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33 publications mentioning mmu-mir-338

Open access articles that are associated with the species Mus musculus and mention the gene name mir-338. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 295
Other miRNAs from this paper: hsa-mir-338
miR-338-3p overexpression suppressed NSCLC cell proliferation and induced apoptosis as well as directly targeted SphK2 and inhibited effect of miR-338-3p on NSCLC A549 and H1299 cells by down -regulating SphK2. [score:11]
Overexpression of miR-338-3p significantly inhibited SphK2 expression and reduced luciferase reporter activity containing the SphK2 3′-untranslated region (3′-UTR) through the first binding site. [score:9]
miR-338-3p suppresses SphK2 expression by directly targeting the SphK2 3′-UTR. [score:8]
Collectively, miR-338-3p inhibited cell proliferation and induced apoptosis of NSCLC cells by targeting and down -regulating SphK2, and miR-338-3p could inhibit NSCLC cells A549 and H1299 growth in vivo, suggesting a potential mechanism of NSCLC progression. [score:8]
Thus, SphK2 is a direct functional target of miR-338-3p, which negatively regulates SphK2 expression by directly binding to its putative binding site in the 3′-UTR sequence. [score:8]
of western blot showed that expression level of SphK2 protein was downregulated in A549 cells after transfected with miR-338-3p, and overexpressed both in cells transfected with pcDNA3.1-SphK2 (without the 3′-UTR) alone and co -transfected with miR-338-3p. [score:8]
Data from miRNA arrays indicate that miR-338-3p is downregulated in NSCLC tissues [33, 34] and miR-338-3p may exert a tumor suppressor role in NSCLC. [score:6]
miR-338-3p significantly downregulated expression of SphK2 in A549 and H1299 cells. [score:6]
miR-338-3p expression in 34 NSCLC clinical samples was downregulated and this was correlated with TNM stage. [score:6]
Identification of targets of miR-338-3p in NSCLC is necessary for understanding the underlying regulatory mechanisms so we used bioinformatics for target gene prediction. [score:6]
miR-338-3p suppresses the translation of a select group of cellular mRNA whose protein products are negative regulators of neurite growth. [score:6]
indicated that SphK2 expression was downregulated in A549 and H1299 cells after transfection with miR-338-3p (Fig.   2b). [score:6]
Fig.  6Inhibitory effect of miR-338-3p on NSCLC is mediated by downregulating SphK2. [score:6]
b Representative images of tumors on indicated days (left panel) and tumor growth curve in mice (right panel) for H1299 cells Western blot indicated that transfection of SphK2-siRNA and miR-338-3p inhibited expression of SphK2, respectively (Fig.   6a, b). [score:5]
h Relative expression of miR-338-3p differed significantly between NHBE cell line and human lung cancer cell lines Bioinformatic analysis using TargetScan and miRanda indicated that the 3′-UTR of SphK2 contains a predicted binding site for miR-338-3p (Fig.   2a). [score:5]
miR-338-3p expression is significantly reduced and SphK2 expression is significantly increased in NSCLC tissues. [score:5]
qRT-PCR results showed that the relative expression of miR-338-3p in NSCLC tumor tissues was much lower than in normal tissues (p < 0.001; Fig.   1d), and the relative expression of miR-338-3p in I + II stage tumor tissues was higher than in III stage tumor tissues of NSCLC (p = 0.023; Fig.   1e). [score:5]
Site-directed mutagenesis of the miR-338-3p target site in the SphK2 3′-UTR (pmiR-GLO-mut) was carried out using a Quikchange site-directed mutagenesis kit (Promega, Madison, WI), with pmiR-GLO-WT as the template. [score:5]
These results indicated that the effects of miR-338-3p on NSCLC cell proliferation and apoptosis were restored by SphK2 lacking the 3′-UTR, suggesting that miR-338-3p suppress NSCLC cell proliferation and induce apoptosis by targeting the 3′-UTR of SphK2. [score:5]
