression in lungs from BK-SS sickle mice and control C57BL/6NJ mice. [score:3]
In the present study, we extended our prior report regarding the regulatory activity of miR-301a on PAI-1. The transcriptional regulation of miR-301a was previously examined in the context of PAI-1 synthesis. [score:3]
miR-301a/ miR-454 target the 3′-UTR of ET-1 mRNA and the 3′-UTR of PAI-1 mRNAs leading to reduction in corresponding ET-1 and PAI-1 levels. [score:3]
Next, we examined binding of miR-301a and miR-454 to their target sequences in the PAI-1 3′-UTR of pGL3-PAI-1-3′-UTR reporter in response to PlGF. [score:3]
The expression of pre- miR-301a and pre- miR-454 mRNA showed a maximal increase in ∼4-fold at 2 h, followed by a gradual decline after 4 h to almost basal level by 8 h (Figure 1B). [score:3]
These data showed that both miR-301a and miR-454 target the 3′-UTR of ET-1 mRNA to attenuate ET-1 synthesis. [score:3]
Figure 3 miR-301a and miR-454 target the 3′-UTR of ET-1 mRNA(A) Schematic of 3′-UTR of ET-1 mRNA showing locations of MRE for miR-301a and miR-454. [score:3]
In addition, fenofibrate addition also augmented by 3-fold the expression of mature miR-301a and miR-454, both of which were attenuated by GW6471 (Figure 2B). [score:3]
In an effort to induce endogenous miR-301a and miR-454, fenofibrate treatment of HMEC augmented the endogenous expression of miR-301a and miR-454 and subsequently reduced the secretion of PlGF -induced, endogenous PAI-1 by ∼90% (Figure 4E). [score:3]
We tested this prediction by examining the effects of synthetic miR-301a and miR-454 on PlGF induced ET-1 mRNA expression in both HMEC and HPMVEC. [score:3]
The specificity of the interaction between miR-301a and miR-454 and their respective MREs in the 3′-UTR of ET-1 mRNA was established by inclusion of the ET-1 3′-UTR in a luciferase translation reporter. [score:3]
The functional consequence of binding miR-301a and miR-454 to target gene mRNAs ET-1 and PAI-1 was demonstrated by use of synthetic miR-301a and miR-454 mimics. [score:3]
Loss of miR-301a and miR-454 expression would therefore render ineffective a proposed feedback loop controlling ET-1 and PAI-1 levels (Figure 5D). [score:3]
PAI-1 3′-UTRs were PCR amplified from BAC clone RP11-213E22 and inserted into the pMIR vector using the Infusion cloning kit (Clontech) and primers listed in Table 1. Deletions of the PPAR-α site and mutation of the HIF-1α -binding site, within the SKA2 promoter, mutations within the miR-301a/ miR-454 -binding sites in the ET-1 and PAI-1 3′-UTRs were all carried out using the Q5 site-directed mutagenesis kit (New England Biolabs) in the corresponding parental vectors using primers listed in Table 1. All constructs and mutations were verified by sequencing. [score:3]
miR-301a and miR-454 target 3′-UTR of ET-1 and attenuate ET-1 mRNA and protein levels In silico analysis of the 3′-UTR of ET-1 mRNA predicted miR-301a/ miR-454 miRNA recognition element (MRE) sequences at nucleotides +45/+65 and +572/+593, as depicted in the schematic of Figure 3(A). [score:3]
We found that fenofibrate treatment of HMEC induced the co -expression of SKA2, the precursors of miR-301a and miR-454 and their mature forms. [score:3]
Figure 2(A) Effect of PPAR-α agonist (fenofibrate) and its antagonist (GW6471) on SKA2, pre- miR-301a and pre- miR-454 RNA expression. [score:3]
A physiological relationship between miR-301a and miR-454 was demonstrated in vitro, as both miRNAs attenuated PlGF -mediated secretion, in human microvascular endothelial cell line (HMEC-1), of both ET-1 and PAI-1. Moreover, these miRNAs co-located in an intron of the spindle and kinetochore -associated protein-2 (SKA2) gene were co-transcriptionally regulated by peroxisome proliferator-activated receptor-α (PPAR-α) and HIF-1α. [score:2]
miR-301a and miR-454, located in the first intron of host gene SKA2, are co-transcriptionally regulated by PPAR-α and HIF-1α. [score:2]
Thus co-regulated reduction in miR-301a and miR-454 appears to significantly contribute to the observed increase in ET-1 and PAI-1 seen in SCD. [score:2]
HMEC cells were transfected with wt pGL3-3′-UTR-ET-1 luc reporter along with indicated miRNA mimics, followed by PlGF treatment for 6 h. (D) Effect of mutation of MRE sites for miR-301a/ miR-454 in wt 3′-UTR-ET-1 luc. [score:2]
However, mutation of the MRE sites located at nt +1367/+1370 (M1) and at positions +1657/+1660 (M2) of the PAI-1 3′-UTR (see schematic in Figure 4A) in the luciferase reporter gene, prevented either exogenous miR-301a or miR-454 from negatively affecting luciferase activity (Figure 4D). [score:2]
Next, we examined whether mutation of MRE sites for miR-301a/ miR-454 in pGL3-PAI-3′-UTR affected reporter activity with exogenous miR-301a and miR-454. [score:2]
As we show in this report, miR-454 is also functional as a post-transcriptional regulator of PAI-1 synthesis and co-synthesized with miR-301a, consequently it was necessary to establish that miR-454 levels paralleled miR-301a in both normal and in SCD. [score:2]
Furthermore, the expression of pre- miR-301a was significantly reduced in lung tissues harvested from sickle mouse mo del [Berkeley sickle mice (BK-SS)] animals compared with C57BK/6NJ controls. [score:2]
As shown in Figure 5(A), miR-301a expression in lung tissue from BK-SS mice compared with control mice was not significantly different. [score:2]
The present study, to the best of our knowledge, is the first demonstration that PPAR-α co-regulates the transcription of SKA2, miR-301a and miR-454; the ET-1 mRNA has complementary sites in the 3′-UTR for the seed sequences of these miRNAs. [score:2]
Thus our studies provide a mechanistic basis for fenofibrate -mediated transcriptional regulation of miR-301a and miR-454 in the present study and miR-199a2 [25] as a rational therapeutic approach to attenuate elevated levels of ET-1 and PAI-1 observed in PH of SCD. [score:2]
miR-454 expression in vivoWe previously demonstrated miR-301a levels are depressed in SCD subjects compared with matching controls [24]. [score:2]
In silico analysis of the 3′-UTR of ET-1 mRNA predicted miR-301a/ miR-454 miRNA recognition element (MRE) sequences at nucleotides +45/+65 and +572/+593, as depicted in the schematic of Figure 3(A). [score:1]
Additionally a re-analysis of the PAI-1 mRNA showed two additional miR-301a sites in its 3′-UTR. [score:1]
Moreover, the induction of SKA2 mRNA, pre- miR-301a and pre- miR-454 was reduced by >80% by GW6471 (Figure 2A). [score:1]
Treatment of HMEC with fenofibrate resulted in a ∼3-fold increase in SKA2 mRNA, pre- miR-301a and pre- miR-454. [score:1]
Our studies showed that lung tissues from BK-SS mice displayed reduced levels of miR-301a consistent with the observation in human SCD patients. [score:1]
We previously showed that miR-301a is depressed in plasma from BK-SS mice [24]. [score:1]
This reporter responded to synthetic miR-301a and miR-454 mimics like endogenous ET-1 mRNA. [score:1]
As shown in Figure 4(B), transfection with miR-301a and miR-454 mimics in HMEC and HPMVEC reduced PlGF -induced PAI-1 mRNA to basal level and below basal level, respectively. [score:1]
The bases in bold font indicate seed sequences of miR-301a/ miR-454 and the base substitutions in the MRE sequences are indicated by asterisks in panel A. HMEC were transfected with wild type PAI-1 3′-UTR-luc or the indicated PAI-1 3′-UTR mutant constructs (M1 or M2) along with either miR-301a or miR-454. [score:1]
The sequences of predicted miR-301a-/ miR-454 -binding sites within ET-1 3′-UTR are shown in panel A. The bases in bold font indicate seed sequences of miR-301a/ miR-454 and the base substitutions created in the corresponding MRE sequences are indicated by asterisks in panel A. HMEC were transfected with wild type ET-1 3′-UTR-luc or the indicated ET-1 3′-UTR mutant constructs (M1 or M2) along with either synthetic miR-301a or miR-454. [score:1]
Thus, we examined the effects of exogenous miR-301a and miR-454 on PlGF -induced PAI-1 mRNA levels in both HMEC and HPMVEC. [score:1]
This was demonstrated using shRNAs specific for PPAR-α and HIF-1α, which antagonized production of SKA2 mRNA as well as both miR-301a and miR-454. [score:1]
Taken together these data showed that pre- miR-301a and pre- miR-454 were co-transcribed with the SKA2 primary transcript, induced by PlGF, and were not products of a secondary transcription unit within the SKA2 intron. [score:1]
HMEC and HPMVEC cells were transfected with miR-301a mimic (90 pmol), miR-454 mimic (90 pmol) or control (NC mimic) overnight, followed by treatment with PlGF for 6 h. (C) Effect of miR-301a and miR-454 synthetic mimics on 3′-UTR-ET-1-luciferase activity. [score:1]
Thus miR-301a and miR-454 comprised a miRNA set which potentially interacted with PAI-1 mRNA. [score:1]
This became of interest because both miR-301a and miR-454 are co-synthesized from the SKA2 transcription unit. [score:1]
The sequences of predicted miR-301a-/ miR-454 -binding sites within PAI-1 3′-UTR are shown. [score:1]
HMEC and HPMVEC cells were transfected with synthetic miR-301a mimic (90 pmol), miR-454 mimic (90 pmol) or control (NC mimic) as described in Figure 3 legend. [score:1]
In silico analysis showed miR-301a is located in the first intron of the SKA2 gene and is co-localized with miR-454 as shown in the gene schematic (Figure 1A). [score:1]
The latter sites have complementarity to the seed region of miR-301a and were also identified as potential miR-454 -binding sites (www. [score:1]
These data showed that both MREs in the 3′-UTR of ET-1 mRNA were required for functional effects of miR-301a and miR-454. [score:1]
Although the miRNA genes are in the correct polarity to be part of the SKA2 transcription unit, it was still conceivable that a smaller transcription unit within the intron was responsible for miR-301a/ miR-454 synthesis. [score:1]
In silico analysis of the 3′-UTR of PAI-1 mRNA showed the presence of miR-301a/ miR-454 recognition elements at nt +1351/+1373 and at nt +1641/+1663 as depicted in the schematic of Figure 4(A). [score:1]
Indeed, PlGF -mediated induction of PAI-1 was achieved by a transcriptional mechanism involving HIF-1α [23] and post-transcriptionally by specific miRNAs (miR-30c and miR-301a) that bind to the 3′-UTR of PAI-1 mRNA [24]. [score:1]
pl) predicted the site at nt +422 to +444 [24], but not the miR-301a sites at nt+1351/+1373 and nt +1641/+1663. [score:1]
As shown in Figure 3B, transfection with both miR-301a and miR-454 mimics reduced PlGF -mediated ET-1 mRNA to basal levels. [score:1]
HMEC cells were pre -treated with GW6471 (15 μM) for 30 min, where indicated, followed by treatment with fenofibrate (100 μM) for 2 h. (B) Effect of fenofibrate on induction of mature miR-301a and miR-454. [score:1]
Mice do not have an orthologue for human miR-454, although the location of miR-301a is syntenic between human and mouse. [score:1]
The first intron of SKA2 gene includes genes for miR-301a and miR-454. [score:1]
The sum of these studies showed that miR-301a and miR-454 could be induced in situ by fenofibrate to antagonize PlGF-induction of PAI-1 synthesis and secretion. [score:1]
In order to clearly establish the relationship between the putative miRNA recognition sites in the ET-1 3′-UTR and miR-301a and miR-454, we mutated both MREs for miR-301a/ miR-454 in pGL3-ET-1 3′-UTR-luc. [score:1]
[1 to 20 of 93 sentences]
3
[+] score: 203
Other miRNAs from this paper: hsa-mir-21, hsa-mir-301b
The experiments in our study were done by ISH on the FFPE tissue, unlike qRT-PCR, ISH could not only semi-quantitative the expression of target gene, but also roughly localize the cell type of the expressed miR-301a on FFPE block section. [score:7]
The OS of BC patients with high miR-301a expression was significantly higher than that of those patients with low miR-301 expression. [score:5]
Data from the Kaplan-Meier Plotter database showed that patients with high expression levels of miR-301a showed a significantly worse OS time than those with low expression levels of miR-301a in both the METABRIC and TCGA databases (Fig.   4a and b, P = 0.001 & P = 0.0039, respectively). [score:5]
Then, the correlations of miR-301a expression with clinicopathological characteristics of patients were statistically analysed and are presented in Table  1. The correlations between miR-301a expression and other parameters were analysed using chi-square tests and are also presented in Table  1. There was a slightly higher chance for the postmenopausal patients to have positive miR-301a expression than the premenopausal group (21.3% vs. [score:5]
As shown in Table  2, high miR-301a expression along with middle tumour size (>2,≤5 cm), lymph node metastasis, high clinical stage and molecular subtype (HER-2 overexpresstion or TNBC) were responsible for poor DFS in BC patients. [score:5]
Here, our study first validated miR-301a expression level and detected the expression of miR-301a and its precise role in 380 BC tissues from both TNBC and non-TNBC patients and analysed its clinicopathological and prognostic significance. [score:5]
Specifically, in the TNBC subgroup, there was a 30.6% difference in DFS at 5 years between patients with high-miR-301a expression tumours versus low-miR-301a expression tumours (55.3% vs. [score:5]
In the non-TNBC subgroup, the 5-year DFS and OS of patients whose tumours expressed high levels of miR-301a were only 56.1% and 83.4%, whereas the DFS and OS of those with low levels of miR-301a expression were 91.7% and 95.4%, respectively. [score:5]
Based on a study by Shi et al., a novel oncogenic role for miR-301 through the regulation of key signalling pathways involving PTEN, FOXF2, and Col2A1 was identified, and miR-301 overexpression was associated with an increased risk of distant relapse and resistance to tamoxifen [26]. [score:4]
Kaplan-Meier survival estimates demonstrated that patients with high expression levels of miR-301a had shorter DFS and OS compared to those with low expression levels of miR-301a in both the TNBC (P = 0.000 & P = 0.000, respectively; Fig.   2b and e) and non-TNBC (P = 0.000 & P = 0.003, respectively; Fig.   2d and f) subgroups. [score:4]
These results indicated that downregulation of miR-301a might be correlated with better survival of BC patients. [score:4]
The 5-year DFS of the high-miR-301a expression group (60.5%) was significantly reduced compared to that of low-miR-301a expression group (90.7%; P = 0.000; Fig.   2a). [score:4]
