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6 publications mentioning mmu-mir-551b

Open access articles that are associated with the species Mus musculus and mention the gene name mir-551b. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

[+] score: 237
a Expression of miR-551b was manipulated by transfecting cells with miR-551b mimic or miR-551b inhibitor, using scramble RNA as a control, and the expression of miR-551b was examined by qPCR, b miR-551b significantly enhanced cell proliferation as assessed by a CCK-8 assay, c monolayer colony formation of cells transfected with miR-551b mimic or miR-551 inhibitor was compared to the scramble control, d cell cycle profiles were determined by flow cytometry, and the results presented as percentages of cells in G0/G1, S, and G2/M phases, e cells with upregulated miR-551b expression showed enhanced invasion through Matrigel in a transwell system. [score:12]
More importantly, in these primary CSCs, inhibiting miR-551b expression using a sequence-specific inhibitor (Fig.   3a) dramatically reduced the colony formation capacity (Fig.   3b), and these data were correlated with a significantly larger G1 but a smaller S population of SP cells treated by miR-551b inhibitor (Fig.   3c). [score:9]
As a result, upregulating miR-551b expression led to significant increase in cell proliferation, while cells with miR-551b inhibitor showed no difference from the scramble transfected cells (Fig.   2b). [score:8]
In lung cancer cells, miR-551b inhibits the expression of catalase and enhances the accumulation of reactive oxygen species and the expression of mucin-1, contributing to the acquired resistance to apoptosis and chemotherapy [48]. [score:7]
The results showed that miR-551b mimic significantly inhibited the expression of Foxo3 and TRIM31, while miR-551b inhibitor led to no obvious change (Fig.   4c, d). [score:7]
Using three microRNA target prediction algorithms, including TargetScan, Pictar, and microRNA, we found that Foxo3 and TRIM31 were among the potential targets of miR-551b. [score:7]
Furthermore, miR-551b was significantly upregulated in the recurrent serous OVCa compared to the primary tumors (Fig.   1c), and the cisplatin-resistant cells expressed more miR-551b than the susceptible cells (Fig.   1d), correlating with its overexpression in the stem cell-enriched SP cells, which are believed to drive tumor recurrence. [score:7]
These data suggested that miR-551b regulates the proliferation and invasion of the OVCa SP cells through its inhibitive effect on the expression of Foxo3 and TRIM31. [score:6]
In a mouse xenograft mo del, miR-551b was targeted to confirm the regulatory roles of miR-551b in OVCa progression and characterize the potentiality of targeting miR-551b in future therapeutic development. [score:5]
A good example of these is miR-551b, which is upregulated in lung squamous cell carcinoma (SCCs) and prostate cancer, and mediates tumor development and progression [26, 27]. [score:5]
miR-551b expression was quantified by qPCR after the SP cells were transfected with miR-551b mimic, miR-551b inhibitor, or scramble RNA control (a). [score:5]
Moreover, our data also suggest that miR-551b contributes to the development of chemoresistance of the SP cells in vitro and in vivo, and its inhibition sensitizes cancer cells to chemotherapy, emphasizing its value in future therapeutic development. [score:5]
This is likely through the suppression of Foxo3 and TRIM31 expression as shown by the binding of miR-551b to the UTRs of Foxo3 and TRIM31 transcripts (Fig.   4) and the reversing of the miR-551 mimic -induced phenotype by exogenous Foxo3 and TRIM31 (Supplemental Fig.  1). [score:5]