b SphK2 protein (Western blot) indicated that transfection of SphK2-siRNAs and miR-338-3p inhibited expression of SphK2 in H1299 cells, respectively. [score:5]
Analysis of patient data indicated that SphK2 expression was significantly correlated with NSCLC TNM stage (p = 0.017), and expression of miR-338-3p was also significantly correlated with NSCLC TNM stage (p = 0.023). [score:5]
Overexpression of miR-338-3p suppresses proliferation of A549 and H1299 cells. [score:5]
b Representative images of tumors on indicated days (left panel) and tumor growth curve in mice (right panel) for H1299 cells indicated that transfection of SphK2-siRNA and miR-338-3p inhibited expression of SphK2, respectively (Fig.   6a, b). [score:5]
Using various approaches, we observed that overexpression of miR-338-3p suppressed NSCLC A549 and H1299 cell proliferation and induced apoptosis in vitro and in vivo. [score:5]
miR-338-3p is mapped to the seventh intron of the apoptosis -associated tyrosine kinase (AATK) gene and miR-338-3p regulates gene AATK expression in rat neurons [15]. [score:4]
Inhibitory effect of miR-338-3p on NSCLC A549 and H1299 cells is mediated by down -regulating SphK2. [score:4]
A dual-luciferase reporter system with luciferase reporter vectors containing either the wild-type or the mutant 3′-UTR of SphK2 verified whether SphK2 is a direct target of miR-338-3p. [score:4]
Thus, miR-338-3p inhibited NSCLC biological effects by down -regulating SphK2. [score:4]
We found that miR-338-3p was downregulated in NSCLC tissues, and was significantly correlated with NSCLC pathological stage. [score:4]
Previous studies indicate that miR-338-3p is downregulated in colorectal and hepatocellular carcinomas and gastric cancer [30– 32]. [score:4]
In tumorigenesis, miR-338-3p is down-regulated in multiple cancers, including gastric, colorectal, and lung cancers [17– 19]. [score:4]
SphK2 was a direct target of miR-338-3p. [score:4]
Three groups were generated for the ensuing experiments: non -transfected group (blank control), scrambled miRNA transfected group (negative control, NC) and miR-338-3p mimics transfected group (inhibitor). [score:3]
qRT-PCR of the relative expression of miR-338-3p showed the opposite results, in human lung cancer cell lines H460, H1299, A549, SPC-A-1 and Calu-3, it was much lower than that in NHBE, and also more obvious in H1299 and A549 cell lines (Fig.   1h). [score:3]
Thus, miR-338-3p inhibited tumorigenicity of NSCLC A549 and H1299 cells in a nude mouse xenograft mo del. [score:3]
Restoration of SphK2 rescues tumor suppression by miR-338-3p. [score:3]
f Expression of SphK2 and miR-338-3p in NSCLC was negatively correlated. [score:3]
miR-338-3p was first reported in prion -induced neurodegeneration: expression of miR-338-3p is reduced in mouse brains infected with mouse-adapted scrape [16]. [score:3]
d miR-338-3p expression differed significantly between cancer tissues and corresponding distant normal tissues (* p < 0.05). [score:3]
NSCLC non-small-cell lung cancer miR-338-3p miRNA-338-3p SphK2 sphingosine kinase 2 CCK-8 cell counting kit 8 3′-UTR 3′-untranslated region AATK apoptosis -associated tyrosine kinase FBS fetal bovine serum DMEM Dulbecco’s minimum essential medium NC negative control GJZ, GWZ, and GQZ: conceived of the study, and participated in its design and coordination and helped to draft the manuscript. [score:3]
Thus, relative expression of SphK2 and miR-338-3p in NSCLC was negatively correlated (Fig.   1f). [score:3]
NSCLC A549 and H1299 cell line stably expressing luciferase infected by lentivirus packaged with vectors LV6-miR-338-3p or LV6 empty vector as described in “”. [score:3]