Moreover, the 5-year OS of the high-miR-301a expression group (74.5%) was significantly reduced compared to that of low-miR-301a expression group (96.1%; P = 0.000; Fig.   2d). [score:4]
Cumulative DFS curves of breast cancer compared patients who received taxane -based chemotherapy with patients who received other chemotherapy in the overall population (a), subgroup with miR-301a negative expression status (b) and subgroup with miR-301a positive expression status (c). [score:4]
Furthermore, previous data failed to validate altered expression of miR-301a in the blood of women with luminal A-like breast cancer, but the concept of a panel or profile of miRNAs for diagnostic purposes is a realistic approach, and to date, combined miRNAs have been reported with higher sensitivity, specificity and reproducibility [38]. [score:3]
Kaplan-Meier curves showing the relationships between miR-301a expression and DFS (a– c) and OS (d– f) in patients with breast cancer (a and d), all breast cancer patients; (b and e), triple -negative breast cancer patients; (c and f), non-triple -negative breast cancer patients). [score:3]
The expression level of miR-301a was prognostic in not only the TNBC subgroup but also the non-TNBC subgroup. [score:3]
More importantly, both the univariate and multivariate survival analyses demonstrated that high miR-301a expression was correlated with shorter DFS and OS in BC patients, which was also consistent with the prognostic significance of miR-301 in other human malignancies, such as gastric cancer [17] and melanoma [18]. [score:3]
To further understand the potential prognostic value of miR-301a on the clinical outcome of breast cancer, the online webtool Kaplan-Meier Plotter was used to determine the prognostic value of the target gene in public breast cancer databases [33]. [score:3]
For example, miR-301a has been described as a potential marker for metastasis in prostate cancer, and its high expression was associated with an increased risk of recurrence [16]. [score:3]
There were no significant correlations between miR-301a expression and variables such as age, tumour size, tumour grade, lymph node status, cancer stage, hormone receptors, HER2 or molecular subtype (P > 0.05). [score:3]
Representative immunostaining images of miR-301a expression are presented in Fig.   1. The average age of all patients was 51.6 years (SD 9.9, median age 50, IQR 45–58 years) at the time of diagnosis. [score:3]
High miR-301a expression was significantly associated with larger tumour size, lymph node metastasis and poor OS for patients with TNBC. [score:3]
First, as the number of patients in this study is smaller, a larger case population is needed to confirm the prognostic value of miR-301a expression in BC. [score:3]
The precise mechanism(s) and targets of miR-301a in breast cancer are not fully elucidated. [score:3]
The relative expression of miR-301a was determined in 380 BC tissue samples. [score:3]
It was shown that a high level of miR-301a expression was an independent molecular biomarker for predicting DFS (HR: 0.193, 95% CI: 0.118–0.316, P = 0.000) and OS (HR: 0.162, 95% CI: 0.073–0.361, P = 0.000) in BC patients (Tables  2 & 3). [score:3]
Despite these previous studies, the validation of miR-301a expression level and its precise role in a whole BC population is still needed. [score:3]
As most studies have concluded, miRNA-301a was identified as an oncogenic miR, which played an important role in activating tumour cell invasion/migration, promoting cell proliferation, inhibiting apoptosis and enhancing chemosensitivity both in vitro and in vivo. [score:3]
These results suggest that analysing miR-301a expression in the breast tissue biopsy specimen at the time of diagnosis could have the potential to identify patients who are at high risk for developing metastasis as well as patients who might be candidates for active surveillance. [score:3]
As mentioned in the staining evaluation, all patients were divided into two groups: high miR-301a expression levels (=3) were detected in 141 (37.1%) of 380 tumours, and low miR-301a expression levels (≤2) were detected in the remaining 239 (62.9%) tumours. [score:3]
We validated our results that higher expression of miR-301a is associated with decreased OS in independent overall public breast cancer databases such as TCGA and METABRIC as well, which provided another powerful piece of evidence to confirm the prognostic value of miR-301a. [score:3]
miR-301a may serve as a potential therapeutic target in patients with breast cancer. [score:3]
Among the 83 patients who experienced disease recurrence or metastasis, 61 patients (73.5%) were miR-301a positive and 22 (26.5%) were negative. [score:3]
Therefore, in this study, we aimed to profile its exact expression level and to identify the potential prognostic role of miR-301a as a biomarker for BC. [score:3]
However, the study has revealed that miR-301a expression was correlated with a poor prognosis only in the specific subtype TNBC [22]. [score:3]
In patients with positive miR-301a expression, patients who had received taxane -based chemotherapy had a better clinical outcome than those who had received other chemotherapy (P = 0.016, Fig.   3c). [score:3]
In situ hybridization for miR-301aWe used ISH to detect miR-301a expression with a digoxigenin(DIG) -labelled miRCURY LNA [TM] probe on TMA sections. [score:3]
Our results were consistent with the basic studies showing that overexpression of miR-301a was more aggressive and played a role in breast cancer progression and metastasis. [score:3]
In the clinical study, the expression level of miR-301a was examined by quantitative reverse transcription polymerase chain reaction (qRT-PCR) in 118 pairs of TNBC tumours [22]. [score:3]
Consistent with findings in previous studies, our results indicated that the status of miR-301a expression in tissues was significantly correlated with poor DFS and OS in breast cancer patients. [score:3]
In BC, studies have revealed that miR-301a expression was also elevated markedly and correlated with a poor prognosis in the specific subtype TNBC 22, 23. [score:3]
The relationships between miR-301a expression and clinicopathological parameters were examined using Pearson’s χ [2] tests or Fisher’s exact tests when necessary. [score:3]
We used ISH to detect miR-301a expression with a digoxigenin(DIG) -labelled miRCURY LNA [TM] probe on TMA sections. [score:3]
Patients expressing high levels of miR-301a had a significantly shorter DFS and OS. [score:3]
Overexpressed miR-301a has also been observed in gastric cancer as well [17]. [score:3]
We analysed the relationship between miR-301a expression and prognosis. [score:3]
Since most of our patients accepted tamoxifen, we were unable to test if expression of miR-301a was relevant to endocrine resistance. [score:3]
MiR-301a expression is associated with clinical survival outcomes in BC patients. [score:2]
To test the clinical relevance of the dysregulated miR-301a in BC, the data were subjected to a survival analysis based on publicly available datasets. [score:2]
MiR-301a has been demonstrated to have prognostic value in both TNBC and non-TNBC patients, our data added weight to the theory that TNBC patients with positive expression of miR-301a would have worse prognosis when compared with non-TNBC patients. [score:2]
You can tell by the intuitionistic Kaplan-Meier curves in Fig.   3 that even patients with positive miR-301a who received taxane -based chemotherapy had a significantly worse disease free survival rate when compared with those with negative miR-301a who received other chemotherapy. [score:2]
Based on literature search, miR-301a specifically has not been published to have any relationship with chemoresistance. [score:1]
Kaplan-Meier analyses, timetables and log-rank tests were used to calculate the effect of miR-301a expression on patient survival and 5-year survival. [score:1]
In situ hybridization for miR-301a. [score:1]
MiR-301a has been reported to be dysregulated not only in breast cancer 22, 23, 26 but also in a variety of malignant tumours, including prostate, gastric, pancreatic, lung, blood, colourectal, and melanoma 17– 19, 21, 25, 27– 29. [score:1]
We learned from data reported by Ma et al. that miR-301a enforced its oncogenic function in breast cancer via inactivating PTEN, consequently activating the Wnt/β-catenin pathway [23]. [score:1]
However, in our study, the patients with positive miR-301a status derived more benefit from taxane based chemotherapy than those with negative miR-301a status. [score:1]
However, a better response to taxane was not observed among miR-301a negative patients (P = 0.350, Fig.   3b). [score:1]
Here, we utilized Kaplan-Meier Plotter to test miR-301a as a biomarker of breast cancer survival [33]. [score:1]
As in our previous studies 31, 32, a staining grade ≤ 2 was defined as miR-301a -negative staining, whereas only grade 3 staining was defined as positive staining. [score:1]
We next investigated the response to chemotherapy according to expression status of miR-301a. [score:1]
The DIG -labelled miRCURY LNA [TM] detection probe for miR-301a was purchased from Exiqon (Vedbeak, Denmark) and the Enhanced Sensitive ISH Detection Kits were from Boster (Wuhan, China). [score:1]
Figure 1Identification of miR-301a in breast tumours by in situ hybridization (ISH). [score:1]
Accumulating evidence indicates that miR-301a acts as an oncomiR, and it has been related to tumour progression in several types of cancer. [score:1]
We are working on the signal pathway and chemosensitivity of miR-301a using cell lines and samples from a pre-designed neoadjuvant chemotherapy project. [score:1]
Intronic miR-301a, which is one of two mature forms of miR-301 (miR-301a and miR-301b), and its host gene, SKA2 (spindle and kinetochore -associated protein 2), are located on chromosome 17q22–23 in the human genome [25]. [score:1]
Next, univariate analyses were performed to evaluate the expression of miR-301a and other clinicopathologic features on the prognosis of BC patients. [score:1]
More clinic and basic research is required to elucidate the mechanism of sensitivity and/or resistance to taxane -based chemotherapy in the miR-301a -positive patients in our study population. [score:1]
Here, the focus is on miR-301. [score:1]
This suggested that miRNA-301a may act as an oncogene in cancer and might provide helpful therapeutic strategies in clinical application. [score:1]
Representative staining of miR-301a in low-magnification (100×) and high-magnification (400×) images. [score:1]
miR-301a was mainly localized in the cytoplasm of breast cancer cells. [score:1]
Patients’ characteristics and miR-301a expression pattern. [score:1]
In conclusion, this study provides new insights into the role of miR-301a, not only in TNBC tumours but also in non-TNBC tumours. [score:1]
Our study demonstrated that miR-301a played a role in not only the TNBC subgroup but also non-TNBC patients. [score:1]
However, there are limited data regarding miR-301a and breast tumours; we found several papers focusing on basic research and only one on clinical research correlating miR-301a with TNBC. [score:1]
We tried to perform subgroup analyses, and the data indicated that miR-301a is associated with a poor overall survival in the lymph node -positive subgroup and has a trend to be significantly related to a decreased OS in the TNBC subgroup based on data from the TCGA database (data not shown). [score:1]
The difference in OS at 5 years between high-miR-301a and low-miR-301a TNBC tumours was 27.1% (68% vs. [score:1]
[1 to 20 of 79 sentences]
4
[+] score: 190
Other miRNAs from this paper: mmu-mir-301a, hsa-mir-20b, mmu-mir-20b, mmu-mir-208b, hsa-mir-208b
MiR-301a-5p directly suppressed the expression of MITF, HDGF, and inhibited the MDM-4 expression to upregulation of p53 during VAN treatment in HK-2 cells. [score:12]
First, inhibition of miR-301a-5p markedly increased expression levels of anti-apoptosis genes of HDGF and MITF, and also upregulated MDM-4 to inhibit p53 expression (Figures 6a and b). [score:12]
In HK-2 cells and mouse mo dels, inhibition of MBD2 downregulates miR-301a-5p to restore anti-apoptosis genes expression including HDGF and MITF, and also increase MDM-4 expression for reduction of p53. [score:10]
Hence, we proposed that miR-301a-5p induced cell apoptosis by suppressing anti-apoptosis genes including HDGF and MITF, and also inhibiting the MDM-4 expression to upregulate p53. [score:10]
Collectively, these data reveal a novel regulatory mechanism by which MBD2 induces miR-301a-5p to suppress the expression of HDGF and MITF, and also inhibit MDM-4 for p53 activation in HK-2 cells (Figure 14). [score:8]
MBD2 siRNA ameliorated VAN induced the expression of MBD2, BAX and active caspase 3. The expression of miR-301a-5p after VAN treatment is suppressed by MBD2 siRNA in HK-2 cells. [score:7]
The target genes of miR-301a-5p were restored, and the expression of p53, BAX and active caspase 3 were suppressed during VAN treatment in MBD2- KO mice. [score:7]
First, we found that miR-301a-5p was significantly upregulated by VAN treatment in vitro and in vivo at indicated time points, which was markedly suppressed in siRNA MBD2 and MBD2 KO mice (Figures 4d and e, and Figure 10). [score:6]
Moreover, we have identified that MBD2 may induce miR-301a-5p to suppress anti-apoptosis genes including HDGF and MITF, and inhibit MDM-4 for p53 activation, together resulting in cell apoptosis and renal injury. [score:5]
These data for the first time suggest that inhibition of miR-301a-5p significantly ameliorates VAN -induced renal cell apoptosis and renal injury in vitro and in vivo (Figures 7 and 13), which indicated that miR-301a-5p may act as an apoptosis promoter, and thus may be referred as a potential therapeutic target for VAN -induced AKI. [score:5]
However, miR-301a-5p as a potential new therapeutic target for other diseases could be further explored. [score:5]
Mechanically, miR-301a-5p suppressed anti-apoptosis genes including HDGF and MITF, and also inhibited MDM-4 for p53 activation. [score:5]
The results revealed that MBD2 induced miR-301a-5p to suppress the expression of HDGF, MITF, and inbitit MDM-4 for p53 activation. [score:5]