Fig.  5Blocking the expression of miR-551b inhibits the growth of ovarian tumors in vivo. [score:5]
Cells were transfected with miR-551b mimic, miR-551b inhibitor, or the scramble RNA, and the changes in the expression of miR-551b were confirmed by qPCR (Fig.   2a). [score:5]
Elevated miR-551b in OVCa enhances the resistance of cancer cells to anoikis by upregulating STAT3 and c-KIT [28]. [score:4]
miR-551b was identified as one of the top 10 upregulated microRNAs in the SP cells. [score:4]
In addition, miR-551b expression is elevated in the recurrent OVCa compared to the primary disease (Fig.   1c) although its functional importance in OVCa recurrence is unknown. [score:4]
Indeed, miR-551b upregulates STAT3 and c-KIT and enhances the resistance of ovarian tumor cells to anoikis [28]. [score:4]
The SP cells were inoculated subcutaneously into the flanks of SCID mice, and the established tumors were treated by intratumoral injection of agomir or antagomir of miR-551b to up- or downregulate miR-551b levels. [score:4]
Supplemental Fig.   1 miR-551b promotes OVCa cell proliferation and invasion by targeting Foxo3 and TRIM31. [score:3]
To define whether Foxo3 and TRIM31 are involved in the miR-551b -mediated cellular functions, Foxo3 or TRIM31 was overexpressed in OVCa cells in the presence or absence of miR-551b mimic (Supplemental Fig.  1A). [score:3]
Ten patients were included in each group, c expression of miR-551b in the primary (Stage III) and recurrent OVCa. [score:3]
Consistent with this, significantly higher levels of miR-551b were detected in tissues from the advanced serous OVCa than the early stage (Fig.   1b), suggesting the association of miR-551b expression with OVCa progression. [score:3]
The observed shifts of the SP cells between G1 and S phases of the cell cycle in response to the manipulation of miR-551b expression are consistent with the known functions of Foxo3 in cell cycle progression [34]. [score:3]
Targeting miR-551b increases the susceptibility of mouse xenografts to cisplatin. [score:3]
Fig.  4Foxo3 and TRIM31 are downstream targets of miR-551b. [score:3]
Identification of the downstream targets of miR-551b. [score:3]
a Sequences of miR-551b, rcmiR-551b, and the potential targeting regions in the 3′ UTRs of Foxo3 and TRIM31 are shown. [score:3]
Using an miR-551b mimic or an specific inhibitor, we explored the roles of miR-551b in cell proliferation, invasion, and susceptibility to cisplatin and identified the downstream effectors. [score:3]
Expression of miR-551b, Foxo3 and TRIM31 in the xenografts was assessed by qPCR and (c). [score:3]
This is consistent with the association of miR-551b expression with the survival of 296 OVCa patients, as demonstrated by previous microRNA profiling [47]. [score:3]
In the results, miR-551b was one of the top 10 microRNAs that were upregulated in the OVCa SP cells compared to the non-SP population. [score:3]
In solid ovarian tumors, miR-551b expression correlates with tumor grades (Fig.   1b), suggesting its close association with cancer progression. [score:3]
Cells were synchronized by serum starving for 24 h and then transfected with miR-551b mimic, inhibitor, or the scramble RNA. [score:3]
The reverse complementary miR-551b (rcmiR-551b), the wild-type and mutant 3′-untranslated regions (UTR) of Foxo3 and TRIM31 were synthesized by TaKaRa (Shanghai, China) and inserted into psiCHECK-2 or pcDNA 3.1 vectors. [score:3]
Our results suggest a tumor-suppressive role of TRIM31 in OVCa cells in response to miR-551b. [score:3]
Moreover, exogenously expressed Foxo3 or TRIM31 also overturned the increase in cell invasion induced by miR-551b (Supplemental Fig.  1E). [score:3]