miR-338-3p significantly inhibited tumorigenicity of NSCLC A549 and H1299 cells in a nude mouse xenograft mo del. [score:3]
Previously, miR-338-3p was shown to act as a tumor suppressor in some cancers [28, 29]. [score:3]
NSCLC A549 and H1299 cell line stably expressing luciferase infected with lentivirus packaged with lentiviral vectors LV6-miR-338-3p or LV6 empty vector (GenePharma, Shanghai, China), and cells were collected and injected into the flanks of nude mice. [score:3]
Therapeutically, miR-338-3p may serve as a potential target in the treatment of human lung cancer. [score:3]
However, the expression pattern of miR-338-3p in lung cancer, particularly in NSCLC, is unreported. [score:3]
e miR-338-3p expression in I + II stage cancer tissues and III stage cancer tissues of NSCLC with different TNM stages (* p < 0.05). [score:3]
Thus, miR-338-3p suppresses viability of NSCLC A549 and H1299 cells. [score:3]
a SphK2 protein was measured using which showed that transfection of SphK2-siRNAs and miR-338-3p inhibited expression of SphK2 in A549 cells, respectively. [score:3]
d CCK-8 array showed that SphK2-siRNA and miR-338-3p inhibited H1299 cell proliferation. [score:3]
Fig.  7Over -expression of SphK2 lacking the 3′-UTR restores the effects of miR-338-3p on NSCLC cell proliferation and apoptosis. [score:3]
miR-338-3p significantly suppressed proliferation and induced apoptosis of NSCLC A549 and H1299 cells in vitro. [score:3]
Fig.  1Expression of miR-338-3p and SphK2 in NSCLC. [score:3]
miR-338-3p inhibits NSCLC cells A549 and H1299 growth in vivo. [score:3]
SphK2 lacking 3′-UTR restored the effects of miR-338-3p on cell proliferation inhibition. [score:3]
Thus, we explored the effect of miR-338-3p targeting SphK2 on proliferation and apoptosis of NSCLC cells. [score:3]
And miR-338-3p inhibited NSCLC cell growth in vivo. [score:3]
a The putative wild-type SphK2 3′-UTR binding sequences in miR-338-3p, and the mutation sequence of SphK2 3′-UTR was not matched with the miR-338-3p. [score:2]
a CCK-8 assay confirmed that miR-338-3p inhibited A549 cell growth. [score:2]
c CCK-8 assay showed that SphK2-siRNA and miR-338-3p inhibited A549 cell proliferation. [score:2]
Using luciferase reporter assays,, and qRT-PCR assays we verified that miR-338-3p directly targets SphK2 by interacting with the first binding site in the 3′-UTR. [score:2]
Luciferase reporter assay and were used to confirm targeting of SphK2 by miR-338-3p. [score:2]
Thus, we studied the regulation of miR-338-3p on SphK2 and the consequent effects on proliferation and apoptosis of human NSCLC cells. [score:2]
b CCK-8 assay confirmed that miR-338-3p inhibited growth of H1299 cells. [score:2]
b– d Cell proliferation by CCK-8 assays and by colony formation assays, cell apoptosis by flow cytometry assays (* p < 0.05) Analysis of patient data indicated that SphK2 expression was significantly correlated with NSCLC TNM stage (p = 0.017), and expression of miR-338-3p was also significantly correlated with NSCLC TNM stage (p = 0.023). [score:2]
However, little is known about the role of miR-338-3p in NSCLC proliferation and apoptosis so we investigated NSCLC progression and development by identifying miRNA targets. [score:2]
Co-transfection of miR-338-3p significantly decreased luciferase activity of the reporter containing pmirGLO-wt 3′-UTR (* p < 0.05), but did not decrease that of the pmirGLO-mut 3′-UTR reporter. [score:1]
d Luciferase reporter vectors that contained wild-type (or mutant-type) 3′-UTR segments of SphK2 were constructed and co -transfected into H1299 cells together with NC or miR-338-3p. [score:1]
c Luciferase reporter vectors that contained wild-type (or mutant-type) 3′-UTR segments of SphK2 were constructed and co -transfected into A549 cells with NC or miR-338-3p. [score:1]