Finally, northern blot analysis of the miR-301a-5p, on days 3 and 7 after VAN treatment, it was markedly downregulated in MBD2- KO mice than in WT mice (Figures 10c and d). [score:4]
12, 15In current study, we found that MBD2 induced MiR-301a-5p to suppress the expression of HDGF, MITF and MDM-4 for cell apoptosis during VAN treatment in vitro. [score:4]
[28] The two downregulated miRNAs, miR-208b-3p induced apoptosis in myocardial cell, [29] however, the role of miR-301a-5p in apoptosis remains unclear (Figure 4b). [score:4]
These data demonstrate that MBD2 regulates the expression of miR-301a-5p. [score:4]
To supply more direct evidence that miR-301a-5p targets HDGF, MITF, and MDM-4, wild-type and mutant luciferase reporter plasmids containing HDGF, MITF and MDM-4 3'-UTR region were co -transfected with a miR-301a-5p analog or a miRNA analog negative control (miR-NAC). [score:4]
As MBD2 involved in methylation regulation, we guess that MBD2 could activate miR-301a-5p by suppression of methylation. [score:4]
As the most remarkable changes were seen in miR-301a-5p, the studies were extended and its expression was also assessed by northern blot analyses in HK-2 cells. [score:3]
These data confirmed our previous in vitro findings that miR-301a-5p is a target of MBD2. [score:3]
Although MBD2 induced the expression of miR-301a-5p in HK-2 cells, the role of miR-301a-5p remains unclear in VAN -induced cells apoptosis. [score:3]
Second, our luciferase reporter assay identified MITF, HDGF and MDM-4 as a target gene of miR-301a-5p in HK-2 cells, and further MDM-4-silencing in HK-2 cells significantly enhanced the p53 accumulation (Figures 6c and d), which was supported by a previous study that MDM-4 was an essential for negative regulation of p53. [score:3]
The expression of miR-208b-3p, miR-301a-5p, miR-1273g-3p and miR-20b-3p was confirmed by real-time PCR (Figure 4c), which is consistent with microarray analysis. [score:3]
Inhibition of miR-301a-5p ameliorated renal dysfunction, renal injury in VAN nephrotoxic AKI mice. [score:3]
MBD2 activates methylated miR-301a-5p promoter activity by suppressing methylation of promoter. [score:3]
As shown in Figure 6a, VAN markedly induced apoptosis in HK-2 cells, which was further inhibited by anti-miR-301a-5p. [score:3]
Our results indicated that MBD2 directly regulated miR-301a-5p, which was supported by evidences as described below. [score:3]
[33] In addition, we also identified MITF, HDGF and MDM-4 as target genes of miR-301a-5p by the prediction of miRBASE (http://mirdb. [score:3]
Although inhibition of miR-301a-5p reduced the apoptosis in vitro, the role of miR-301a-5p in the pathogenesis of VAN nephrotoxic AKI remains unclear. [score:3]
We found that VAN treatment significantly induced activation of p53 and the expression of BAX, less cleaved/active caspase 3, and reduced HDGF, MITF and MDM-4 protein, which was significantly reversed by anti-miR-301a-5p treatment (Figures 7b and c). [score:3]
After VAN treatment, the miR-301a-5p expression increases notably by 12 h, and by 24 h a steep increase was observed. [score:3]
[28] The expression levels of miR-208b-3p and miR-301a-5p were consistently high in VAN group, which was decreased in siRNA MBD2 with VAN group. [score:3]
Furthermore, we construct CpG-free pCpGI luciferase reporter plasmid that included CG DNA methylation target sequences in promoter region of miR-301a-5p. [score:3]
To further depth understanding of molecular mechanism of MBD2 for regulation of apoptosis, we focus on the miR-301a-5p. [score:2]
Although miR-301a-5p is responsible for the HK-2 cells apoptosis, the regulation mechanism of it remains unclear. [score:2]
As shown in Figure 5b, the antibody directed against MBD2 immunoprecipitated the DNA fragments from HK-2 cells containing the potential binding sites of mBS1-5, supporting the hypothesis that MBD2 can physically interact with the miR-301a-5p promoter region. [score:2]
Compared with naked methylated DNA, the methylated miR-301a-5p pCpGI was demethylated in endogenous MBD2-bound DNA, the demethylation of it was further enhanced in ecpotic MBD2 expression (Figure 5d). [score:2]
42, 43 HK-2 cells were cultured in Dulbecco’s modified Eagle’s medium (Sigma-Aldrich) supplemented with 10% fetal bovine serum, 0.5% penicillin and streptomycin in 5% CO [2] incubator at 37° C. For transfection experiment, transfection of miR-301a-5p analog (100 nM) or negative control (miR-neg; Sigma, St. [score:1]
Construction of methylation promoter of miR-301a-5p CpG-free pCpGI luciferase reporter, MBD2 and mtMBD2 (the deletion of the methylated DNA -binding domain) plasmids as described previously. [score:1]
The miR-301a-5p induced by VAN was blocked in MBD2- KO mice. [score:1]
Histological analysis confirmed the VAN -induced kidney tissue damage, which was significantly ameliorated in anti-miR-301a-5p mice (Figure 13c). [score:1]
We examined whether the binding of MBD2 with the ectopic miR-301a-5p promoter region leads to a change in its methylation state. [score:1]
Male C57BL/6 mice were injected with LNA -modified antisense oligonucleotide of miR-301a-5p (anti-miR-301a-5p) or LNA -modified oligonucleotide of the scrambled sequence (scramble), levels of BUN and serum creatinine were similarly low in these mice, indicating normal renal function. [score:1]
At day 7 of VAN treatment, scrambled mice developed moderate renal failure, with 121.2 mg/dl BUN and 0.48 mg/dl serum creatinine, whereas anti-miR-301a-5p mice had 62.6 mg/dl BUN and 0.24 mg/dl serum creatinine (Figures 13a and b). [score:1]
To clarify its role, HK-2 cells were treated with anti-miR-301a-5p treatment. [score:1]
In addition, the experiment on role of miR-301a-5p, male C57BL/6 mice were injected by tail vein with or without 20 mg/kg LNA -modified antisense oligonucleotide of miR-301a-5p (anti-miR-301a-5p) or LNA -modified oligonucleotide of scrambled sequence (scrambled) for 7 days. [score:1]
In addition, MBD2 activates the miR-301a-5p promoter via reducing the metalyation (Figures 5c and d). [score:1]
In vitro studies have demonstrated that miR-301a-5p mediates apoptosis during VAN treatment. [score:1]
Second, as shown in the saline group (Figure 10b), level of miR-301a-5p was likewise low in these mice, after VAN treatment, it was markedly increased in MBD2-WT mice, which was ameliorated in tissues of MBD2- KO mice. [score:1]
After co -transfected with MBD2 plasmid, the transcriptional activity of methylated miR-301a-5p pCpGI is significantly increased, it is not increased with the mutant plasmid of MBD2 methylated DNA binding domain deletion (Figure 5c). [score:1]
These data show that binding of MBD2 to promoter of miR-301a-5p is associated with demethylation. [score:1]
In current experiment, first, real-time PCR showed that VAN induced significant increase of miR-301a-5p on day 1, and gradually increase of it on days 3 and 7 (Figure 10a). [score:1]
In scrambled mice, the tubular damage score was 3.9 after VAN AKI, whereas the score was markedly decreased to 1.3 after VAN AKI for anti-miR-301a-5p tissues (Figure 13d). [score:1]
[1 to 20 of 54 sentences]
5
[+] score: 131
Hypoxia led to p38 and JNK phosphorylation, which was inhibited by miRNA-301a overexpression, and miRNA-301a inhibitor treatment interrupted the inhibitory effect of miRNA-301a on p38 and JNK phosphorylation (Figure 4B). [score:9]
Hypoxia consistently caused increased ASK1 mRNA and protein expression levels, as shown in Figure 1, whereas miRNA-301a mimic treatment caused decreases in ASK protein expression and phosphorylation as well as ASK1 mRNA expression. [score:7]
To determine whether miRNA-301a regulates cell survival by targeting ASK1 under hypoxic conditions, cell viability was examined under hypoxic conditions, followed by treatment with a miR-301a mimic or inhibitor. [score:6]
In our study, as miRNA-301a expressed by stem cells could be released into the adjacent environment, which includes other cell types, determining the effect of miRNA-301a on regulating ASK1 expression in other cardiac cell types is important. [score:6]
To investigate the signaling molecules that are regulated by miRNA-301a, which target ASK1 under hypoxic conditions, we first examined the ASK1 mRNA and protein expression levels under hypoxic conditions with or without miRNA-301a overexpression. [score:6]
We used a miRNA that targets ASK1 as a regulatory tool to modulate ASK1 expression and stem cell activation under hypoxic conditions and investigated the regulatory effect of miRNA-301a on ASK1 -mediated apoptosis in hASCs. [score:5]
In this study, we investigated the overexpression of miRNA-301a in human ASCs (hASCs) and found that this miRNA increased cell survival by inhibiting ASK1 expression under hypoxic conditions. [score:5]
We also observed that the expression level of ASK1 was associated with cell death, and that miRNA-301a overexpression could attenuate the activation of hypoxia -induced apoptotic signaling in hASCs. [score:5]
Our data indicated that miRNA-301a suppressed the hypoxia -induced expression and activation of proapoptosis-related factors (JNK, p38, and NFκB). [score:5]
miRNA-301a mimic treatment showed a significant protective effect against cell death, but a miRNA-301a inhibitor blocked the protective effect of miRNA-301a overexpression (Figure 3A). [score:5]
Considering these findings, we speculate that controversial effects may not occur among different cell types, and we anticipate a consistent effect of miRNA-301a regulation of ASK1 expression and activation on hASCs [miR-301] transplanted into infarcted hearts. [score:4]
2.4. miRNA-301a Represses the Apoptotic Pathway via Down-Regulation of the ASK1-Mediated Signaling Pathway during Hypoxia. [score:4]
To determine whether miRNA-301a regulates the ASK1 -mediated apoptotic pathway, we examined JNK and p38 activation under hypoxic conditions with or without miRNA-301a overexpression. [score:4]
Moreover, the regulation of ASK1 expression and activation by miRNA-301a considerably improved stem cell survival and increased ischemic heart function (Figure 5). [score:4]
As an apoptosis -associated transcription factor, NFκB was investigated to determine the anti-apoptotic effect of ASK1 inhibition by miRNA-301a overexpression. [score:3]
Mature miRNA-301a mimics (Genolution Pharmaceuticals, Seoul, Korea) and miRNA-301a inhibitors (Integrated DNA Technologies, Coralville, IA, USA) were used at final concentrations of 50 nM. [score:3]
Hypoxic stress resulted in NFκB phosphorylation, whereas miRNA-301a mimic treatment attenuated NFκB phosphorylation; this effect was reversed by miRNA-301a inhibitor treatment (Figure 4B). [score:3]
miRNA-301a was not able to inhibit caspase 3 activation (Figure S6). [score:3]
Therefore, we further examined caspase 3 activation to determine whether miRNA-301a inhibits the mitochondrial -dependent apoptosis mediated by ASK1. [score:3]
The threshold cycle (C [t]) of miR-301a and U6 expression was automatically defined, located in the linear amplification phase of the PCR, and normalized to the control U6 (Δ C [t] value). [score:3]
Additionally, these effects were reversed by miR-301a inhibitor treatment of these cells (Figure 4A,B). [score:3]
We investigated the protective effects of ASK1 inhibition by candidate miRNA transfection on cell death under hypoxic conditions, and we found that around eight miRNAs, including miR-301a overexpression, showed the protective effect against cell death (Figure S2). [score:3]
In addition, we confirmed that endogenous miR-301a expression decreased until 24 h in hASCs under hypoxic conditions (Figure 2D). [score:3]
Patel N. Tahara S. M. Malik P. Kalra V. K. Involvement of mir-30c and mir-301a in immediate induction of plasminogen activator inhibitor-1 by placental growth factor in human pulmonary endothelial cells Biochem. [score:3]
Although we did not investigate these proteins which can support ASK1 function in the present study, miRNA-301a inhibited ASK1 phosphorylation through transcriptional and translational repression of ASK1, resulting in the attenuation of cell death (Figure 3 and Figure 4). [score:3]
2.2. miRNA-301a Targeted ASK1 in hASCs. [score:3]
This study is the first demonstration of ASK1 modulation using a miRNA in transplanted stem cells in a MI mo del and suggests that the suppression of ASK1 by miRNA-301a is a promising approach to prevent massive death of stem cells after transplantation. [score:3]
Then, we used an annexin V assay to test the anti-apoptotic effect of miRNA-301a under hypoxic conditions and confirmed the anti-apoptotic effect of ASK1 inhibition using miRNA-301a under hypoxic conditions (Figure 3B and Figure S4). [score:2]
Luciferase assay using vectors containing the 3′ UTR of ASK1 confirmed that miRNA-301a targets ASK1 (Figure 2C). [score:2]
Additionally, miRNA-301a treatment was capable of attenuating hASCs apoptosis by regulating cytosolic in hypoxia -treated cells and in a MI heart. [score:2]
2.3. miRNA-301a Has Anti-Apoptotic Effects on hASCs under Hypoxic Conditions. [score:1]
To determine whether miRNA-301a -transfected hASCs (hASCs [miR-301]) have a therapeutic effect on ischemic myocardium, cardiac functional improvements by hASCs [miR-301] were analyzed in normal and MI rat hearts after hASC [miR-301] transplantation. [score:1]
The relative difference in the expression level of miR-301a in the sorted cells (ΔΔ C [t]) was calculated and presented as the fold induction (2–ΔΔ Ct). [score:1]
Although few studies have reported on an association between miRNA-301a and ASK1 in cardiomyocytes, the role of ASK1 in apoptosis has been well established. [score:1]
Figure 5C shows that transplanted hASCs [miR-301] had greater survivorship rates than transplanted hASCs at injected sites, with less cell death observed in hASCs [miR-301] injected heart tissue (Figure 5D). [score:1]
The fibrosis area was significantly reduced by hASCs [miR-301] injection in ischemic hearts (Figure 5B). [score:1]
miRNA-301a was also reported to be related to vascular dysfunction in human pulmonary endothelial cells [35]. [score:1]
Effect of hASC [miR-301] on Ischemic MyocardiumTo determine whether miRNA-301a -transfected hASCs (hASCs [miR-301]) have a therapeutic effect on ischemic myocardium, cardiac functional improvements by hASCs [miR-301] were analyzed in normal and MI rat hearts after hASC [miR-301] transplantation. [score:1]
Effect of hASC [miR-301] on Ischemic Myocardium. [score:1]