Consistent with our in vitro observations, inhibitions of Foxo3 and TRIM31 by miR-551b were observed in mouse xenografts (Fig.   5), suggesting the occurrence of the signaling in vivo. [score:3]
This mechanism may extend to other anchorage-free settings since miR-551b expression is also enhanced in the circulating prostate cancer cells [27]. [score:3]
The results demonstrated a decreased susceptibility of cells treated with miR-551b mimic to cisplatin and an increased responsiveness of cells with miR-551b inhibitor (Fig.   3d). [score:3]
The IC [50] values for cells with the scramble RNA, miR-551b mimic, and miR-551b inhibitor were 2.33, 3.41, and 1.49 µg/ml, respectively. [score:3]
Cells were transfected in an Opti-MEM medium (Invitrogen) with miR-551b mimic, miR-551b inhibitor, scramble RNA (GeneCopoeia, Rockville, MD) or psiCHECK-2 plasmid (Promega, Madison, WI) using Lipofectamine 2000 (Invitrogen), following the manufacturer’s instructions. [score:3]
When the targeting sequences in the 3′-UTRs were mutated, the miR-551b -mediated effects were completely abolished (Fig.   4c, d), suggesting the interaction of miR-551b with the 3′-UTRs of Foxo3 and TRIM31. [score:3]
The OVCa SP cells were transfected with miR-551b in the presence and absence of Foxo3 or TRIM31 overexpression. [score:3]
The SP cells transfected with miR-551b mimic, miR-551b inhibitor, or the scramble RNA were exposed to a range of doses of cisplatin, and their viability assessed after 3 days. [score:3]
a qPCR analysis indicates a higher level of miR-551b in the side population of the ascites-derived OVCa cell line than the non-side population, b expression of miR-551b in ovarian serous cystadenocarcinoma tissues with varied levels of differentiation was examined by qPCR, in comparison with ovarian serous cystadenoma. [score:3]
demonstrated that miR-551b significantly promoted, consistently with our data in Fig.   2b, while exogenous Foxo3 and TRIM31 inhibited cell proliferation (Supplemental Fig.  1B, C). [score:3]
The results indicated a significant increase in the number of cells migrating through Matrigel when the primary OVCa cells were transfected with miR-551b mimic, whereas those with miR-551b inhibitor showed no apparent difference, compared to the cells with the scramble control (Fig.   2e). [score:2]
Further in vitro and in vivo assays suggested that miR-551b mediated the proliferation, invasion, and chemoresistance, likely through its control over the expression of Foxo3 and TRIM31. [score:2]
To further dissect the functions of miR-551b in OVCa cells, we sorted out the SP cells from the ascitic OVCa cell population and performed the soft agar colony formation assay after manipulating their miR-551b expression (Fig.   3a). [score:2]
Corresponding to this, mice treated with miR-551b agomir survived for a shorter period than the control, while the treatment with miR-551b antagomir prolonged the survival (Fig.   5b). [score:1]
In an attempt to explore the mechanism of miR-551b functioning, we have shown that miR-551b functions through Foxo3 and TRIM31. [score:1]
In summary, our results demonstrate that miR-551b is significantly higher in OVCa SP cells than the non-SP cells. [score:1]
We next asked how miR-551b executes its important functions in the proliferation, invasion, and chemoresistance of OVCa cells. [score:1]
The two proteins counteracted against miR-551b and negated the increase in S phase cells population caused by this microRNA (Supplemental Fig.  1D). [score:1]
The data suggested that the mediation of Foxo3 and TRIM31 by miR-551b was occurring in vivo and might play a key role in the observed impacts of miR-551b on tumor growth (Fig.   5a). [score:1]
Our in vitro data in Fig.   3d suggested that miR-551b mediated the resistance of the SP cells against cisplatin. [score:1]