Also, colony formation in the miR-338-3p group was much lower than that of NCs in A549 and H1299 cells (Fig.   3c). [score:1]
a At 48 h after transfection with miR-338-3p or NC, A549 cells or H1299 cells was collected for analysis of apoptosis. [score:1]
and luciferase reporter assays were used to determine whether SphK2 is regulated by miR-338-3p. [score:1]
Flow cytometry was used to study the effect of miR-338-3p on NSCLC apoptosis. [score:1]
NSCLC cell line was co -transfected with miR-338-3p and pcDNA3.1-SphK2 without the 3′-UTR. [score:1]
Co-transfection of miR-338-3p significantly decreased luciferase activity of the reporter containing wild-type 3′-UTR, but did not decrease that of the mutant 3′-UTR reporter (* p < 0.05) in A549 cells (Fig.   2c). [score:1]
miR-338-3p induces apoptosis of A549 and H1299 NSCLC. [score:1]
Also, co-transfection of miR-338-3p significantly decreased luciferase activity of the reporter containing the wild-type 3′-UTR reporter in H1299 cells (* p < 0.05; Fig.   2d). [score:1]
The miR-338-3p mimics (GMR-miR MicroRNA-338-3p mimics) used in this study were synthesized by Shanghai GenePharma Co. [score:1]
of CCK-8 assay and colony formation assay showed that the proliferation inhibitory effects of miR-338-3p on A549 cells were partly restored by pcDNA3.1-SphK2 lacking the 3′-UTR (Fig.   7b, c), and the apoptosis promoted effects of miR-338-3p were also partly restored (Fig.   7d). [score:1]
Expression of miR-338-3p and SphK2 in NSCLC A549 and H1299 cell lines was measured using qRT-PCR and. [score:1]
f Flow cytometry showed that SphK2-siRNA and miR-338-3p induced A549 and H1299 apoptosis To investigate whether the effects of miR-338-3p on the cell proliferation and apoptosis of NSCLC cells was mediated by SphK2 repression, we overexpressed SphK2 lacking the 3′-UTR in NSCLC cell lines and co -transfected with miR-338-3p. [score:1]
CCK-8 assay showed that SphK2-siRNA inhibited proliferation of A549 and H1299 cells compared to NCs, and this was similar to cells transfected with miR-338-3p (Fig.   6c, d). [score:1]
e showed that SphK2-siRNA and miR-338-3p reduced A549 and H1299 cell colony growth. [score:1]
Cells were transfected with miR-338-3p mimics using Lipofectamine™ 2000 (Invitrogen, Carlsbad, CA) according to the manufacturer’s instructions. [score:1]
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2
[+] score: 274
Other miRNAs from this paper: mmu-mir-1a-1, mmu-mir-1a-2, mmu-mir-1b
As shown in Fig. 3A and B, miR-338-3p overexpression down-regulated expression of HIF-1 target genes vascular endothelial growth factor (VEGF), glucose transporter 1 (GLUT-1), and multidrug resistance gene (MDR1, produces P-glycoprotein; P-gp) at the transcriptional and the translational levels under hypoxia. [score:12]
Previous studies have shown that other cell regulatory elements such as cyclin D1 [37] and smoothened [38] also are targets of miR-338-3p that are aberrantly expressed due to downregulated miR-338-3p expression in HCC. [score:11]
Our study found that miR-338-3p overexpression down-regulated expression of VEGF, GLUT-1 and MDR1, which are all known to be regulated by HIF-1 and are important in tumorigenesis [39]– [41]. [score:9]
miR-338-3p suppresses HIF-1α expression by directly targeting the HIF1A 3′UTR. [score:8]
We next used RT-PCR and western blot to examine whether miR-338-3p overexpression results in down-regulation of the HIF signaling pathway. [score:6]
[24], [25] To confirm that miR-338-3p regulates HIF-1α expression, we assessed HIF-1α protein levels in HepG2, SMMC7721, and Huh-7 cells expressing ectopic miR-338-3p, using western blot. [score:6]