We found that the miRNA-301a binding site is highly conserved in the 3′ UTR of ASK1 mRNA. [score:1]
In addition, we further investigated the protective effect using siRNA for ASK1 under hypoxic conditions, as ASK1 is one of the major targets of miRNA-301a (Figure S3). [score:1]
[1 to 20 of 41 sentences]
6
[+] score: 51
miR-301a inhibition in CD4 [+] T cells reduced IL-17 secretion and the expression of Th17 marker genes, such as RORα, RORγt, and AhR; however, this inhibition did not affect TBX21 or FOXP3 expression. [score:9]
In the current study, the miRNA expression changes produced following the stimulation of CD3 [+] T cells with anti-CD3 antibodies suggests that Th17/Treg polarization was associated with the induction of miR-146a, miR-21, and miR-155 expression; that together with miR-301 up-regulation, this process would result in a Treg bias. [score:8]
OKT3 and FvFcR both up-regulated miR-301a expression in CD3 [+] T cells; OKT3 stimulation led to particularly strong expression (Fig.   2h). [score:8]
a miR-155, b miR-21, c miR-146a, d miR-210, e miR-17, f miR-590-5p, g miR-106b, h miR-301a miR-155 was consistently overexpressed following both antibody treatments: OKT3 seemed to induce stronger expression than FvFcR (Fig.   2a). [score:5]
a miR-155, b miR-21, c miR-146a, d miR-210, e miR-17, f miR-590-5p, g miR-106b, h miR-301a miR-155 was consistently overexpressed following both antibody treatments: OKT3 seemed to induce stronger expression than FvFcR (Fig.   2a). [score:5]
Eight of the tested miRNAs (miR-155, miR-21, miR-146a, miR-210, miR-17, miR-590-5p, miR-106b and miR-301a) were statistically significantly up- or down-regulated relative to untreated cells. [score:4]
This strong expression suggests that miR-301a modulates Th17 development [37]. [score:4]
miR-301a expression was particularly robust in Th17 cells both in vivo and in vitro. [score:3]
Furthermore, it has been reported that miR-301a inhibits PIAS3, a molecule known to interfere with the STAT3 signaling pathway [28, 37]. [score:3]
As they were the least variable, the CD3 [+] T cell expression profiles of eight distinct miRNAs, miR-155, miR-21, miR-146a, miR-210, miR-17, miR-590-5p, miR-106b and miR-301a, were further investigated (Fig.   2 and Additional file 1: Table S5). [score:1]
Treating PBMCs with anti-CD3 antibodies led to a consistent increase in miR-301a levels among CD3 [+] T cells. [score:1]
[1 to 20 of 11 sentences]
7
[+] score: 36
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-21, hsa-mir-23a, hsa-mir-27a, hsa-mir-29a, hsa-mir-101-1, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-16-2, hsa-mir-10a, hsa-mir-10b, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-181a-1, hsa-mir-223, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-23b, hsa-mir-27b, hsa-mir-146a, hsa-mir-150, hsa-mir-155, hsa-mir-181b-2, hsa-mir-29c, hsa-mir-101-2, hsa-mir-378a, hsa-mir-381, hsa-mir-340, hsa-mir-146b, hsa-mir-181d, hsa-mir-548a-1, hsa-mir-548b, hsa-mir-548a-2, hsa-mir-590, hsa-mir-548a-3, hsa-mir-548c, hsa-mir-548d-1, hsa-mir-548d-2, hsa-mir-378d-2, hsa-mir-301b, hsa-mir-548e, hsa-mir-548j, hsa-mir-548k, hsa-mir-548l, hsa-mir-548f-1, hsa-mir-548f-2, hsa-mir-548f-3, hsa-mir-548f-4, hsa-mir-548f-5, hsa-mir-548g, hsa-mir-548n, hsa-mir-548m, hsa-mir-548o, hsa-mir-548h-1, hsa-mir-548h-2, hsa-mir-548h-3, hsa-mir-548h-4, hsa-mir-548p, hsa-mir-548i-1, hsa-mir-548i-2, hsa-mir-548i-3, hsa-mir-548i-4, hsa-mir-548q, hsa-mir-548s, hsa-mir-378b, hsa-mir-548t, hsa-mir-548u, hsa-mir-548v, hsa-mir-548w, hsa-mir-548x, hsa-mir-378c, hsa-mir-23c, hsa-mir-548y, hsa-mir-548z, hsa-mir-548aa-1, hsa-mir-548aa-2, hsa-mir-548o-2, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-548h-5, hsa-mir-548ab, hsa-mir-378f, hsa-mir-378g, hsa-mir-548ac, hsa-mir-548ad, hsa-mir-548ae-1, hsa-mir-548ae-2, hsa-mir-548ag-1, hsa-mir-548ag-2, hsa-mir-548ah, hsa-mir-378h, hsa-mir-548ai, hsa-mir-548aj-1, hsa-mir-548aj-2, hsa-mir-548x-2, hsa-mir-548ak, hsa-mir-548al, hsa-mir-378i, hsa-mir-548am, hsa-mir-548an, hsa-mir-548ao, hsa-mir-548ap, hsa-mir-548aq, hsa-mir-548ar, hsa-mir-548as, hsa-mir-548at, hsa-mir-548au, hsa-mir-548av, hsa-mir-548aw, hsa-mir-548ax, hsa-mir-378j, hsa-mir-548ay, hsa-mir-548az, hsa-mir-548ba, hsa-mir-548bb, hsa-mir-548bc
Namely, HHV-6A specifically induced an early up-regulation of miR-590 (1 d. p. i. ), miR-15a and miR-21 (3 d. p. i. ), a sustained up-regulation of miR-29b, miR-101 (3 and 6 d. p. i. ), miR-301a and miR-548e (1 and 6 d. p. i. ) and a late up-regulation of miR-340 and miR-381 (6 d. p. i. ) By contrast, HHV-6B infection specifically up-modulated the expression of miR-301b (2 and 3 d. p. i. ) and miR-548e (1 and 3 d. p. i. ), whereas it down-regulated miR-590 (2 and 3 d. p. i. ) and miR-15a (6 d. p. i. ). [score:15]
In particular, both HHV-6A and 6B induced an early up-regulation of miR-301a and miR-548e (1 d. p. i. ), an increase of miR-101 and a decrease of miR-let-7c and miR-340 at 3 d. p. i., and a down-regulation of miR-23 at late time-points p. i. (6 d. p. i. ). [score:7]
On the contrary, the increase of miR-301a (up-regulated by both viruses) has been reported to block the IRF1 innate immune response against Japanese encephalitis virus and might therefore favor HHV-6 pathogenesis by inhibiting IFNβ production (Hazra et al., 2017). [score:6]
Interestingly, miR-301 was also up-regulated in T cells in the central nervous system of animals with experimental autoimmune encephalomyelitis (Mycko et al., 2012), an animal mo del for the process of autoimmune demyelination occurring during multiple sclerosis, a disease with a possible association with HHV-6 infection (Leibovitch and Jacobson, 2014). [score:6]
MicroRNA-301a regulation of a T-helper 17 immune response controls autoimmune demyelination. [score:1]
The host microRNA miR-301a blocks the IRF1 -mediated neuronal innate immune response to Japanese encephalitis virus infection. [score:1]
[1 to 20 of 6 sentences]
8
[+] score: 27
Other miRNAs from this paper: mmu-mir-301a, mmu-mir-200a, hsa-mir-200a
Several reports have already shown that i) miR-200a directly regulates A2, a receptor for the oncogene Eph, and decreases cancer cell migration via downstream activation of AMPKα [43], and ii) miR-301a appears to directly down-regulate AMPKα1 in osteosarcoma cells [44]. [score:7]
These findings support our results indicating that telmisartan inhibited cancer proliferation and tumor growth via AMPK activation, which was likely enhanced by the down-regulation of miR-200a and miR-301a. [score:6]
To clarify the relationship between p-AMPKα and these miRNAs, we further assayed the effect of miR-201a-3p and miR-301a-3p overexpression on the expression and phosphorylation of AMPKα in OE19 cells treated with or without telmisartan. [score:4]
Among these microRNAs, miR-200a and miR-301a were significantly down-regulated in OE19 cells treated with telmisartan. [score:4]
However, the expression of p-AMPKα was induced by telmisartan, and this effect was slightly attenuated by miR-301a-3p (Supplementary Figure 6). [score:3]
Thus, miR-301a-3p may regulate the phosphorylation of AMPKα through the AMPKα/mTOR signaling pathway to control cell proliferation in EAC cells. [score:2]
miR-200a-3p mimics, miR-301a-3p mimics, and negative control miRNA were obtained from Thermo Scientific (Waltham, MA, USA). [score:1]
[1 to 20 of 7 sentences]
9
[+] score: 22
A significant number of genes associated with metastasis were overexpressed in tumors classified into the serum miRNA cluster 1. (A) Box plots representing microarray expression results for miR-141, miR-200b, miR-193b and miR-301 from two different studies performed in lung primary tumors. [score:5]
A supervised diagnostic miRNA signature composed of 4 miRNAs (miR-141, miR-200b, miR-193b and miR-301) which were up-regulated in NSCLC tumors and serum was selected to validate its diagnostic value in an independent cohort of age and sex-matched serum samples. [score:4]
We identified 4 miRNAs that fulfilled these criteria: miR-141, miR-200b, miR-193b and miR-301, since they were significantly overexpressed in lung AC and/or SCC versus normal lung samples (Fig. 3A) as well as in the serum of NSCLC patients versus NC (Fig. 3B). [score:3]
Validation results showed that all 4 miRNAs were significantly overexpressed in the NSCLC sera (p < 0.001) and the log [2] fold-change for miR-141, miR-200b, miR-193b and miR-301 were 2.67, 2.98, 2.52 and 2.01 respectively. [score:3]
All four miRNAs were significantly overexpressed (p < 0.001) in lung tumors, except miR-301 that was not significantly higher in lung SCC. [score:3]
MiR-301 was found overexpressed among vesicle-related miRNAs from plasma in NSCLC 20, but it has not been previously reported as a serum -based marker for cancer diagnosis. [score:3]
To validate these findings, we measured by RT-PCR the expression level of miR-141, miR-200b, miR-193b and miR-301 in the serum of an independent cohort of 84 NSCLC and 23 age and sex-matched NC subjects. [score:1]
[1 to 20 of 7 sentences]
10
[+] score: 20
Among these miRs, we identified two (miR-10b* and miR-139-5p) that were down-regulated and three (miR-425, miR-454 and miR-301a) that were up-regulated for all three subtypes (Fig 1D and E and Supporting Information Fig S1A). [score:7]
Thus, up-regulation of miR-425, miR-454 and miR-301a and down-regulation of miR-10b* and miR-139-5p were definitively confirmed. [score:7]
5-aza-dC treatment did not affect the expression of the three up-regulated miRs (miR-425, miR-454 and miR-301a; Supporting Information Fig S2C). [score:6]
[1 to 20 of 3 sentences]
11
[+] score: 19
Interestingly, 7 of the 12 miRNAs that were up-regulated in the presence of IFN-α (miR-30b,miR-30c, miR-130a, miR-192, miR-301, miR-324-5p and miR-565) were also down-regulated in HCV -infected Huh7.5 cells. [score:7]
Seven miRNAs (miR-30b, miR-30c, miR-130a, miR-192, miR-301, miR-324-5p, and miR-565) were down-regulated in HCV-infected Huh7.5 cells (p<0.05) and subsequently up-regulated following interferon-α treatment (p<0.01). [score:7]
The GOMir tool JTarget, using five major miRNA-mRNA prediction databases, identified a list of mRNA targets for miR-30, miR-130a, miR-192, miR-301 and miR-324-5p [21]. [score:5]
[1 to 20 of 3 sentences]
12
[+] score: 15
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-26b, hsa-mir-29a, hsa-mir-30a, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-106a, mmu-let-7g, mmu-let-7i, mmu-mir-15b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-130a, mmu-mir-138-2, mmu-mir-181a-2, mmu-mir-182, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-30e, hsa-mir-10a, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-182, hsa-mir-181a-1, mmu-mir-297a-1, mmu-mir-297a-2, mmu-mir-301a, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, mmu-mir-106a, mmu-mir-106b, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-30b, hsa-mir-125b-1, hsa-mir-130a, hsa-mir-138-2, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-138-1, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-15a, mmu-mir-26b, mmu-mir-29a, mmu-mir-29c, mmu-mir-34a, rno-mir-301a, rno-let-7d, rno-mir-344a-1, mmu-mir-344-1, rno-mir-346, mmu-mir-346, rno-mir-352, hsa-mir-181b-2, mmu-mir-10a, mmu-mir-181a-1, mmu-mir-29b-2, mmu-mir-138-1, mmu-mir-181b-1, mmu-mir-181c, mmu-mir-125b-1, hsa-mir-106b, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-34b, hsa-mir-34c, hsa-mir-30e, hsa-mir-362, mmu-mir-362, hsa-mir-369, hsa-mir-374a, mmu-mir-181b-2, hsa-mir-346, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-10a, rno-mir-15b, rno-mir-26b, rno-mir-29b-2, rno-mir-29a, rno-mir-29b-1, rno-mir-29c-1, rno-mir-30c-1, rno-mir-30e, rno-mir-30b, rno-mir-30d, rno-mir-30a, rno-mir-30c-2, rno-mir-34b, rno-mir-34c, rno-mir-34a, rno-mir-106b, rno-mir-125a, rno-mir-125b-1, rno-mir-125b-2, rno-mir-130a, rno-mir-138-2, rno-mir-138-1, rno-mir-181c, rno-mir-181a-2, rno-mir-181b-1, rno-mir-181b-2, rno-mir-181a-1, hsa-mir-449a, mmu-mir-449a, rno-mir-449a, mmu-mir-463, mmu-mir-466a, hsa-mir-483, hsa-mir-493, hsa-mir-181d, hsa-mir-499a, hsa-mir-504, mmu-mir-483, rno-mir-483, mmu-mir-369, rno-mir-493, rno-mir-369, rno-mir-374, hsa-mir-579, hsa-mir-582, hsa-mir-615, hsa-mir-652, hsa-mir-449b, rno-mir-499, hsa-mir-767, hsa-mir-449c, hsa-mir-762, mmu-mir-301b, mmu-mir-374b, mmu-mir-762, mmu-mir-344d-3, mmu-mir-344d-1, mmu-mir-673, mmu-mir-344d-2, mmu-mir-449c, mmu-mir-692-1, mmu-mir-692-2, mmu-mir-669b, mmu-mir-499, mmu-mir-652, mmu-mir-615, mmu-mir-804, mmu-mir-181d, mmu-mir-879, mmu-mir-297a-3, mmu-mir-297a-4, mmu-mir-344-2, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-466b-3, mmu-mir-466c-1, mmu-mir-466e, mmu-mir-466f-1, mmu-mir-466f-2, mmu-mir-466f-3, mmu-mir-466g, mmu-mir-466h, mmu-mir-493, mmu-mir-504, mmu-mir-466d, mmu-mir-449b, hsa-mir-374b, hsa-mir-301b, rno-mir-466b-1, rno-mir-466b-2, rno-mir-466c, rno-mir-879, mmu-mir-582, rno-mir-181d, rno-mir-182, rno-mir-301b, rno-mir-463, rno-mir-673, rno-mir-652, mmu-mir-466l, mmu-mir-669k, mmu-mir-466i, mmu-mir-669i, mmu-mir-669h, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-466j, mmu-mir-1193, mmu-mir-767, rno-mir-362, rno-mir-504, rno-mir-582, rno-mir-615, mmu-mir-3080, mmu-mir-466m, mmu-mir-466o, mmu-mir-466c-2, mmu-mir-466b-4, mmu-mir-466b-5, mmu-mir-466b-6, mmu-mir-466b-7, mmu-mir-466p, mmu-mir-466n, mmu-mir-344e, mmu-mir-344b, mmu-mir-344c, mmu-mir-344g, mmu-mir-344f, mmu-mir-374c, mmu-mir-466b-8, hsa-mir-466, hsa-mir-1193, rno-mir-449c, rno-mir-344b-2, rno-mir-466d, rno-mir-344a-2, rno-mir-1193, rno-mir-344b-1, hsa-mir-374c, hsa-mir-499b, mmu-mir-466q, mmu-mir-344h-1, mmu-mir-344h-2, mmu-mir-344i, rno-mir-344i, rno-mir-344g, mmu-let-7j, mmu-mir-30f, mmu-let-7k, mmu-mir-692-3, rno-let-7g, rno-mir-15a, rno-mir-762, mmu-mir-466c-3, rno-mir-29c-2, rno-mir-29b-3, rno-mir-344b-3, rno-mir-466b-3, rno-mir-466b-4
Such a situation occurred for miR-26b, miR-30, and miR-374 downregulation, and for miR-34, miR-301, and miR-352 upregulation [121]. [score:7]
Of these miRNAs, 12 were upregulated (miR-34b, miR-138, miR-297a, miR-301, miR-449, miR-466, miR-493, miR-579, miR-582, miR. [score:4]
Three dysregulated miRNAs (miR-301, miR-369, and miR-669k) overlapped in the lungs of adenoma-bearing mice and of microadenoma-bearing mice. [score:2]
These miRNAs were miR-301, miR-369, and miR-669k, whose main functions are to regulate cell proliferation, autophagy, and aerobic glycolysis, which are mechanisms involved in the initial stage of the functional transformation of cells into their neoplastic counterpart. [score:2]