miR-551b promotes the colony formation of the SP cells and confers them chemoresistance. [score:1]
The current study demonstrates that miR-551b is over 100-fold higher in the SP cells than in the non-SP population of cells, implicating that this microRNA is required to maintain the phenotypic features of the SP cells. [score:1]
Importantly, both Foxo3 and TRIM31 apparently abrogated the induction of proliferation by miR-551b when either was co -transfected with miR-551b (Supplemental Fig.  1B, C). [score:1]
Ovarian cancer Side population of cancer cells miR-551b Cell proliferation Cell invasion Drug resistance Ovarian cancer (OVCa) is the most common and one of the most lethal gynecological malignancies in the world [1]. [score:1]
Consistently, SP cells transfected with miR-551b mimic had a smaller G1 but a larger S population of cells than those treated with the scramble RNA (Fig.   3c). [score:1]
a p < 0.05; b p < 0.01 vs the scramble control; c p < 0.05 vs the miR-551b mimic -treated only. [score:1]
miR-551b promotes the proliferation and invasion of OVCa cells. [score:1]
This result was validated by a separate qPCR analysis for miR-551b (Fig.   1a). [score:1]
Mice were treated by intraperitoneal administration of miR-551b agomir, miR-551b antagomir, or saline, together with 25 mg/kg cisplatin. [score:1]
In the intraperitoneal mouse xenograft mo del, mice were injected intraperitoneally with SP cells and were treated for 4 weeks with miR-551b agomir, miR-551b antagomir, or the vehicle, in the presence of 25 mg/kg cisplatin (intraperitoneal delivery). [score:1]
We identified miR-551b as one of the most significantly elevated microRNAs in the SP cells in comparison with the non-SP cells in OVCa. [score:1]
Mouse xenograft mo del was employed to confirm our in vitro observations, which suggested key roles of miR-551b in the proliferation and invasion of OVCa cells. [score:1]
Data were averaged from three repeated experiments, e the mediation of Foxo3 and TRIM31 by miR-551b was confirmed by qPCR and, respectively. [score:1]
Further studies are needed to define whether miR-551b is involved in other processes important for OVCa metastases, such as spheroid formation and the colonization of OVCa cells on the surfaces of adjacent organs in the peritoneal cavity [27, 46]. [score:1]
The cells were co -transfected with 0.8 µg/well of plasmid and 30 nM of miR-551b mimic or its inhibitor and incubated for 24 h. The samples were then analyzed using a dual luciferase reporter assay kit (Promega), and the assays were performed in triplicate and repeated three times. [score:1]
miR-551b is elevated in OVCa. [score:1]
In the subcutaneous mouse xenograft mo dels, the tumor burden in mice was significantly increased by the 4-week treatment of miR-551 agomir, but reduced by miR-551b antagomir (a), and correlated with these, mice injected with miR-551b agomir had poorer survival (p = 0.0035), while those with miR-551b antagomir showed better survival in comparison with the control mice (b). [score:1]
In Fig.   2d, flow cytometry analysis demonstrated that increased miR-551b reduced the cell population in the G1 phase while increasing that in the S phase, suggesting that this microRNA may promote the transition from G1 to S phase. [score:1]
The results indicated that the SP cells transfected with miR-551b mimic produced more colonies than the scramble control (Fig.   3b). [score:1]
The enhancement of cell proliferation by miR-551b was supported by the profiling of the cell cycle. [score:1]
On the other hand, mice co-administrated with miR-551b antagomir and cisplatin grew significantly fewer tumors (Fig.   5d), and as a result, these mice survived much longer periods than the other two treatment groups (Fig.   5e). [score:1]