Consistent with the results of our HIF-1α overexpression study, down-regulation of HIF-1α, using HIF1A siRNA, significantly decreased HIF-1α protein levels, reduced HepG2 cell viability and induced cell apoptosis, whereas miR-338-3p did not show further effects when co -transfected with HIF1A siRNA (Figs. 5E-5H; p≤0.01). [score:6]
As shown in Fig. 5A and 5B, re-introduction of HIF-1α rescued HIF-1α protein levels downregulated by miR-338-3p and abrogated the inhibitory effect of miR-338-3p on cell viability. [score:6]
Undoubtedly, regulation of such other targets may contribute to the inhibitory effects of miR-338-3p on HCC. [score:6]
Moreover, miR-338-3p down-regulated tumor HIF-1α expression in mice treated with or without sorafenib (Fig. 7C). [score:6]
In this study, we found that miR-338-3p directly targeted HIF-1α and suppressed the HIF signaling pathway. [score:6]
Our results showed that miR-338-3p inhibits cell viability and induces cell apoptosis by directly targeting HIF-1α. [score:6]
0115565.g003 Figure 3 (A) Effect of miR-338-3p on HIF-1α target genes expression including VEGF, GLUT-1 and MDR1, determined by RT- PCR. [score:5]
Even though recent evidence indicates the inhibitory effect of miR-338-3p on human cancers, such as colorectal [27], neuroblastoma [28], gastric [29], and osteosarcoma [30], there is little knowledge about miR-338-3p and its targets in HCC. [score:5]
Predicted targets of miR-338-3p are factors involved in many biological processes, such as cell proliferation, differentiation, and cell death, as well as diseases such as Alzheimer's, arthritis, and cancer. [score:5]
Our study found that miR-338-3p expression is markedly down-regulated in HCC patient samples and HCC cell lines as compared to normal liver cells. [score:5]
To explore the functional significance of HIF-1α in the inhibitory effects of miR-338-3p on HCC tumorigenesis, we overexpressed HIF-1α in miR-338-3p -transfected HepG2 cells and determined whether HIF-1α can reverse miR-338-3p -mediated regulation of cell viability and apoptosis using western blot, MTT assay and flow cytometry. [score:5]
Taken together, these findings suggested that miR-338-3p is down-regulated in human HCC. [score:4]
However, considering our observation that HIF-1α overexpression rescued the cell from the anti-HCC activity of miR-338-3p, it is likely that regulation of HIF-1α by miR-338-3p is a key anti-tumor aspect in HCC. [score:4]
To further elucidate the mechanisms through which miR-338-3p reduces HCC resistance to sorafenib, we tested the effect of miR-338-3p on P-gp gene expression, since inducing P-gp protein expression is considered one of the most important mechanisms of HIF-1α on chemoresistance [10], [26]. [score:4]
The inhibitory effect of miR-338-3p on HCC is mediated by down -regulating HIF-1α. [score:4]
Down-regulation of miR-338-3p in human Hepatocarcinoma (HCC) tissues and cell lines. [score:4]
To our knowledge, our study is the first to show regulation of P-gp expression by miR-338-3p. [score:4]
Inhibitory effect of miR-338-3p on HCC cells is mediated by down -regulating HIF-1α. [score:4]
In summary, these results indicate that HIF-1α is a direct target gene of miR-338-3p in human HCC cells. [score:4]
miR-338-3p directly targets HIF-1α. [score:4]
Furthermore, our data showed that miR-338-3p potentiated growth inhibitory function of sorafenib in HCC. [score:3]
HepG2 cells were infected with 20 MOI of miR-338-3p -expressing lentivirus or control lentivirus by spin infection for 2 h, followed by incubation at 37°C for 2 h. HepG cells (2×10 [6]) in 0.1 ml Hank's balanced salt solution were injected subcutaneously into the right scapular region of nude mice. [score:3]
We also analyzed miR-338-3p expression in liver cell line L02 and five human HCC cell lines (HepG2, SMMC-7721, BEK-7402, Hep3B, and Huh-7). [score:3]