[1 to 20 of 4 sentences]
13
[+] score: 14
Moreover, miR-130b [99], miR-301a [100], miR-106a [101], miR-103a [102], miR-495 [103], and miR-532-5p [104] directly inhibit RUNX3 translation at the post-transcriptional level. [score:6]
In addition, increased H3K9 dimethylation and reduced H3 acetylation, as well as the increased miR-130b, miR-301a, miR-106a, miR-103a, miR-495, and miR-532-5p, synergistically inhibited the expression of RUNX3 Numerous studies have demonstrated that H. pylori infection is closely related to abnormal CpG island methylation. [score:5]
In addition, increased H3K9 dimethylation and reduced H3 acetylation, as well as the increased miR-130b, miR-301a, miR-106a, miR-103a, miR-495, and miR-532-5p, synergistically inhibited the expression of RUNX3 The exploitation of characteristic epigenetic alterations during the malignant transformation of gastric mucosa allows for the prevention, diagnosis, treatment, and prognostic evaluation of gastric cancer from a new perspective independent of protein expression. [score:3]
[1 to 20 of 3 sentences]
14
[+] score: 13
MiR-301a also down-regulates the expression of an inhibitor of NF-κB, Nkrf [38]. [score:7]
Interestingly, miR-454-3p and a third putative BTG1 target, miR-301a, are encoded within the first intron of SKA2, whose depletion affects the cell cycle by inducing a metaphase-like delay [37]. [score:3]
NF-κB binds directly to the SKA2 promoter region to activate the transcription of SKA2 and miR-301a and also enhances persistent NF-κB activation to facilitate tumor growth [37, 39], thus suggesting a feedback loop to moderate SKA2 function. [score:2]
These miRNAs included hsa-mir-130, hsa-mir-301a, hsa-mir-302, hsa-mir-454-3p, and hsa-mir-19b. [score:1]
[1 to 20 of 4 sentences]
15
[+] score: 11
The suitability of candidate EC reference genes was assessed using geNorm and NormFinder software, with hsa-miR-301a and hsa-miR-339-5p found to be the most uniformly expressed EC reference genes on TLDA card A and hsa-miR-425* and RNU24 for TLDA card B. A panel of 18 potential EC reference genes that were not significantly differentially expressed between CD133+ NSCs/ CD133- NPCs and primary human MB specimens was identified. [score:5]
The ranking of the candidate EC reference genes determined by these programs is summarised in Table 3, and consistent results were obtained for both TLDA card A and card B. Normfinder and geNorm identified hsa-miR-301a and hsa-miR-339-5p as the two most uniformly expressed EC reference genes on TLDA card A, closely followed by hsa-miR-210 and RNU48. [score:3]
Based on our findings, EC reference gene pairs hsa-miR-301a and hsa-miR-339-5p and hsa-miR-425* and RNU24 are recommended for the normalisation of miRNAs on TLDA card A and card B, respectively, in primary MB specimens relative to ESC-derived NSCs/ NPCs. [score:1]
This suggests that the combination of hsa-miR-339-5p and hsa-miR-301a should be used for data normalisation in preference to the single EC reference genes. [score:1]
Our initial statistical analyses identified a number of candidate EC reference genes uniformly expressed across experimental groups, with both NormFinder and geNorm identifying hsa-miR-339-5p and hsa-miR-301a as the most stable EC reference genes for TLDA card A, and hsa-miR-425* and RNU24 as the most stable for TLDA card B. The practical consequences of miRNA normalisation were then evaluated using TLDA card B candidate EC reference genes and miRNAs as a case study. [score:1]
[1 to 20 of 5 sentences]
16
[+] score: 10
Recently, Wang et al. reported that miR-301a is upregulated in gastric cancer and directly downregulates RUNX3 expression [47]. [score:10]
[1 to 20 of 1 sentences]
17
[+] score: 10
Six miRNAs were overexpressed (hsa-miR-193a-3p, hsa-miR-29b-1-5p, hsa-miR-505-5p, hsa-miR-194-5p, hsa-miR-99b-3p, and hsa-miR-200b-3p) and 14 (hsa-miR-3663-3p, hsa-miR-513a-5p, hsa-miR-146b-5p, hsa-miR-1972, hsa-miR-718, hsa-miR-3138, hsa-miR-21-5p, hsa-miR-630, hsa-miR-575, hsa-miR-301a-3p, hsa-miR-636, hsa-miR-34a-3p, hsa-miR-21-3p, and hsa-miR-516a-5p) were downregulated in aortic tissue from AS patients (Table 2). [score:6]
Six overexpressed miRNAs (hsa-miR-193a-3p, hsa-miR-29b-1-5p, hsa-miR-505-5p, hsa-miR-194-5p, hsa-miR-99b-3p, and hsa-miR-200b-3p) and 14 downregulated miRNAs (hsa-miR-3663-3p, hsa-miR-513a-5p, hsa-miR-146b-5p, hsa-miR-1972, hsa-miR-718, hsa-miR-3138, hsa-miR-21-5p, hsa-miR-630, hsa-miR-575, hsa-miR-301a-3p, hsa-miR-636, hsa-miR-34a-3p, hsa-miR-21-3p, and hsa-miR-516a-5p) were identified in patients with AS, relative to normal controls, and their general characteristics and functional annotations were analyzed using bioinformatic tools. [score:4]
[1 to 20 of 2 sentences]
18
[+] score: 10
Other miRNAs from this paper: mmu-mir-301a, mmu-mir-301b, hsa-mir-301b
It is possible, however, that living cells have evolved a buffering mechanism whereby the loss of Oct4 down-regulates mir-301, which in turn up-regulates its paralogs Pou4f1, Pou3f2 or Pou4f2, which compensate for the function of Oct4. [score:7]
Previous experiments have shown that Oct4 can affect transcription of the microRNA mir-301 [39], which in turn targets the Oct4 paralogs Pou4f1, Pou3f2 and Pou4f2. [score:3]
[1 to 20 of 2 sentences]
19
[+] score: 10
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-20a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-27a, hsa-mir-92a-1, hsa-mir-92a-2, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-15b, mmu-mir-23b, mmu-mir-27b, mmu-mir-130a, mmu-mir-133a-1, mmu-mir-140, mmu-mir-24-1, hsa-mir-196a-1, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, mmu-mir-206, hsa-mir-30c-2, hsa-mir-196a-2, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-200b, mmu-mir-301a, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-15b, hsa-mir-23b, hsa-mir-27b, hsa-mir-130a, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-140, hsa-mir-206, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-196a-1, mmu-mir-196a-2, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-15a, mmu-mir-18a, mmu-mir-20a, mmu-mir-24-2, mmu-mir-27a, mmu-mir-92a-2, hsa-mir-200c, hsa-mir-1-1, mmu-mir-1a-2, mmu-mir-17, mmu-mir-19a, mmu-mir-200c, mmu-mir-199a-2, mmu-mir-199b, mmu-mir-19b-1, mmu-mir-92a-1, hsa-mir-30c-1, hsa-mir-200a, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, hsa-mir-196b, mmu-mir-196b, dre-mir-196a-1, dre-mir-199-1, dre-mir-199-2, dre-mir-199-3, hsa-mir-18b, dre-let-7a-1, dre-let-7a-2, dre-let-7a-3, dre-let-7a-4, dre-let-7a-5, dre-let-7a-6, dre-let-7b, dre-let-7c-1, dre-let-7c-2, dre-let-7d-1, dre-let-7d-2, dre-let-7e, dre-let-7f, dre-let-7g-1, dre-let-7g-2, dre-let-7h, dre-let-7i, dre-mir-1-2, dre-mir-1-1, dre-mir-15a-1, dre-mir-15a-2, dre-mir-15b, dre-mir-17a-1, dre-mir-17a-2, dre-mir-18a, dre-mir-18b, dre-mir-18c, dre-mir-19a, dre-mir-20a, dre-mir-23b, dre-mir-24-4, dre-mir-24-2, dre-mir-24-3, dre-mir-24-1, dre-mir-27a, dre-mir-27b, dre-mir-27c, dre-mir-27d, dre-mir-27e, dre-mir-30c, dre-mir-92a-1, dre-mir-92a-2, dre-mir-92b, dre-mir-130a, dre-mir-133a-2, dre-mir-133a-1, dre-mir-133b, dre-mir-133c, dre-mir-140, dre-mir-196a-2, dre-mir-196b, dre-mir-200a, dre-mir-200b, dre-mir-200c, dre-mir-206-1, dre-mir-206-2, dre-mir-301a, dre-let-7j, hsa-mir-92b, mmu-mir-666, mmu-mir-18b, mmu-mir-92b, mmu-mir-1b, dre-mir-196c, dre-mir-196d, mmu-mir-3074-1, mmu-mir-3074-2, hsa-mir-3074, mmu-mir-133c, mmu-let-7j, mmu-let-7k, dre-mir-24b
miRNA Embryonic age Expression profile mir15a 48 and 72 hpf Midbrain, MHB, notochord mir15b 48 and 72 hpf Midbrain, neurocranium, notochord mir23b 30, 48, and 72 hpf Somites, lens, pharyngeal arches, notochord mir27b 48 and 72 hpf mir30c 48 and 72 hpf Brain, neurocranium, eye, heart mir130a 48 and 72 hpf Brain, gut tube, heart, eye mir133b 30, 48, and 72 hpf Notochord mir301a 48 and 72 hpf Forming cartilage Midbrain, neurocranium, eye, trigeminal ganglia Figure 5 Expression of mir23b in zebrafish embryos. [score:5]
miRNA Embryonic age Expression profile mir15a 48 and 72 hpf Midbrain, MHB, notochord mir15b 48 and 72 hpf Midbrain, neurocranium, notochord mir23b 30, 48, and 72 hpf Somites, lens, pharyngeal arches, notochord mir27b 48 and 72 hpf mir30c 48 and 72 hpf Brain, neurocranium, eye, heart mir130a 48 and 72 hpf Brain, gut tube, heart, eye mir133b 30, 48, and 72 hpf Notochord mir301a 48 and 72 hpf Forming cartilage Midbrain, neurocranium, eye, trigeminal ganglia Figure 5 Expression of mir23b in zebrafish embryos. [score:5]
[1 to 20 of 2 sentences]
20
[+] score: 10
Wang et al. reported that miR-301a is upregulated in gastric cancer, and directly downregulates Runx3 expression [28]. [score:10]
[1 to 20 of 1 sentences]
21
[+] score: 10
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-22, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-33a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-96, hsa-mir-101-1, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-107, hsa-mir-16-2, hsa-mir-196a-1, hsa-mir-198, hsa-mir-129-1, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-10a, hsa-mir-10b, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-182, hsa-mir-183, hsa-mir-196a-2, hsa-mir-199b, hsa-mir-203a, hsa-mir-204, hsa-mir-210, hsa-mir-211, hsa-mir-212, hsa-mir-181a-1, hsa-mir-214, hsa-mir-215, hsa-mir-216a, hsa-mir-217, hsa-mir-219a-1, hsa-mir-221, hsa-mir-222, hsa-mir-223, hsa-mir-224, hsa-mir-200b, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-15b, hsa-mir-23b, hsa-mir-30b, hsa-mir-122, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-128-1, hsa-mir-130a, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-137, hsa-mir-138-2, hsa-mir-140, hsa-mir-141, hsa-mir-142, hsa-mir-143, hsa-mir-145, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-127, hsa-mir-129-2, hsa-mir-138-1, hsa-mir-146a, hsa-mir-150, hsa-mir-184, hsa-mir-185, hsa-mir-195, hsa-mir-206, hsa-mir-320a, hsa-mir-200c, hsa-mir-1-1, hsa-mir-155, hsa-mir-181b-2, hsa-mir-128-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-101-2, hsa-mir-219a-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-99b, hsa-mir-296, hsa-mir-130b, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-365a, hsa-mir-365b, hsa-mir-375, hsa-mir-376a-1, hsa-mir-378a, hsa-mir-382, hsa-mir-383, hsa-mir-151a, hsa-mir-148b, hsa-mir-338, hsa-mir-133b, hsa-mir-325, hsa-mir-196b, hsa-mir-424, hsa-mir-20b, hsa-mir-429, hsa-mir-451a, hsa-mir-409, hsa-mir-412, hsa-mir-376b, hsa-mir-483, hsa-mir-146b, hsa-mir-202, hsa-mir-181d, hsa-mir-499a, hsa-mir-376a-2, hsa-mir-92b, hsa-mir-33b, hsa-mir-151b, hsa-mir-320b-1, hsa-mir-320c-1, hsa-mir-320b-2, hsa-mir-378d-2, hsa-mir-301b, hsa-mir-216b, hsa-mir-103b-1, hsa-mir-103b-2, hsa-mir-320d-1, hsa-mir-320c-2, hsa-mir-320d-2, hsa-mir-378b, hsa-mir-320e, hsa-mir-378c, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, hsa-mir-219b, hsa-mir-203b, hsa-mir-451b, hsa-mir-499b, hsa-mir-378j
This report indicated that bmp3, hsp60, and msxb genes had role in regeneration and were predicted targets of up- or downregulated miR-200b, miR-2/miR-338, and miR-301, respectively. [score:6]
Ramachandra et al. (2008) Oocyte and early embryo miR-34 Zebrafish Knockdown, microarray, qRT–PCR Nervous system development Soni et al. (2013) Oocyte miR-15, miR-29, miR-92, miR-101, miR-126, miR-181-3p, miR-196, miR-202-5p, miR-202-3p, miR-221, miR-301, miR-338, and miR-2184 Rainbow trout Microarray ? [score:3]
Soares et al. (2009) let-7i, miR-15b, miR-17a-3p, miR-21, miR-92b, miR-128, miR-133, miR-146a,b, miR-150, miR-194a, miR-204, miR-210-3p, miR-301a, miR-429, miR-730, miR-733, miR-738, Zebrafish Microarray, northern blot, qRT-PCR, ISH Yin, Lepilina, et al. (2012) Muscle miR-1, miR-21, miR-133a,b,c, miR-203b Zebrafish NGS, qRT–PCR ? [score:1]
[1 to 20 of 3 sentences]
22
[+] score: 9
With the exception of miR-301, all of these putative REST target miRNAs were found to be expressed in both NT2-N and PHN, and many of them were differentially expressed between neurons and astrocytes suggesting that they may be regulators of neuronal development and function (Fig. 8). [score:9]
[1 to 20 of 1 sentences]
23
[+] score: 9
miR-301a was also shown to directly target and suppress PTEN, maintaining constitutively activated Wnt/β-catenin signaling, which leads to the enhancement of breast cancer invasion and metastasis (96). [score:6]
In breast cancer, PTEN is targeted by miR-29b (94) and miR-301 (95). [score:3]
[1 to 20 of 2 sentences]
24
[+] score: 9
However, the related family members miR-130a and miR-130b (that is, with the same seed regions as miR-301a and likely overlapping targets) both increased basal reporter activity by 4.5-fold (P = 0.04) and 3.6-fold (P = 0.06), respectively (see Additional file 1, Table S2). [score:3]
They found miR-301a was the strongest inducer (approximately 5-fold increase in reporter activity) and that it functioned by targeting NFKB repressing factor (NKRF). [score:3]
Hence, our results are in agreement with the Lu et al. study suggesting that the miR-301/miR-130 family positively regulates NF-κB signaling. [score:2]
miR-301a was not a hit in our screen (P = 0.18; average fold change = 2.3). [score:1]
[1 to 20 of 4 sentences]
25
[+] score: 9
miR-16, miR-31, miR-33a, miR-146a, miR-155, and miR-301a can suppress or promote IL-8 expression and secretion by inhibiting the expression of different proteins [31– 36]. [score:9]
[1 to 20 of 1 sentences]
26
[+] score: 9
Turini Gonzales Marioto et al. (97) evaluated the miRNA profiles in mice intravenously administered P. brasiliensis and showed that the most upregulated miRNAs at 28 days included miR-126a-5p, miR-340-5p, miR-30b-5p, miR-19b-3p, miR-221-3p, miR-20a-5p, miR-130a-3p, and miR-301a-3p, whereas after 56 days, miRNAs from the let-7 family, as well as miR-26b-5p, and miR-369-3p were the greatest upregulated miRNAs (97). [score:5]
In a chemical allergen mo del examining the murine miRNA profile following dermal exposure to toluene 2,4-diisocyanate, miR-21, miR-22, miR-27b, miR-31, miR-126, miR-155, miR-210, and miR-301a expression were increased (57). [score:3]
While this study identified miRNAs that are known to participate in the immune response associated with asthma (miR-21, miR-31, miR-126, and miR-155), new miRNAs were proposed as potential biomarkers for allergic sensitization to toluene 2,4-diisocyanate (miR-22, miR-27b, miR-301a, and miR-210). [score:1]