Our data support significant roles of miR-551b in the proliferation and invasion of the ascitic SP cells in vitro and the growth of tumor xenografts in mice (Fig.   5). [score:1]
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[+] score: 163
To identify the putative targets of miR-551b, the TargetScan was performed and 3′-UTR of ERBB4 mRNA was recognized as the potential target of miR-551b (Figure 5A). [score:7]
Therefore, higher ERBB4 expression resulted in malignant GC (including EMT process, invasion and metastasis) and miR-551b negatively regulated ERBB4 expresssion. [score:6]
In summary, miR-551b regulates EMT and GC metastasis by inhibiting the expression of ERBB4 that significantly correlates with poor survival time. [score:6]
Our data was corroborated by the analysis in GC patient samples demonstrating miR-551b was downregulated in advanced tumor samples and its expression correlated with GC patient survival time. [score:6]
Due to the low expression of miR-551b in GC tissue, it is postulated to function as a tumor suppressor [18]. [score:5]
By analyzing the TCGA data and clinical samples, we demonstrated that ERBB4 was a target of miR-551b; ERBB4 was overexpressed in GC tissues and significantly associated with the survival of GC patients. [score:5]
miR-551b regulates ERBB4 translationally. [score:4]
Further, miR-551b was significantly downregulated in GC tissues. [score:4]
However, showed that treatment with miR-551b mimics downregulated ERBB4 protein levels (Figure 7C and 7D). [score:4]
We further explored the mode of miR-551b regulation of ERBB4 by analyzing the effect of miR-551b mimics on mRNA and protein expression levels of ERBB4. [score:4]
ERBB4 is a direct target of miR-551b. [score:4]
miR-551b regulates ERBB4 translation. [score:4]
miR-551b is down-regulated in gastric cancer. [score:4]
This suggested that miR-551b regulated ERBB4 translation and not at the transcriptional level. [score:4]
Based on in vitro transwell migration and invasion assays, we demonstrated that miR-551b mimic treated MNK45 and SGC7901 cells were inhibited significantly in migrating through the matrigel, further suggesting that miR-551b inhibited tumor invasion and metastasis. [score:4]
This suggested that miR-551b inhibited GC metastasis. [score:3]
Again, the expression of miR-551b was significantly lower in tumor tissues than the matched adjacent normal tissues (Figure 1C). [score:3]
Since miR-551b mimics inhibited invasiveness and metastasis of GC cell lines in vitro, we wanted to study the effects of miR-551b on the epithelial to mesenchymal transition (EMT) that confers metastatic ability to tumor cells. [score:3]
The dual-luciferase reporter assay was used to validate if ERBB4 was a direct target of miR-551b. [score:3]
High expression of miR-551b is associated with long term survival. [score:3]
miR-551b inhibits the EMT induced by TGF-β1. [score:3]
miR-551b mimics inhibit EMT induction by TGF-β1 in gastric cancer cell lines. [score:3]
These results suggested that TGF-β1 induce EMT in gastric cancer cells and miR-551b inhibited EMT. [score:3]
demonstrated that treatment with ERBB4 inhibitor AST-1306 resulted in increased E-Cadherin and reduced N-Cadherin and Vimentin in both MNK45 and SGC7901 cells, similar to miR-551b mimic transfected cells (Figure 6E and 6F). [score:3]
Fold expression of miR-551b in control or miR-551b mimic treated SGC7901 (left) and MNK45 (right) cells is shown. [score:3]
This suggested that miR-551b specifically targeted ERBB4. [score:3]
Thus, our data points that miR-551b is a potential prognostic factor and a therapeutic target for gastric cancer. [score:3]