miR-338-3p mimic, miR-338-3p inhibitor, miR-338-3p mutant and negative control (NC) were purchased from Shanghai Gene-Pharma Co. [score:3]
To further demonstrate that miR-338-3p directly regulates HIF-1α by interacting with its 3′UTR, we co -transfected the pGL luciferase reporter plasmid harboring the wild type or mutant 3′-UTR of HIF-1α, along with miR-338-3p or NC-miRNA (Fig. 2D). [score:3]
These findings suggest that miR-338-3p is a potential HCC suppressor and plays an important role in preventing HCC drug resistance. [score:3]
Additionally, apoptosis induced by miR-338-3p was also significantly attenuated by HIF-1α overexpression (Fig. 5C-D; p≤0.01). [score:3]
We examined the tumor suppressor properties of miR-338-3p in HCC cells and in nude mice. [score:3]
Because recent studies have reported that inhibition of HIF-1α can overcome hypoxia -mediated sorafenib resistance in HCC [20], we tested whether miR-338-3p could sensitize HCC cells to sorafenib treatment. [score:3]
miR-338-3p inhibits HIF signaling pathway. [score:3]
miR-338-3p expression is significantly reduced in HCC tissues and cell lines. [score:3]
The results showed that HIF-1α levels, under hypoxia, were consistently reduced by miR-338-3p overexpression in all three types of cell lines (Fig. 2B). [score:3]
Our further studies will focus on other targets of miR-338-3p and their specific roles under both normoxic and hypoxic conditions. [score:3]
miR-338-3p inhibits the HIF pathway. [score:3]
Our study identified one key target of miR-338-3p, HIF-1α. [score:3]
15 µM) treatment under hypoxia; n = 4. (B) % apoptotic cells assessed two days after sorafenib (15 µM) treatment under hypoxia; n = 4. (C) Cytoplasmic and nuclear expression of HIF-1α in NC- or miR-338-3p -transfected (50 nM) HepG2 cells treated with or without sorafenib (15 µM), as detected by immunofluorescence staining. [score:3]
Inhibited or silent HIF-1α can increase HCC sensitivity to sorafenib, which provides a rationale for testing combined therapy with miR-338-3p and sorafenib. [score:3]
The results showed that the inhibitory effect of miR-338-3p on HCC cells were more significant under hypoxia than under normoxia (S2 Fig. ). [score:3]
These results indicate that miR-338-3p elicits anti-HCC effects by targeting HIF-1α. [score:3]
miR-338-3p and sorafenib synergistically inhibit subcutaneous tumor growth. [score:3]
Consistently, miR-338-3p was down-regulated in all HCC cell lines examined compared to L02 cells (Fig. 1B). [score:3]
S1 Fig miR-338-3p inhibitor has no effect on HIF1A 3′UTR luciferase reporter activity. [score:3]
As shown in Fig. 4A, ectopic expression of miR-338-3p markedly reduced HCC cell viability in all three types of HCC cell lines. [score:3]
miR-338-3p and sorafenib synergistically inhibited subcutaneous tumor growth. [score:3]
The expression levels of miR-338-3p were quantified using TaqMan miRNA assay kit (Applied Biosystems, Foster City, CA). [score:2]
To establish whether miR-338-3p plays a suppressing role in HCC tumorigenesis, we analyzed cell viability using MTT assay and apoptosis using flow cytometry, in HCC cells transfected with miR-338-3p. [score:2]
Furthermore, miR-338-3p could reduce HCC cell viability and promote cell apoptosis by directly binding to the 3′-UTR of HIF-1α. [score:2]
Taken together, our results provide strong evidence that miR-338-3p can antagonize hypoxia -mediated sorafenib resistance by regulating HIF-1α. [score:2]
Luciferase reporter assay of cells transfected with the HIF1A 3′UTR luciferase reporter plasmid with increasing amounts (20 to 50 nM) of NC or miR-338-3p-in (miR-338-3p -inhibitor in HCC cells two days post-transfection. [score:2]
We did not observe significant difference in luciferase activity in cells transfected with miR-338-3p inhibitor compared to NC. [score:2]