[1 to 20 of 3 sentences]
27
[+] score: 9
This would explain the high variability of the expression levels observed in the exposed group compared with the other two groups for bta-mir-19b, bta-mir-19b2, bta-mir-301a and bta-mir-32 that were all differentially expressed between the PP vs NN groups. [score:4]
A decreased expression of mir-301a has been associated with both viral [38] and mycobacterial infection [63]. [score:3]
Mir-301a is an activator of NF-kB [62] and was under-expressed in PP vs NN groups. [score:2]
[1 to 20 of 3 sentences]
28
[+] score: 9
Six miRNAs, 3 less expressed (miR-324-3p, miR-516a-3p, miR-659-3p) and 3 more expressed (miR-137, miR-301a-3p, miR-873-5p) in BM-infiltrating cells than in primary tumors, were significantly differentially expressed also in this new set of samples (Table 2). [score:7]
To validate the differential expression of the selected 20 miRNAs, reverse-transcribed and pre-amplified miRNA fractions from 10 additional BM-infiltrating and 10 primary tumors were amplified in a 96 well plate in triplicate using the specific TaqMan [©] human microRNA assays (hsa-miR-324-3p, catalog #002161; hsa-miR-516-3p, catalog #001149; hsa-miR-628-5p, catalog #002433; hsa-miR-659-3p, catalog #001514; hsa-miR-10b, catalog #002218; hsa-miR-128, catalog #002216; mmu-miR-137, catalog #01129; mmu-miR-140, catalog #001187; hsa-miR-16, catalog #000391, hsa-miR-191, catalog #002299; hsa-miR-301, catalog #000528; hsa-miR-361-3p, catalog #002116; hsa-miR-365, catalog #001020; hsa-miR-548d-3p, catalog #001605; hsa-miR-572, catalog #001614; hsa-miR-576-5p, catalog #002350, hsa-miR-616, catalog #001589; hsa-miR-628-3p, catalog #002434; hsa-miR-873, catalog #002356; hsa-miR-98, catalog #000577; U6 snRNA, catalog #001973, Life Technologies). [score:2]
[1 to 20 of 2 sentences]
29
[+] score: 8
9 −3.8 hsa-miR-424 −4.2 −2 −4.5 hsa-miR-24-1* −3.9 −2.3 −4.1 hsa-miR-542-3p −2.9 −2.2 −3.8 hsa-miR-29b −2.6 −2.1 −3.3 hsa-miR-301a −2.4 −1.8 −2 hsa-miR-107 −2 −1.7 −2.2 hsa-miR-101 −1.8 −1.9 −1.8 hsa-miR-188-5p −1.7 −1.6 −1.8Based on the 3 lists of DEMs, we focused our attention on the miRNAs whose expression was influenced specifically by the oncogenic alteration of AKT1, PIK3CA or PTEN, and, alternatively, on those commonly deregulated by two or three of the above-mentioned alterations. [score:4]
9 −3.8 hsa-miR-424 −4.2 −2 −4.5 hsa-miR-24-1* −3.9 −2.3 −4.1 hsa-miR-542-3p −2.9 −2.2 −3.8 hsa-miR-29b −2.6 −2.1 −3.3 hsa-miR-301a −2.4 −1.8 −2 hsa-miR-107 −2 −1.7 −2.2 hsa-miR-101 −1.8 −1.9 −1.8 hsa-miR-188-5p −1.7 −1.6 −1.8 Based on the 3 lists of DEMs, we focused our attention on the miRNAs whose expression was influenced specifically by the oncogenic alteration of AKT1, PIK3CA or PTEN, and, alternatively, on those commonly deregulated by two or three of the above-mentioned alterations. [score:4]
[1 to 20 of 2 sentences]
30
[+] score: 8
In particular, CUL3, over expressed in kidney and prostate cancers, is a target of several dysregulated MIRs: MIR22, MIR23A, MIR23B, MIR218-1, MIR218-2, and MIR301, which are down regulated in kidney cancers, and of MIR22, MIR23A, MIR181A, and MIR181C, which are down regulated in prostate cancers (Table 5). [score:8]
[1 to 20 of 1 sentences]
31
[+] score: 8
In the second group, there were six miRNAs with an expression level that was four times lower in BCSCs than in MCF-7 cells: miR-200a, miR-301, miR-188, miR-21, miR-181d and miR-29b. [score:3]
Moreover, miR-301, miR-296, miR-21 and miR-373* have been reported to be expressed in human embryonic stem cells and other stem cells, indicating that these miRNAs may play a constitutive role in maintaining the biological characteristics of stem cells [40, 41]. [score:1]
We performed real-time RT-PCR for 10 miRNAs: miR-122a, miR-188, miR-200a, miR-21, miR-224, miR-296, miR-301, miR-31, miR-373* and miR-200C. [score:1]
The analysed miRNAs included miR-122a, miR-188, miR-200a, miR-21, miR-224, miR-296, miR-301, miR-31, miR-373* and miR-200C. [score:1]
Parts of the amplification curves for miR-188, miR-200a miR-301 and miR-31 are shown (B). [score:1]
Part of amplification curves for miR-188, miR-200a miR-301 and miR-31 are shown in Figure 3B. [score:1]
[1 to 20 of 6 sentences]
32
[+] score: 8
Other miRNAs from this paper: hsa-mir-630, hsa-mir-301b
In prostate cancer, luteolin exerts anticancer effects through various mechanisms such as suppression of androgen receptor expression and vascular endothelial growth factor receptor 2 (VEGFR-2) mediated angiogenesis at > 10 μM, and induction of cytotoxicity, apoptosis and cell cycle arrest via regulation of IGF-1/Akt pathway, Akt-Mdm2 pathway, epidermal growth factor signaling pathway and expression levels of miR-630 and miR-301 at > 10 μM [26– 30]. [score:8]
[1 to 20 of 1 sentences]
33
[+] score: 8
It was demonstrated that LTL could inhibit the proliferation of and induce apoptosis in prostate cancer cells by downregulating the expression of miR-301 [22]. [score:8]
[1 to 20 of 1 sentences]
34
[+] score: 8
Others associated with inflammation and immune response (Contreras and Rao 2012) that have been linked to the NF-κB pathway for which we did not observe an association in this study were: miR-181b, previously associated with CYLD, which has a negative regulator effect on NF-κB; miR-301a, which has previously been shown to indirectly activate NF-κB via downregulation of NF-κB repressing factor (NKBF); miR-155, previously associated with BCR-related genes and the expression of IL8 (Ma et al. 2011). [score:8]
[1 to 20 of 1 sentences]
35
[+] score: 8
In the MCF7-specific MIR interaction network (Supplementary Figure S11), disease-related MIRs, such as mir-21, mir-301a and mir-454 have been shown to play a role in the regulation of breast cancer (64–66). [score:4]
MIRs such as miR-194-2, miR-21, miR-301a, miR-454 and miR-92b, each target nearly one-third of the communities, for example. [score:3]
The nodes representing three cell-specific MIRs, mir-142, mir-301a and mir-454, are indicated. [score:1]
[1 to 20 of 3 sentences]
36
[+] score: 8
Although we did find miR-27a-3p to significantly inhibit TLR8 in human PBMCs, our experimental evidence does not support a strong inhibitory activity for miR-301a-3p in either mouse or human mo dels. [score:5]
Interestingly, miR-27a-3p and miR-301a-3p AMOs belong to this list of potential inhibitors. [score:3]
[1 to 20 of 2 sentences]
37
[+] score: 8
YIPF2 19p13.2 G VIP unknown ZNHIT3 17q12 G HHUB unknown C11orf75 11q21 B HHUB unknown miR-23b-3p CEACAM1 19q13.2 B HUB T-cell developmentmiR-30c-5pmiR-30d-5p IFNGR2 21q22.11 B HUB T-cell developmentmiR-30c-5pmiR-30d-5p CD59 11p13 C HUB T-cell development let-7f-1-3p CGN 1q21 C HUB T-cell development miR-125b-5p [b]miR-766-3pmiR-125a-5p HSPA13 21q11 C HHUB T-cell development miR-181a-5p [b]miR-200c-3p miR-205-5p ARHGEF4 2q22 D HHUB T-cell development miR-301a-3p DLG3 Xq13.1 D HHUB T-cell development MORC3 21q22.13 D HHUB Epigenetic controllet-7b-3pmiR-200c-3p APP 21q21.3 E VIP Thymic microenviron. [score:8]
[1 to 20 of 1 sentences]
38
[+] score: 7
In total, 65 microRNAs were identified to exhibit differential expression in either LHR expressing S KOV3 cells or LH -treated cells, a few of which have been found in the genomic fragile regions that are associated with abnormal deletion or amplification in cancer, such as miR-21, miR-101-1, miR-210 and miR-301a. [score:5]
Interestingly, more positively correlated microRNA-mRNA pairs than negatively correlated pairs were observed for all microRNAs with the exception of nine, miR-181B2, miR-582, miR-497, miR-559, miR-561, miR-101-1, miR-187, miR-572 and miR-301A (Figure 5). [score:1]
For example, the loss of 11p15 (covering miR-210) is found in ovarian cancer [31] and 17q23 (covering miR-301a and miR-21) is amplified in breast cancer [32], as well as those reported in [33], [34]. [score:1]
[1 to 20 of 3 sentences]
39
[+] score: 7
Potentially, editing of these miRNAs could therefore be a side effect of other regulatory functions performed by ADARs, which might in turn explain why the deeply conserved editing sites of miR-140*, miR-301a and miR-455 all lie outside of the seed sequence and other parts of the miRNA that may influence targeting properties [22]. [score:4]
Remarkably, we found that miR-301a and miR-455 were edited in bony fishes, implying that both miRNAs have experienced site-specific RNA editing during the past 450 million years [20]. [score:1]
Editing of miR-140* and miR-301a had not been reported previously, consistent with our detection of a strong editing signal in opossum and chicken, but not in human and mouse (Table  1). [score:1]
Our results hint at an even earlier emergence of miR-27a and miR-301a editing, which might also be shared with sharks and lampreys, respectively, although the signal is too weak for us to exclude completely that it stems from sequencing errors. [score:1]
[1 to 20 of 4 sentences]
40
[+] score: 7
Other miRNAs from this paper: hsa-let-7c, hsa-let-7d, hsa-mir-16-1, hsa-mir-21, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-28, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-99a, hsa-mir-101-1, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-27b, mmu-mir-30a, mmu-mir-99a, mmu-mir-101a, mmu-mir-125b-2, mmu-mir-126a, mmu-mir-128-1, mmu-mir-9-2, mmu-mir-142a, mmu-mir-144, mmu-mir-145a, mmu-mir-151, mmu-mir-152, mmu-mir-185, mmu-mir-186, mmu-mir-24-1, mmu-mir-203, mmu-mir-205, hsa-mir-148a, hsa-mir-34a, hsa-mir-203a, hsa-mir-205, hsa-mir-210, hsa-mir-221, mmu-mir-301a, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-27b, hsa-mir-125b-1, hsa-mir-128-1, hsa-mir-142, hsa-mir-144, hsa-mir-145, hsa-mir-152, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125b-2, hsa-mir-126, hsa-mir-185, hsa-mir-186, mmu-mir-148a, mmu-mir-200a, mmu-let-7c-1, mmu-let-7c-2, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-21a, mmu-mir-24-2, mmu-mir-29a, mmu-mir-31, mmu-mir-34a, mmu-mir-148b, mmu-mir-339, mmu-mir-101b, mmu-mir-28a, mmu-mir-210, mmu-mir-221, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-125b-1, mmu-mir-128-2, hsa-mir-128-2, hsa-mir-200a, hsa-mir-101-2, hsa-mir-151a, hsa-mir-148b, hsa-mir-339, hsa-mir-335, mmu-mir-335, hsa-mir-449a, mmu-mir-449a, hsa-mir-450a-1, mmu-mir-450a-1, hsa-mir-486-1, hsa-mir-146b, hsa-mir-450a-2, hsa-mir-503, mmu-mir-486a, mmu-mir-542, mmu-mir-450a-2, mmu-mir-503, hsa-mir-542, hsa-mir-151b, mmu-mir-301b, mmu-mir-146b, mmu-mir-708, hsa-mir-708, hsa-mir-301b, hsa-mir-1246, hsa-mir-1277, hsa-mir-1307, hsa-mir-2115, mmu-mir-486b, mmu-mir-28c, mmu-mir-101c, mmu-mir-28b, hsa-mir-203b, hsa-mir-5680, hsa-mir-5681a, mmu-mir-145b, mmu-mir-21b, mmu-mir-21c, hsa-mir-486-2, mmu-mir-126b, mmu-mir-142b, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
Of the up-regulated miRNAs (in the metastatic library), miR-210 has been reported to be up-regulated in prostate carcinomas relative to BPH samples [23] and miR-301 has been linked to prostate cancer metastasis [37]. [score:7]
[1 to 20 of 1 sentences]
41
[+] score: 7
Overexpression of miR-301a-3p inhibits the target gene Smad4, enhancing pancreatic ductal adenocarcinoma (PDAC) cells colony, invasion and migration abilities in vitro as well as tumorigenesis in vivo [8]. [score:7]
[1 to 20 of 1 sentences]
42
[+] score: 7
Alternatively, the change in expression may be a result of an upstream alteration in the regulatory mechanisms, for example NONO; another example is that NKRF expression is regulated by miR-301a [40]. [score:7]
[1 to 20 of 1 sentences]
43
[+] score: 7
Seven over-expressed microRNAs that were altered at least four fold, including hsa-miR-671-5p, hsa-miR-542-5p, hsa-miR-542-3p, hsa-miR-1185, hsa-miR-539, hsa-miR-148a and hsa-miR-301a, (Figure 4A) and six over-expressed microRNAs that were highly expressed (normalized data ≥6), including hsa-miR-1290, hsa-miR-136, hsa-miR-424, hsa-miR-30a, hsa-miR-148a and hsa-miR-1246 (Figure 4B), were selected for further qRT-PCR analyses. [score:7]
[1 to 20 of 1 sentences]
44
[+] score: 6
For instance, mir-215 and mir-301 are downregulated in colon cancer, and mir-129 is overexpressed in prostate cancer. [score:6]
[1 to 20 of 1 sentences]
45
[+] score: 6
Dou L. Wang S. Sui X. Meng X. Shen T. Huang X. Guo J. Fang W. Man Y. Xi J. MiR-301a mediates the effect of IL-6 on the AKT/GSK pathway and hepatic glycogenesis by regulating PTEN expression Cell. [score:3]
Therefore, miRNAs targeting PTEN such as miR-499, miR-26b, and miR-301a are beneficial for improving insulin sensitivity [49, 50, 51]. [score:3]
[1 to 20 of 2 sentences]
46
[+] score: 6
Developmental expression profiling of the murine CNS revealed 12 miRNAs (miR-9, miR-17-5p, miR-124a, miR-125a, miR-125b, miR-130a, miR-140, miR-181a, miR-199a, miR-205, miR-214, miR-301) with significantly higher expression at embryonic versus postnatal time points. [score:6]
[1 to 20 of 1 sentences]
47
[+] score: 6
In addition, three down-regulated miRNAs (miR-206, miR-301 and miR-187) also were predicated to target on AIV genome. [score:6]
[1 to 20 of 1 sentences]
48
[+] score: 6
Calin et al. reported that one cluster of FRAs at chromosome 17q23 contains three HPV16 integration events and four miRNA genes (miR-21, miR-301, miR-142s, and miR-142as); they conclude that these miRNAs are possible targets of such viral integration that may lead to deregulation of miRNAs expression [8]. [score:6]
[1 to 20 of 1 sentences]
49
[+] score: 5
In addition, the plasma level of miR-301a is down-regulated in patients with sickle cell anemia, compared to normal controls, which is related to PAI-1 suppression [23]. [score:5]
[1 to 20 of 1 sentences]
50
[+] score: 5
In breast cancer, global miRNA expression profiling studies have identified significant alterations in a number of oncogenic and tumor-suppressive miRNAs, including miR-221, miR-21, miR-125, and miR-301 [9- 11]. [score:5]
[1 to 20 of 1 sentences]
51
[+] score: 5
In addition, 17 miRNAs (miR-136, miR-143, miR-148a, miR-15b, miR-18a, miR-181a, miR-181a*, miR-20b, miR-27b, miR-29b, miR-30d, miR-30e*, miR-301a, miR-376a, miR-376b, miR-410 and miR-7), which are differentially expressed in our retinal induction treatment, are involved in the regulation of developing mouse retina 25. [score:4]
Six of them (hsa-let-7f-1, hsa-let-7i, hsa-miR-125a, hsa-miR-15b, hsa-miR-18a and hsa-miR-301a) were commonly found in the differentiation treatment of ESC into retinal pigment epithelial cells 13. [score:1]