miR-551b inhibits invasion and migration of GC cell lines in vitro. [score:3]
shows that miR-551b mimics significantly inhibit tumor growth and extend life span. [score:3]
In this study, we demonstrated that miR-551b significant inhibited EMT, invasion and metastasis of GC cells. [score:3]
The heat map analysis showed that miR-551b was significantly downregulated in the tumor tissues compared to the normal stomach tissues (Figure 1A and 1B). [score:3]
was also used to confirm the correlation between ERBB4 and EMT Transcription factor -binding sites in the promoter region of human miR-551b were predicted by TargetScan and PicTar4 biological analysis website: http://www. [score:3]
Therefore, we postulated that miR-551b had tumor suppressor function based on our comparative analysis of GC cell lines MNK45 and SGC7901 with normal stomach cell line GES. [score:3]
ERBB4 is the target of miR-551b. [score:3]
We demonstrated that miR-551b inhibited EMT transition when the miR-551b mimic treated MNK45 and SGC7901 cells compared to control cells, based on cellular morphology as well as E-Cadherin versus N-Cadherin and Vimentin protein levels. [score:2]
Figure 3miR-551b significantly inhibits invasion and migration of (A) MNK45 and (B) SGC7901 cells treated miR-551b mimics compared to the control. [score:2]
miR-551b is known to regulate the malignant behavior of GC [17]. [score:2]
Together, these results strongly suggest that ERBB4 promotes EMT and metastasis in GC based on its regulation by miR-551b. [score:2]
DAPI stained images (100x) of miR-551b mimic transfected (C) MNK45 and (D) SGC7901 cells (right) compared to control group (left) demonstrating inhibited invasion (top) and migration (bottom) are shown. [score:2]
Figure 8 (A and B) Live imaging of subcutaneous and peritoneal tumor growth at 14 days in untreated (left) and miR-551b mimic treated GC cells (right) demonstrating that miR-551b diminishes tumor growth in nude mice. [score:1]
Figure 5 (A) Sequence alignment of miR-551b with the 3′ UTR of ERBB4 and the mutated miR-551b binding site are shown. [score:1]
However, the specific role and mechanism of miR-551b in the metastasis of GC is unclear. [score:1]
We observed by RT-PCR that ERBB4 mRNA levels in both the MNK45 and SGC7901 cells that were transfected with miR-551b mimics were comparable to the negative controls (Figure 7A and 7B). [score:1]
miR-551b supresses tumor growth in vivo and prolonged the survival timeFinally, to confirm the anti-tumor effects of miR-551b in vivo, we used a xenograft mouse mo del. [score:1]
Further analysis demonstrated that low miR-551b levels in TCGA gastric cancer data was closely related to the poor survival rate of GC patients suggesting that miR-551b was a prognostic indicator of GC (Figure 1E). [score:1]
miR-551b inhibits invasion and migration of GC cell lines in vitroSince miR-551b levels were low in the MNK45 and SGC7901 gastric cancer cells, we treated the cells with miR-551b mimic to generate cells with significantly enhanced miR-551b levels (Figure 2) and compared the consequences using in vitro invasion and migration assays. [score:1]
miR-551b mimic transfection. [score:1]
SGC7901 or MNK45 cells (1×10 [5] per well) were grown in a 6-well plate overnight followed by transfection with miR-551b mimics with Lipofectamine 2000 (Beyotime Biotechnology, Hangzhou, China), according to manufacturer's instructions. [score:1]
Also, Kaplan-Meier survival curves were used to analyze the effects of miR-551b mimics on the mice survival. [score:1]
The miR-551b mimics were synthesized by GenePharma (Shanghai, China) and the negative control was purchased from RiboBio Co. [score:1]