To determine whether miR-338-3p is involved in regulation of human HCC tumorigenesis, we first detected miR-338-3p levels in HCC tumor and adjacent non-tumor tissues, using RT-PCR (n = 15). [score:2]
As shown in Fig. 1A, miR-338-3p expression was significantly less in 14 HCC samples and significantly more in one HCC sample compared to normal adjacent liver tissue. [score:2]
0115565.g001 Figure 1 (A) Real-time PCR analysis of miR-338-3p expression in 15 HCC specimens compared to their pair-matched adjacent non-tumor tissues (NTT). [score:2]
Overexpression of miR-338-3p resulted in significant reduction of HIF1A 3′ UTR firefly luciferase reporter activity containing wild type but not mutant binding sites compared to that of NC-miRNA (Fig. 2E; p≤0.01). [score:2]
Deregulation of miR-338-3p has been reported for many different cancer types. [score:2]
We demonstrated that miR-338-3p can sensitize HCC cells to sorafenib. [score:1]
Mice were randomly divided into four groups (n = 8) that received either lentivirus vector, lentivirus vector +sorafenib, lentivirus-miR-338-3p, or lentivirus-miR-338-3p + sorafenib. [score:1]
0115565.g005 Figure 5 (A) HIF-1α levels in HepG2 cells transfected with miR-338-3p and/or HIF-1α determined by western blot. [score:1]
As expected, miR-338-3p, in a dose -dependent manner, decreased the relative luciferase activity (Fig. 3C; p≤0.01). [score:1]
S2 Fig miR-338-3p reduces HCC cell viability under normoxia. [score:1]
Mice treated with sorafenib and/or miR-338-3p showed moderate weight loss (Fig. 7D). [score:1]
In summary, combined treatment with sorafenib and miR-338-3p exerted a more potent anti-tumor growth effect than either alone. [score:1]
Next, we investigated the effect of miR-338-3p on HIF-1α expression under hypoxia in HepG2 cells with or without sorafenib treatment. [score:1]
Using the DNA Intelligent Analysis -miRPath v2.0 program, we observed that HIF-1α contains conserved miR-338-3p recognition sites in its 3′-UTR (Fig. 2A). [score:1]
miR-338-3p reduces HCC cell viability and promotes cell apoptosis. [score:1]
However, the overall staining and nuclear accumulation of HIF-1α was markedly reduced with miR-338-3p transfection (Fig. 6C). [score:1]
We observed that miR-338-3p sensitized human HCC cells to sorafenib in vitro. [score:1]
We wanted to determine whether miR-338-3p potentiates sensitivity of HCC cells to sorafenib, which is the only drug that currently improves overall survival of HCC patients [59]. [score:1]
Taken together, these results suggested anti-cell growth properties of miR-338-3p in HCC cells. [score:1]
Moreover, to determine whether miR-338-3p could affect the transcriptional activity of HIF-1α, we co -transfected HIF-1α luciferase reporter plasmid with miR-338-3p or NC-miRNA into HepG2 cells. [score:1]
miR-338-3p reduces HCC cell viability and induces cell apoptosis under hypoxia. [score:1]
In this regard, the chemosensitizing effect of miR-338-3p is an important feature for its potential therapeutic roles for HCC. [score:1]
However, P-gp levels were significantly reduced in miR-338-3p -transfected cells (Fig. 6D). [score:1]
However, tumors treated with miR-338-3p or sorafenib were smaller than control tumors. [score:1]
This may be due to the low endogenous levels of miR-338-3p in HCC cells (S1 Fig. ). [score:1]
HepG2 cells were transfected with 50 µM NC or miR-338-3p for 48 h. RT-PCR was performed 24 h after cells were incubated under hypoxia. [score:1]
These results support the possibility that HIF-1α functions as a tumor promoter in the liver, and indicates potential applications for miR-338-3p in anticancer therapy. [score:1]
Using miRNA-specific RT-PCR, we confirmed that the miR-338-3p level had increased more than 10-fold after transfection (Fig. 2C). [score:1]