[1 to 20 of 2 sentences]
52
[+] score: 5
Except for miR-301, no studies have shown direct regulation of FOXF2 by a miRNA. [score:3]
Recently miR-301 was defined as an oncogene and it was reported to mediate proliferation via regulating FOXF2 in breast cancer [36]. [score:2]
[1 to 20 of 2 sentences]
53
[+] score: 5
In addition, Ma et al. demonstrated that overexpressed microRNA-301a in breast cancer promoted tumor metastasis by targeting PTEN and activating Wnt/beta-catenin signaling [27]. [score:5]
[1 to 20 of 1 sentences]
54
[+] score: 5
Similarly, we have verified that miR-301a up-regulates by inhibiting Nkrf [26], yet the role of miR-454 (the other member of the 301a∼454 cluster) in the pathway needs further investigation. [score:4]
miR-301a has recently been implicated as an inducer in pancreatic cancer [26]. [score:1]
[1 to 20 of 2 sentences]
55
[+] score: 5
qRT-PCR analysis of miR-130b, miR-301a, and miR-200b expression as well as DICER1, zeb2, CDH1, and vimentin mRNA expression levels in Ishikawa and AN3CA cells treated with 10 μM 5'-aza-CdR and 10 μM TSA. [score:5]
[1 to 20 of 1 sentences]
56
[+] score: 5
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-25, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-92a-1, hsa-mir-93, hsa-mir-98, hsa-mir-101-1, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-106a, hsa-mir-16-2, hsa-mir-192, hsa-mir-196a-1, hsa-mir-197, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-10b, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-182, hsa-mir-183, hsa-mir-196a-2, hsa-mir-205, hsa-mir-181a-1, hsa-mir-221, hsa-mir-222, hsa-mir-200b, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-15b, hsa-mir-122, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-128-1, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-137, hsa-mir-140, hsa-mir-141, hsa-mir-143, hsa-mir-145, hsa-mir-152, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-146a, hsa-mir-150, hsa-mir-194-1, hsa-mir-206, hsa-mir-200c, hsa-mir-1-1, hsa-mir-155, hsa-mir-128-2, hsa-mir-194-2, hsa-mir-106b, hsa-mir-29c, hsa-mir-200a, hsa-mir-101-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-26a-2, hsa-mir-372, hsa-mir-374a, hsa-mir-375, hsa-mir-328, hsa-mir-133b, hsa-mir-20b, hsa-mir-429, hsa-mir-449a, hsa-mir-486-1, hsa-mir-146b, hsa-mir-494, hsa-mir-503, hsa-mir-574, hsa-mir-628, hsa-mir-630, hsa-mir-449b, hsa-mir-449c, hsa-mir-708, hsa-mir-301b, hsa-mir-1827, hsa-mir-486-2
MiR-301 is another oncomir upregulated in several types of cancer, including NSCLC, and involved in smad4 repression through the direct binding to 3′ UTR [90- 91]. [score:5]
[1 to 20 of 1 sentences]
57
[+] score: 5
For example, miR-625, miR-103/miR-107, miR-21 and miR-301 have been found to promote CRC to invade and metastasize by stimulating multiple metastasis-promoting genes [27– 30], whereas miR-99, miR-137, miR-132 and miR-128 function as tumor suppressors to inhibit the metastasis of CRC [31– 34]. [score:5]
[1 to 20 of 1 sentences]
58
[+] score: 4
We found a decrease of miR-301a and miR-200c in TPC-TWIST1 cells (Table S2); these miRNAs were reported to be down-regulated in ATC [34]. [score:4]
[1 to 20 of 1 sentences]
59
[+] score: 4
We also identified EB upregulated miRNAs that have not been previously reported such as miR-130a, miR-301a, and miR-135, miR-190, miR-30c, and miR-30e. [score:4]
[1 to 20 of 1 sentences]
60
[+] score: 4
Of the 15 pairs, including 18 miRNAs, mir-181a-5p and mir-301a-3p formed hubs co-expressed with 7 and 3 other miRNAs, respectively (Supplementary Fig.   S3). [score:3]
The second group, of miR-301a-3p, miR-30e-3p, miR-182-5p, and miR-30e-5p showed no pathway that was not also identified using random lists of 4 miRNAs and miRPath. [score:1]
[1 to 20 of 2 sentences]
61
[+] score: 4
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-20a, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-29a, hsa-mir-30a, hsa-mir-93, hsa-mir-101-1, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-107, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-15b, mmu-mir-23b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-101a, mmu-mir-124-3, mmu-mir-125a, mmu-mir-130a, mmu-mir-9-2, mmu-mir-135a-1, mmu-mir-136, mmu-mir-138-2, mmu-mir-140, mmu-mir-144, mmu-mir-145a, mmu-mir-146a, mmu-mir-149, mmu-mir-152, mmu-mir-10b, mmu-mir-181a-2, mmu-mir-182, mmu-mir-183, mmu-mir-185, mmu-mir-24-1, mmu-mir-191, mmu-mir-193a, mmu-mir-195a, mmu-mir-200b, mmu-mir-204, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-30e, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-10a, hsa-mir-10b, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-182, hsa-mir-183, hsa-mir-204, hsa-mir-181a-1, hsa-mir-221, hsa-mir-222, hsa-mir-200b, mmu-mir-301a, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, mmu-mir-130b, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-23b, hsa-mir-30b, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-130a, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-138-2, hsa-mir-140, hsa-mir-144, hsa-mir-145, hsa-mir-152, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-136, hsa-mir-138-1, hsa-mir-146a, hsa-mir-149, hsa-mir-185, hsa-mir-193a, hsa-mir-195, hsa-mir-320a, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-15a, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-20a, mmu-mir-23a, mmu-mir-24-2, mmu-mir-26a-1, mmu-mir-26b, mmu-mir-29a, mmu-mir-29c, mmu-mir-93, mmu-mir-34a, mmu-mir-330, mmu-mir-339, mmu-mir-340, mmu-mir-135b, mmu-mir-101b, hsa-mir-200c, hsa-mir-181b-2, mmu-mir-107, mmu-mir-10a, mmu-mir-17, mmu-mir-200c, mmu-mir-181a-1, mmu-mir-320, mmu-mir-26a-2, mmu-mir-221, mmu-mir-222, mmu-mir-29b-2, mmu-mir-135a-2, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-138-1, mmu-mir-181b-1, mmu-mir-181c, mmu-mir-7a-1, mmu-mir-7a-2, mmu-mir-7b, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-101-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-130b, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-361, mmu-mir-361, hsa-mir-376a-1, mmu-mir-376a, hsa-mir-340, hsa-mir-330, hsa-mir-135b, hsa-mir-339, hsa-mir-335, mmu-mir-335, mmu-mir-181b-2, mmu-mir-376b, mmu-mir-434, mmu-mir-467a-1, hsa-mir-376b, hsa-mir-485, hsa-mir-146b, hsa-mir-193b, hsa-mir-181d, mmu-mir-485, mmu-mir-541, hsa-mir-376a-2, hsa-mir-320b-1, hsa-mir-320c-1, hsa-mir-320b-2, mmu-mir-301b, mmu-mir-674, mmu-mir-146b, mmu-mir-467b, mmu-mir-669c, mmu-mir-708, mmu-mir-676, mmu-mir-181d, mmu-mir-193b, mmu-mir-467c, mmu-mir-467d, hsa-mir-541, hsa-mir-708, hsa-mir-301b, mmu-mir-467e, mmu-mir-467f, mmu-mir-467g, mmu-mir-467h, hsa-mir-320d-1, hsa-mir-320c-2, hsa-mir-320d-2, mmu-mir-467a-2, mmu-mir-467a-3, mmu-mir-467a-4, mmu-mir-467a-5, mmu-mir-467a-6, mmu-mir-467a-7, mmu-mir-467a-8, mmu-mir-467a-9, mmu-mir-467a-10, hsa-mir-320e, hsa-mir-676, mmu-mir-101c, mmu-mir-195b, mmu-mir-145b, mmu-let-7j, mmu-mir-130c, mmu-mir-30f, mmu-let-7k, mmu-mir-9b-2, mmu-mir-124b, mmu-mir-9b-1, mmu-mir-9b-3
The miRNA families that change expression in both mouse and human were: let-7, miR-7, miR-15, miR-101, miR-140, miR-152 (all validated by qPCR, P < 0.05), as well as miR-17, miR-34, miR-135, miR-144, miR-146, miR-301, miR-339, miR-368 (qPCR not performed). [score:3]
26E-0212mmu-miR-101b-3pmir-1010.297.791.72E-059.11E-0437mmu-miR-101a-3pmir-1010.2410.121.17E-031.92E-0250mmu-miR-107-3pmir-1030.228.773.24E-034.12E-0264mmu-miR-124-5pmir-1240.156.327.13E-037.09E-0233mmu-miR-301a-3pmir-1300.228.396.90E-041.29E-0259mmu-miR-130a-3pmir-1300.168.305.94E-036.44E-0252mmu-miR-135b-5pmir-1350.227.924.08E-034.99E-0274mmu-miR-136-5pmir-1360.229.061.09E-029. [score:1]
[1 to 20 of 2 sentences]
62
[+] score: 4
For H1N1 infected cells, at 18 and 24-hour post-infection, miR-188-5p, miR-1260, miR-1274a, miR-1274b, miR141, miR183*, miR-18b, miR-19a, miR21*, miR-301a, miR-572, miR-720, and miR-939 were found to be up-regulated (>1.5-fold, p<0.05) (Table 1). [score:4]
[1 to 20 of 1 sentences]
63
[+] score: 4
Recently SERPINE1 expression was shown to be regulated by miR-30c and miR-301a in pulmonary endothelial cells [14]. [score:4]
[1 to 20 of 1 sentences]
64
[+] score: 3
The assay results revealed four highly up-regulated miRNAs (up to 60-fold change) at 24 hpi: miR-29b, miR-155, miR-301a and miR-301b. [score:3]
[1 to 20 of 1 sentences]
65
[+] score: 3
Additionally, the expression level of miR-301, 194, and 122 was lower in the high graded fibrotic liver tissue than in low graded fibrotic liver tissue [18] [19] [20](GEO Series accession number GSE16922). [score:3]
[1 to 20 of 1 sentences]
66
[+] score: 3
In our primary screen, two major miR-130 miRNAs, miR-130a-3p and miR-130b-3p (denominated as miR-130a/b hereafter), and another family member, miR-301a, were shown to effectively inhibit HCV infection (Supplementary Fig.   11a). [score:3]
[1 to 20 of 1 sentences]
67
[+] score: 3
In our study, we have identified several miRNAs abnormally expressed in pancreatic cancer, such as miR-21, miR-301a and miR-155. [score:3]
[1 to 20 of 1 sentences]
68
[+] score: 3
Of these, 5 miRNAs (miR-137, miR-214-3p, miR-301a-3p, miR-330-3p and miR-383-5p) affect all four categories, linking them strongly to leukemia pathogenesis and highlighting their potential as therapeutic targets. [score:3]
[1 to 20 of 1 sentences]
69
[+] score: 3
Among these, only a few cellular miRNAs including miR-423, miR-301a, and miR-155 bound viral transcripts and reduced their expression. [score:3]
[1 to 20 of 1 sentences]
70
[+] score: 3
miR-301a +miR-301a expression was significantly differentiated in smoker versus non-smoker [52]. [score:3]
[1 to 20 of 1 sentences]
71
[+] score: 3
We use bioinformatics analyses to screen SDF-1 targeting miRNAs, e. g. miR-301a, miR-301b, miR-3666, miR-130a, miR-130b, miR-4295, miR-454, etc. [score:3]
[1 to 20 of 1 sentences]
72
[+] score: 3
Moreover, compared with the healthy gingiva, in periodontitis cases, six miRNAs (let-7a, let-7c, miR-130a, miR-301a, miR-520d and miR-548a) were up-regulated more than eightfold [25]. [score:3]
[1 to 20 of 1 sentences]
73
[+] score: 3
Using miR-30c-5p as a normalizer in qRT-PCR, we validated expression levels of miR-301a-3p (Figure 4B; r = 0.969, p-value = 0.003). [score:3]
[1 to 20 of 1 sentences]
74
[+] score: 3
Other miRNAs from this paper: hsa-mir-146a, hsa-mir-361, hsa-mir-448
For example, miR-146a and miR-301a promotes breast cancer progression by targeting EMT markers and PTEN, respectively [7, 10]. [score:3]
[1 to 20 of 1 sentences]
75
[+] score: 3
Recently, it has been established that the expression of hepatic miRNA (miR-22b, miR-140, miR-210a, mir-301, miR-457b, and let-7d) is increased in fluoxetine (the active ingredient in Prozac®) exposed female zebrafish (Craig et al., 2014). [score:3]
[1 to 20 of 1 sentences]
76
[+] score: 3
Increasing evidence has ascertained that a large number of miRs exhibit dysregulated expression in primary cancer specimens compared to tissues from healthy patient populations, including miR-21, miR-125b, miR-143, miR-145, miR-10b, miR-26a, miR-155 and miR-301 (27, 28). [score:3]
[1 to 20 of 1 sentences]
77
[+] score: 3
For example, Lee EJ 2007 et al. [44] showed that the miRNAs miR155, miR21, miR222, Let7, miR376a, miR301, miR100, miR125, miR142 and others are overexpressed significantly in human PC. [score:3]
[1 to 20 of 1 sentences]
78
[+] score: 3
Third, expression of miR-29b, miR-34a/c, miR-141, miR-199, miR-210c and miR-301a did not change significantly during malignant progression (Figure 2B). [score:3]
[1 to 20 of 1 sentences]
79
[+] score: 3
With the application of in situ RT-PCR, Lee et al. showed that the aberrantly expressed miR-221, miR-301 and miR-376a were localized to pancreatic cancer cells but not to stroma or normal acini or ducts. [score:3]
[1 to 20 of 1 sentences]
80
[+] score: 3
For example, Lu et al. found that miR-301a whose expression level is specifically elevated in pancreatic cancer tissues, contributes to the persistent activation of NF-κB -mediated pro-oncogenic signaling pathway [157]. [score:3]
[1 to 20 of 1 sentences]
81
[+] score: 2
Namely, pregnant rats fed SO and FO diets during the first 12 days of pregnancy showed significant lower expression of miR-449c-5p, miR-134–5p, miR-188, miR-32, miR130a, miR-144–3p, miR-431, miR-142–5p, miR-33, miR-340–5p, miR-301a, miR-30a, miR-106b, and miR-136–5p, as compared with OO, LO, and PO diets. [score:2]
[1 to 20 of 1 sentences]
82
[+] score: 2
Finally, when comparing colon cancer tissue directly to rectal cancer tissue, the ROC analysis indicated that hsa-miR-7-5p and hsa-miR-301a-5p had a fairly good specificity for detecting colon cancer (vs. [score:2]
[1 to 20 of 1 sentences]
83
[+] score: 2
Other miRNAs from this paper: hsa-mir-200b, hsa-mir-515-1, hsa-mir-515-2, hsa-mir-548a-1, hsa-mir-548b, hsa-mir-548a-2, hsa-mir-548a-3, hsa-mir-548c, hsa-mir-548d-1, hsa-mir-548d-2, hsa-mir-548e, hsa-mir-548j, hsa-mir-548k, hsa-mir-548l, hsa-mir-548f-1, hsa-mir-548f-2, hsa-mir-548f-3, hsa-mir-548f-4, hsa-mir-548f-5, hsa-mir-548g, hsa-mir-548n, hsa-mir-548m, hsa-mir-548o, hsa-mir-548h-1, hsa-mir-548h-2, hsa-mir-548h-3, hsa-mir-548h-4, hsa-mir-548p, hsa-mir-548i-1, hsa-mir-548i-2, hsa-mir-548i-3, hsa-mir-548i-4, mml-mir-301a, mml-mir-548a, mml-mir-548b, mml-mir-548c, mml-mir-548d, mml-mir-548e, mml-mir-548f, ptr-mir-301a, ptr-mir-515-1, ptr-mir-515-2, ptr-mir-548a-1, ptr-mir-548a-2, ptr-mir-548b, ptr-mir-548c, ptr-mir-548f-1, ptr-mir-548f-2, ptr-mir-548h, ptr-mir-548i-1, ptr-mir-548i-2, ptr-mir-548i-3, ptr-mir-548i-4, ptr-mir-548i-5, ptr-mir-548j, ptr-mir-548k, ptr-mir-548l, ptr-mir-548n, ptr-mir-548p, hsa-mir-2115, hsa-mir-548q, hsa-mir-2681, hsa-mir-548s, hsa-mir-548t, hsa-mir-548u, hsa-mir-548v, hsa-mir-548w, hsa-mir-3065, hsa-mir-548x, ppy-mir-515-1, ppy-mir-515-2, hsa-mir-548y, hsa-mir-548z, hsa-mir-548aa-1, hsa-mir-548aa-2, hsa-mir-548o-2, hsa-mir-548h-5, hsa-mir-548ab, hsa-mir-548ac, hsa-mir-548ad, hsa-mir-548ae-1, hsa-mir-548ae-2, hsa-mir-548ag-1, hsa-mir-548ag-2, hsa-mir-548ah, hsa-mir-548ai, hsa-mir-548aj-1, hsa-mir-548aj-2, hsa-mir-548x-2, hsa-mir-548ak, hsa-mir-548al, hsa-mir-4511, hsa-mir-548am, hsa-mir-548an, hsa-mir-4691, hsa-mir-203b, hsa-mir-4760, hsa-mir-4762, hsa-mir-548ao, hsa-mir-548ap, hsa-mir-548aq, hsa-mir-548ar, hsa-mir-548as, hsa-mir-548at, hsa-mir-548au, hsa-mir-548av, hsa-mir-548aw, hsa-mir-548ax, ptr-mir-548o, ptr-mir-548e, ggo-mir-548b, ggo-mir-203b, ggo-mir-548c, ggo-mir-548e, ggo-mir-548a, ggo-mir-548d, ggo-mir-548f, ggo-mir-200b, ppy-mir-548e, ppy-mir-548a, ppy-mir-548h, ppy-mir-548f, ppy-mir-548c, hsa-mir-548ay, hsa-mir-548az, mml-mir-548g, mml-mir-548h, mml-mir-548i, mml-mir-548j, hsa-mir-548ba, hsa-mir-548bb, ggo-mir-515-1, ggo-mir-515-2, ppy-mir-515-3, hsa-mir-548bc, ggo-mir-301a, ppy-mir-301a