Then, control and miR-551b mimic transfected MNK45 or SGC7901 cells (2×10 [7]/ml) were injected with 100μl peritoneally or subcutaneously into nude mice and the tumor growth/volume was followed every 7 days for 5 weeks. [score:1]
We observed that cells transfected with the miR-551b mimic showed significant reduction in migration and invasion (Figure 3A-3D). [score:1]
Figure 7ally (A and B) Relative levels of ERBB4 mRNA in untreated and miR-551b mimic treated MNK45 and SGC7901 cells based on RT-PCR is shown. [score:1]
To examine the effect of miR-551b on the growth and metastasis of tumor cells in vivo, GC cell lines, SGC-7901 and MNK45 were transfected with luciferase vector (Sangon Biotech, Shanghai, China) with or without miR-551b mimic. [score:1]
Most importantly, miR-551b mimic treated cells resulted in significantly enhanced survival time of tumor bearing nude mice (Figure 8D). [score:1]
The sequences of the human miR-551b promoter region were inserted into pGL3-basic vector (Sangon Biotech, Shanghai, China). [score:1]
Finally, to confirm the anti-tumor effects of miR-551b in vivo, we used a xenograft mouse mo del. [score:1]
Relative expression of miR-551b was calculated by the ΔΔCq method. [score:1]
miR-551b supresses tumor growth in vivo and prolonged the survival time. [score:1]
Therefore, we conducted both in vitro and in vivo experiments to investigate the molecular mechanism of miR-551b in inhibiting metastasis and EMT of GC. [score:1]
For further confirmation, miR-551b levels were quantified in 27 frozen gastric cancer specimens paired with adjacent normal tissues. [score:1]
First, MNK45 and SGC7901 cells were transfected with either miR-551b -mimics or control and then injected into the subcutaneous or peritoneum of nude mice. [score:1]
In contrast, cells treated with miR-551b mimic demonstrated quadrilateral shape and no characteristic microfilament organization along with enhanced E-Cadherin and reduced N-Cadherin and Vimentin levels that suggested inhibition of EMT (Figure 4D and 4F). [score:1]
We observed that co-transfection of miR-551b mimics significantly enhanced the luciferase activity of the ERBB4 3′-UTR reporter, but, the luciferase activity of ERBB4 reporter with mutated miR-551b binding sites remained basal (Figure 5D-5G). [score:1]
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[+] score: 15
Other miRNAs from this paper: mmu-mir-30a, mmu-mir-101a, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-132, mmu-mir-134, mmu-mir-135a-1, mmu-mir-138-2, mmu-mir-142a, mmu-mir-150, mmu-mir-154, mmu-mir-182, mmu-mir-183, mmu-mir-24-1, mmu-mir-194-1, mmu-mir-200b, mmu-mir-122, mmu-mir-296, mmu-mir-21a, mmu-mir-27a, mmu-mir-92a-2, mmu-mir-96, rno-mir-322-1, mmu-mir-322, rno-mir-330, mmu-mir-330, rno-mir-339, mmu-mir-339, rno-mir-342, mmu-mir-342, rno-mir-135b, mmu-mir-135b, mmu-mir-19a, mmu-mir-100, mmu-mir-139, mmu-mir-212, mmu-mir-181a-1, mmu-mir-214, mmu-mir-224, mmu-mir-135a-2, mmu-mir-92a-1, mmu-mir-138-1, mmu-mir-181b-1, mmu-mir-125b-1, mmu-mir-194-2, mmu-mir-377, mmu-mir-383, mmu-mir-181b-2, rno-mir-19a, rno-mir-21, rno-mir-24-1, rno-mir-27a, rno-mir-30a, rno-mir-92a-1, rno-mir-92a-2, rno-mir-96, rno-mir-100, rno-mir-101a, rno-mir-122, rno-mir-125a, rno-mir-125b-1, rno-mir-125b-2, rno-mir-132, rno-mir-134, rno-mir-135a, rno-mir-138-2, rno-mir-138-1, rno-mir-139, rno-mir-142, rno-mir-150, rno-mir-154, rno-mir-181b-1, rno-mir-181b-2, rno-mir-183, rno-mir-194-1, rno-mir-194-2, rno-mir-200b, rno-mir-212, rno-mir-181a-1, rno-mir-214, rno-mir-296, mmu-mir-376b, mmu-mir-370, mmu-mir-433, rno-mir-433, mmu-mir-466a, rno-mir-383, rno-mir-224, mmu-mir-483, rno-mir-483, rno-mir-370, rno-mir-377, mmu-mir-542, rno-mir-542-1, mmu-mir-494, mmu-mir-20b, mmu-mir-503, rno-mir-494, rno-mir-376b, rno-mir-20b, rno-mir-503-1, mmu-mir-1224, mmu-mir-672, mmu-mir-455, mmu-mir-490, 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-504, mmu-mir-466d, mmu-mir-872, mmu-mir-877, rno-mir-466b-1, rno-mir-466b-2, rno-mir-466c, rno-mir-872, rno-mir-877, rno-mir-182, rno-mir-455, rno-mir-672, mmu-mir-466l, mmu-mir-466i, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-466j, rno-mir-551b, rno-mir-490, rno-mir-1224, rno-mir-504, 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-466b-8, rno-mir-466d, mmu-mir-466q, mmu-mir-21b, mmu-mir-21c, mmu-mir-142b, mmu-mir-466c-3, rno-mir-322-2, rno-mir-503-2, rno-mir-466b-3, rno-mir-466b-4, rno-mir-542-2, rno-mir-542-3
Both ACTH and 17α-E2 up-regulated the expression of miRNA-212, miRNA-132, miRNA-154, miRNA-494, miRNA-872, miRNA-194, and miRNA-24-1, but reduced the expression of miRNA-322, miRNA-20b, miRNA-339, miRNA-27a, miRNA-551b, and miRNA-1224. [score:8]
The levels of miR-27a and miR-551b were down-regulated by all three hormones, ACTH, 17α-E2 and DEX. [score:4]
Finally the expression levels of miRNA-27a and miRNA-551b were significantly reduced in adrenals of ACTH, 17α-E2 or DEX treated animals. [score:3]
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[+] score: 5
Of the latter, miR126, miR136, miR206, miR451 and miR551b showed significant, gradual down-regulation (>2 times) after birth or during development (ED16>4W>4W). [score:5]
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[+] score: 3
The glucosamyl (N-acetyl) transferase 1 (GNCT1), a member of the beta-1,6-N-acetylglucosaminyltransferase gene family, is the primary target gene of miR-551, as shown in this pathway. [score:3]
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[+] score: 1
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-93, mmu-let-7g, mmu-let-7i, mmu-mir-126a, mmu-mir-302a, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-126, 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-93, hsa-mir-302a, mmu-mir-466a, hsa-mir-551b, hsa-mir-548a-1, hsa-mir-548b, hsa-mir-548a-2, hsa-mir-548a-3, hsa-mir-548c, hsa-mir-626, hsa-mir-548d-1, hsa-mir-548d-2, mmu-mir-763, mmu-mir-680-2, mmu-mir-692-1, mmu-mir-327, 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-466d, mmu-mir-466l, mmu-mir-466i, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-466j, mmu-mir-467g, hsa-mir-1233-1, hsa-mir-1234, hsa-mir-548e, hsa-mir-548j, hsa-mir-548k, hsa-mir-1299, 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-1255a, hsa-mir-548g, hsa-mir-548n, hsa-mir-548m, hsa-mir-548o, hsa-mir-1268a, 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-103b-2, hsa-mir-320d-2, hsa-mir-548q, 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-466b-8, hsa-mir-548s, hsa-mir-466, hsa-mir-548t, hsa-mir-548u, hsa-mir-548v, hsa-mir-3176, hsa-mir-548w, hsa-mir-548x, mmu-mir-3471-1, hsa-mir-4281, hsa-mir-1302-11, hsa-mir-548y, hsa-mir-548z, hsa-mir-548aa-1, hsa-mir-548aa-2, hsa-mir-548o-2, hsa-mir-1268b, 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-3689c, hsa-mir-548x-2, hsa-mir-548ak, hsa-mir-548al, hsa-mir-548am, hsa-mir-548an, hsa-mir-548ao, hsa-mir-548ap, mmu-mir-466q, hsa-mir-548aq, hsa-mir-548ar, hsa-mir-548as, hsa-mir-548at, hsa-mir-548au, hsa-mir-548av, hsa-mir-548aw, hsa-mir-548ax, mmu-let-7j, hsa-mir-548ay, hsa-mir-548az, mmu-let-7k, mmu-mir-126b, hsa-mir-548ba, hsa-mir-548bb, mmu-mir-466c-3, hsa-mir-548bc
For example, HSA-MIR-3176, HSA-MIR-3689c, MMU-MIR-551b and MMU-MIR-692-1, that are respectively TE-derived, mis-annotated, TE-derived and TE-derived miRNAs, show TE sequences inside precursors only if they are submitted with the extended sequence in CENSOR. [score:1]
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