Eight common TFs: ETS1, FOXC1, FOXL1, GATA2, HOXA5, MZF1_1-4, Nkx2-5 and SPIB could bind the upstream sequences of the two out of three intronic miRNAs and no TFBSs have been found in the potential regulatory sequences of ppy-mir-301a and ppy-mir-4419a (Tables S6, S8). [score:2]
[1 to 20 of 1 sentences]
84
[+] score: 2
Other miRNAs from this paper: hsa-mir-29a, hsa-mir-204, hsa-mir-1183, hsa-mir-3160-2, hsa-mir-6529
miRNAs were identified by Blasting Turbot 3 database sequences against the miRBase Contig number Read number Turbot 3 database annotation miRBase accession name miRBase annotation6,51454Early growth response 1MI0020478 Cricetulus griseus miR-29a stem-loop32,3923LSU rRNAMI0022328 Bos taurus miR-6529 stem-loop1,984r97Serine/threonine-protein phosphatase 2AMI0014190 Homo sapiens miR-3160-2 stem-loop34,898r2Similar to dynamin 3MI0000247 Mus musculus miR-204 stem-loop49,8972Similar to Elongation factor 1-gammaMI0015615 Ciona intestinalis miR-4064 stem-loop40,4423Similar to ORFaMI0019438 Oryzias latipes miR-133-2 stem-loop40,442r3Similarity to transposasesMI0001124 Oryza sativa miR169i stem-loop10,002r1Spindle and kinetochore -associated protein 2-likeMI0018844 Anolis carolinensis miR-301a stem-loop8,914r22UnknownMI0019711 Glycine max miR5769 stem-loop 10,002 1 Unnamed protein product MI006276 Homo sapiens miR-1183 stem-loop This is the first time that the transcriptome of the reproductive and the immune systems of turbot have been wi dely explored together. [score:1]
miRNAs were identified by Blasting Turbot 3 database sequences against the miRBase Contig number Read number Turbot 3 database annotation miRBase accession name miRBase annotation6,51454Early growth response 1MI0020478 Cricetulus griseus miR-29a stem-loop32,3923LSU rRNAMI0022328 Bos taurus miR-6529 stem-loop1,984r97Serine/threonine-protein phosphatase 2AMI0014190 Homo sapiens miR-3160-2 stem-loop34,898r2Similar to dynamin 3MI0000247 Mus musculus miR-204 stem-loop49,8972Similar to Elongation factor 1-gammaMI0015615 Ciona intestinalis miR-4064 stem-loop40,4423Similar to ORFaMI0019438 Oryzias latipes miR-133-2 stem-loop40,442r3Similarity to transposasesMI0001124 Oryza sativa miR169i stem-loop10,002r1Spindle and kinetochore -associated protein 2-likeMI0018844 Anolis carolinensis miR-301a stem-loop8,914r22UnknownMI0019711 Glycine max miR5769 stem-loop 10,002 1 Unnamed protein product MI006276 Homo sapiens miR-1183 stem-loop The progression in the construction of the turbot database is summarized in Table  1. First, the Turbot 1 database was created from almost ten thousand high-quality EST sequences from three cDNA libraries of three immune relevant organs (liver, head kidney and spleen) generated from turbot infected with A. salmonicida subspecies salmonicida and P. dicentrarchi, as well as from non-infected fish [36]. [score:1]
[1 to 20 of 2 sentences]
85
[+] score: 2
Other miRNAs from this paper: rno-mir-301a
Zhang W Zhang T Jin R Zhao H Hu J Feng B MicroRNA-301a promotes migration and invasion by targeting TGFBR2 in human colorectal cancerJ Exp Clin Cancer Res. [score:2]
[1 to 20 of 1 sentences]
86
[+] score: 2
The results of our luciferase reporter assay showed that six candidates (mir-20a, mir-106a, mir-106b, mir-148a, mir-182 and mir-301a) could be Clock -targeting miRNAs (Additional file 3B and C). [score:2]
[1 to 20 of 1 sentences]
87
[+] score: 2
For example, we found significant overexpression of miR-103, miR-107, miR-301 and miR-338 in lung cancer cells as compared to HBECs. [score:2]
[1 to 20 of 1 sentences]
88
[+] score: 2
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-32, hsa-mir-33a, hsa-mir-99a, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-107, mmu-let-7g, mmu-let-7i, mmu-mir-15b, mmu-mir-99a, mmu-mir-126a, mmu-mir-128-1, mmu-mir-130a, mmu-mir-140, mmu-mir-154, mmu-mir-204, mmu-mir-143, hsa-mir-204, hsa-mir-211, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-222, hsa-mir-223, mmu-mir-301a, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-128-1, hsa-mir-130a, hsa-mir-140, hsa-mir-143, hsa-mir-126, hsa-mir-129-2, hsa-mir-154, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-26a-1, mmu-mir-26b, mmu-mir-29a, mmu-mir-29c, mmu-mir-27a, mmu-mir-129-2, mmu-mir-103-1, mmu-mir-103-2, mmu-mir-340, mmu-mir-107, mmu-mir-32, mmu-mir-218-1, mmu-mir-218-2, mmu-mir-223, mmu-mir-26a-2, mmu-mir-211, mmu-mir-222, mmu-mir-128-2, hsa-mir-128-2, hsa-mir-29c, hsa-mir-101-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-26a-2, hsa-mir-379, mmu-mir-379, hsa-mir-340, mmu-mir-409, hsa-mir-409, hsa-mir-499a, hsa-mir-455, hsa-mir-670, mmu-mir-1249, mmu-mir-670, mmu-mir-499, mmu-mir-455, bta-mir-26a-2, bta-mir-29a, bta-let-7f-2, bta-mir-101-2, bta-mir-103-1, bta-mir-16b, bta-mir-222, bta-mir-26b, bta-mir-27a, bta-mir-499, bta-mir-99a, bta-mir-126, bta-mir-128-1, bta-mir-34b, bta-mir-107, bta-mir-140, bta-mir-15b, bta-mir-218-2, bta-let-7d, bta-mir-29c, bta-mir-455, bta-let-7g, bta-let-7a-1, bta-let-7f-1, bta-let-7i, bta-mir-34c, bta-let-7a-2, bta-let-7a-3, bta-let-7b, bta-let-7c, bta-let-7e, bta-mir-103-2, bta-mir-204, hsa-mir-1249, hsa-mir-1306, hsa-mir-103b-1, hsa-mir-103b-2, bta-mir-128-2, bta-mir-129-2, bta-mir-130a, bta-mir-143, bta-mir-154a, bta-mir-211, bta-mir-218-1, bta-mir-223, bta-mir-26a-1, bta-mir-301a, bta-mir-32, bta-mir-33a, bta-mir-340, bta-mir-379, bta-mir-409a, bta-mir-670, mmu-mir-1306, bta-mir-1306, bta-mir-1249, bta-mir-2284i, bta-mir-2285a, bta-mir-2284s, bta-mir-2285d, bta-mir-2284l, bta-mir-2284j, bta-mir-2284t, bta-mir-2285b-1, bta-mir-2284d, bta-mir-2284n, bta-mir-2284g, bta-mir-2284p, bta-mir-2284u, bta-mir-2284f, bta-mir-2284a, bta-mir-2284k, bta-mir-2284c, bta-mir-2284v, bta-mir-2285c, bta-mir-2284q, bta-mir-2284m, bta-mir-2284b, bta-mir-2284r, bta-mir-2284h, bta-mir-2284o, bta-mir-2284e, hsa-mir-1260b, bta-mir-2284w, bta-mir-2284x, bta-mir-409b, hsa-mir-499b, bta-mir-1260b, bta-mir-2284y-1, bta-mir-2285e-1, bta-mir-2285e-2, bta-mir-2285f-1, bta-mir-2285f-2, bta-mir-2285g-1, bta-mir-2285h, bta-mir-2285i, bta-mir-2285j-1, bta-mir-2285j-2, bta-mir-2285k-1, bta-mir-2285l, bta-mir-6119, mmu-let-7j, bta-mir-2285o-1, bta-mir-2285o-2, bta-mir-2285n-1, bta-mir-2285n-2, bta-mir-2285p, bta-mir-2285m-1, bta-mir-2285m-2, bta-mir-2284y-2, bta-mir-2285n-3, bta-mir-2285n-4, bta-mir-2284y-3, bta-mir-154c, bta-mir-154b, bta-mir-2285o-3, bta-mir-2285o-4, bta-mir-2285m-3, bta-mir-2284y-4, bta-mir-2284y-5, bta-mir-2284y-6, bta-mir-2285m-4, bta-mir-2285o-5, bta-mir-2285m-5, bta-mir-2285n-5, bta-mir-2285n-6, bta-mir-2284y-7, bta-mir-2285n-7, bta-mir-2284z-1, bta-mir-2284aa-1, bta-mir-2285k-2, bta-mir-2284z-3, bta-mir-2284aa-2, bta-mir-2284aa-3, bta-mir-2285k-3, bta-mir-2285k-4, bta-mir-2284z-4, bta-mir-2285k-5, bta-mir-2284z-5, bta-mir-2284z-6, bta-mir-2284z-7, bta-mir-2284aa-4, bta-mir-2285q, bta-mir-2285r, bta-mir-2285s, bta-mir-2285t, bta-mir-2285b-2, bta-mir-2285v, bta-mir-2284z-2, mmu-let-7k, mmu-mir-126b, bta-mir-2285g-2, bta-mir-2285g-3, bta-mir-2285af-1, bta-mir-2285af-2, bta-mir-2285y, bta-mir-2285w, bta-mir-2285x, bta-mir-2285z, bta-mir-2285u, bta-mir-2285aa, bta-mir-2285ab, bta-mir-2284ab, bta-mir-2285ac, bta-mir-2285ad, bta-mir-2284ac, bta-mir-2285ae, chi-let-7a, chi-let-7b, chi-let-7c, chi-let-7d, chi-let-7e, chi-let-7f, chi-let-7g, chi-let-7i, chi-mir-103, chi-mir-107, chi-mir-1249, chi-mir-126, chi-mir-1306, chi-mir-130a, chi-mir-140, chi-mir-143, chi-mir-154a, chi-mir-154b, chi-mir-15b, chi-mir-16b, chi-mir-204, chi-mir-211, chi-mir-222, chi-mir-223, chi-mir-2284a, chi-mir-2284b, chi-mir-2284c, chi-mir-2284d, chi-mir-2284e, chi-mir-26a, chi-mir-26b, chi-mir-27a, chi-mir-29a, chi-mir-29c, chi-mir-301a, chi-mir-33a, chi-mir-340, chi-mir-34b, chi-mir-34c, chi-mir-379, chi-mir-409, chi-mir-455, chi-mir-499, chi-mir-99a, bta-mir-2285ag, bta-mir-2285ah, bta-mir-2285ai, bta-mir-2285aj, bta-mir-2285ak, bta-mir-2285al, bta-mir-2285am, bta-mir-2285ar, bta-mir-2285as-1, bta-mir-2285as-2, bta-mir-2285as-3, bta-mir-2285at-1, bta-mir-2285at-2, bta-mir-2285at-3, bta-mir-2285at-4, bta-mir-2285au, bta-mir-2285av, bta-mir-2285aw, bta-mir-2285ax-1, bta-mir-2285ax-2, bta-mir-2285ax-3, bta-mir-2285ay, bta-mir-2285az, bta-mir-2285an, bta-mir-2285ao-1, bta-mir-2285ao-2, bta-mir-2285ap, bta-mir-2285ao-3, bta-mir-2285aq-1, bta-mir-2285aq-2, bta-mir-2285ba-1, bta-mir-2285ba-2, bta-mir-2285bb, bta-mir-2285bc, bta-mir-2285bd, bta-mir-2285be, bta-mir-2285bf-1, bta-mir-2285bf-2, bta-mir-2285bf-3, bta-mir-2285bg, bta-mir-2285bh, bta-mir-2285bi-1, bta-mir-2285bi-2, bta-mir-2285bj-1, bta-mir-2285bj-2, bta-mir-2285bk, bta-mir-2285bl, bta-mir-2285bm, bta-mir-2285bn, bta-mir-2285bo, bta-mir-2285bp, bta-mir-2285bq, bta-mir-2285br, bta-mir-2285bs, bta-mir-2285bt, bta-mir-2285bu-1, bta-mir-2285bu-2, bta-mir-2285bv, bta-mir-2285bw, bta-mir-2285bx, bta-mir-2285by, bta-mir-2285bz, bta-mir-2285ca, bta-mir-2285cb, bta-mir-2285cc, bta-mir-2285cd, bta-mir-2285ce, bta-mir-2285cf, bta-mir-2285cg, bta-mir-2285ch, bta-mir-2285ci, bta-mir-2285cj, bta-mir-2285ck, bta-mir-2285cl, bta-mir-2285cm, bta-mir-2285cn, bta-mir-2285co, bta-mir-2285cp, bta-mir-2285cq, bta-mir-2285cr-1, bta-mir-2285cr-2, bta-mir-2285cs, bta-mir-2285ct, bta-mir-2285cu, bta-mir-2285cv-1, bta-mir-2285cv-2, bta-mir-2285cw-1, bta-mir-2285cw-2, bta-mir-2285cx, bta-mir-2285cy, bta-mir-2285cz, bta-mir-2285da, bta-mir-2285db, bta-mir-2285dc, bta-mir-2285dd, bta-mir-2285de, bta-mir-2285df, bta-mir-2285dg, bta-mir-2285dh, bta-mir-2285di, bta-mir-2285dj, bta-mir-2285dk, bta-mir-2285dl-1, bta-mir-2285dl-2, bta-mir-2285dm
In addition, among these ten miRNA, mir-128-2, mir-218-2 and mir-301a were found in the ARPP21 (cAMP-regulated phosphoprotein), SLIT3 (Slit homolog 3) and SKA2 (Spindle and kinetochore associated complex subunit 2) genes in human, mouse, cow and chicken [65]. [score:2]
[1 to 20 of 1 sentences]
89
[+] score: 1
From the prediction, the experimental data from cow milk study validated 9 transportable milk miRNAs in human blood, including bta-miR-487b, miR-181b, miR-421, miR-215, let-7c, miR-301a, miR-432, miR-127, and miR-184. [score:1]
[1 to 20 of 1 sentences]
90
[+] score: 1
0013219hsa-miR-301a-3p0.2070.0048517hsa-miR-45000.4130.0096213hsa-miR-451b0.2100.0055917hsa-miR-36540.4150.004007hsa-miR-1070.2160.0001010hsa-miR-223-3p0.4160.00199Xhsa-miR-196b-3p0.2260.000837hsa-miR-3607-5p0.4210.004125hsa-miR-5581-3p0.2299.8E-051hsa-miR-93-3p0.4220.001297hsa-miR-44170.2300.001241hsa-miR-24-3p0.4270.037889hsa-miR-185-5p0.2390.0136722hsa-miR-365a-3p0.4330.0003016hsa-miR-12750.2400.013796hsa-miR-1260b0.4340. [score:1]
[1 to 20 of 1 sentences]
91
[+] score: 1
In the Figure, the red arrows (for miR-19a-3p, miR-28-5p and miR-301-3p) indicate these sequences are mapped to the genome sequence with one mismatch. [score:1]
[1 to 20 of 1 sentences]
92
[+] score: 1
For instance, miR-30e, miR-182, and miR-301a promote NF-κB activity to enhance tumor growth, invasiveness or angiogenesis [24– 26]. [score:1]
[1 to 20 of 1 sentences]
93
[+] score: 1
Other miRNAs from this paper: hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-22, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-98, hsa-mir-99a, hsa-mir-100, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-106a, hsa-mir-16-2, hsa-mir-196a-1, hsa-mir-199a-1, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-10a, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-196a-2, hsa-mir-199a-2, hsa-mir-210, hsa-mir-181a-1, hsa-mir-214, hsa-mir-222, hsa-mir-223, hsa-mir-27b, hsa-mir-30b, hsa-mir-122, hsa-mir-125b-1, hsa-mir-130a, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-140, hsa-mir-141, hsa-mir-142, hsa-mir-143, hsa-mir-145, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-127, hsa-mir-146a, hsa-mir-150, hsa-mir-186, hsa-mir-188, hsa-mir-195, hsa-mir-200c, hsa-mir-155, hsa-mir-181b-2, hsa-mir-106b, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-34b, hsa-mir-34c, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-363, hsa-mir-302c, hsa-mir-370, hsa-mir-373, hsa-mir-374a, hsa-mir-328, hsa-mir-342, hsa-mir-326, hsa-mir-135b, hsa-mir-338, hsa-mir-335, hsa-mir-345, hsa-mir-424, hsa-mir-20b, hsa-mir-146b, hsa-mir-520a, hsa-mir-518a-1, hsa-mir-518a-2, hsa-mir-500a, hsa-mir-513a-1, hsa-mir-513a-2, hsa-mir-92b, hsa-mir-574, hsa-mir-614, hsa-mir-617, hsa-mir-630, hsa-mir-654, hsa-mir-374b, hsa-mir-301b, hsa-mir-1204, hsa-mir-513b, hsa-mir-513c, hsa-mir-500b, hsa-mir-374c
Few FL-specific miRNAs included miR-9/9*, miR-301, miR-338, and miR-213 [51]. [score:1]
[1 to 20 of 1 sentences]
94
[+] score: 1
Selected miRNAs for further analysis in this report are miR-152, -128, -27a, -214, -454; with results concerning the role of miR-130a and miR-301a in another context to be reported elsewhere (Woo et al. unpublished). [score:1]
[1 to 20 of 1 sentences]
95
[+] score: 1
Furthermore, in a subsequent study, there were five circulating miRNAs identified as potential biomarkers of drug-resistant epilepsy, and miR-301a-3p had the highest sensitivity and specificity (47). [score:1]
[1 to 20 of 1 sentences]
96
[+] score: 1
We discovered pro-proliferative miRNAs (miR-9 [*], miR-93, miR-130a, miR-130b, miR-301, miR-302b, miR-302d, miR-363, miR-372, miR-373), and anti-proliferative miRNAs (miR-7, miR-124a, miR-192, miR-193a, miR-193b, miR-199a [*], miR-432 [*], miR-497, miR-506, miR-517c) in A2780 cells. [score:1]
[1 to 20 of 1 sentences]
97
[+] score: 1
In addition, all rat IGF/Insulin node microRNAs (except miR-301a) were present in humans (black in Figure 3E ), albeit at a lower level (4-fold instead of 16-fold enriched). [score:1]
[1 to 20 of 1 sentences]
98
[+] score: 1
The results revealed potentially conserved sites for approximately nine miRNA family candidates (miR-30c, miR-34a/c, miR-449b, miR-181, miR-301a, miR-421, miR-299-5p, miR-609 and miR-99a) in the PAI-1 mRNA 3′ UTR. [score:1]
[1 to 20 of 1 sentences]
99
[+] score: 1
Panguluri SK Tur J Chapalamadugu KC Katnik C Cuevas J Tipparaju SM MicroRNA-301a mediated regulation of Kv4.2 in diabetes: identification of key modulatorsPLoS One. [score:1]
[1 to 20 of 1 sentences]
100
[+] score: 1
Mir-130b and miR-301 were not found to be significantly different in amplified samples by SAM analysis. [score:1]
[1 to 20 of 1 sentences]