Collectively, our data demonstrates the functional link between miR-338-3p and the HIF signaling pathway in human HCC cells. [score:1]
However, cells pre -transfected with miR-338-3p can overcome hypoxia -mediated sorafenib resistance. [score:1]
Notably, tumors treated with miR-338-3p and sorafenib were significantly smaller than tumors treated with either miR-338-3 or sorafenib alone (Figs. 7A and 7B). [score:1]
We also found that miR-338-3p combined with sorafenib has synergistic effects against HCC tumor growth in vivo. [score:1]
miR-338-3p sensitizes HCC cells to sorafenib. [score:1]
Similarly, miR-338-3p significantly increased early and late apoptotic cell populations of human HCC cells (Figs. 4B and 4C; p≤0.01). [score:1]
miR-338-3p sensitizes HCC cells to sorafenib treatment. [score:1]
n = 4. (D) Six nucleotides (red) of HIF 3′UTR were mutated to prevent binding with miR-338-3p. [score:1]
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3
[+] score: 83
We analyzed the expression of the following genes by western blot analysis of the encoded proteins: BCL2, NOTCH1 and SIRT1 (miR-34a-5p targets), ATP5G1 (miR-338-3p target) and JNK and p38 (miR-350 targets). [score:9]
Representative cropped blots of BCL2 (miR-34a-5p target), ATP5G1 (miR-338-3p target), p38, JNK (miR-350 targets) and activated p-JNK and p-p38, along with the results of protein quantification performed by laser densitometry (n = 4–5 per group, 5 months-old mice). [score:7]
miR-34a-5p targets Bcl2, Sirt1 and Notch1 genes, influencing apoptosis and mitochondrial energy metabolism, among other processes 29, 30; miR-338-3p regulates the expression of several subunits of mitochondrial oxidative phosphorylation complexes [31], and miR-350 regulates p38 and JNK stress kinases [32]. [score:7]
miRNA RQ Validated target genes Biological process Role in disease miR-31-3p 4.5 RhoA Proliferation and migration Cancer 53 miR-691 3.4 No data No data No data miR-700-3p 3.1 No data No data No data miR-29a-5p 3.1 No data No data Cancer 54 miR-501-3p 3 Gria1 Neuro-transmision No data 55 miR-338-3p* 2.7 Aatk, Atp5g1, CoxIV Axonal guidance, apoptosis, mitochondrial function Cancer, neurodegeneration 42, 56 miR-139-3p 2.7 MMP11 Extracellular matrix organization Cancer 57 miR-34a-5p* 2.5 Bcl-2, Notch1, Map2k1, Sirt1 Apoptosis, mitochondrial function, oxidative stress response Cancer, Alzheimer, cardiomyopathy 29, 30, 34, 43, 44 miR-335-3p 2.1 Ank3 No data No data 58 miR-1949 1.7 Rb1 Cell cycle control Cancer 59 miR-326-3p 0.5 Bcl-xl, Notch1/2 Apoptosis, proliferation Cancer 60, 61 miR-671-5p 0.3 Smarcb1 Proliferation Cancer 62 miR-503-3p 0.2 No data No data No data miR-350* 0.2 p38, Jnk Apoptosis Cardiac hypertrophy 32 [*]miRNAs selected for further studies. [score:5]
To gain insight into the possible role of selected miRNAs in the organ pathophysiology of the disease we quantified the relative expression of miR-34a-5p, miR-338-3p and miR-350 in brain, heart and liver of PA mice and age-matched controls (two months-old, n = 4; five and 10 months-old, n = 5). [score:5]
As previously mentioned, the regulation of the selected target genes by miR-34a-5p, miR-338-3p and miR-350 has been validated in experimental mo dels, as referenced in miRTarbase 31– 36. [score:4]
Most relevant is the discovery in PA patients’ plasma of a specific miRNA signature that includes several miRNAs which were also found dysregulated in the mouse mo del of the disease, among them miR-34a-5p and miR-338-3p. [score:4]
The results confirmed that miR-34a-5p, miR-338-3p and miR-350 are upregulated in brain and heart tissues of PA mice at 2 and 5 months of age, while in 10 months-old mice miRNA levels tend to normalize (Fig.   2). [score:4]
miR-34a-5p, miR-338-3p and miR-350 are up-regulated in different tissues of PA mice. [score:4]
revealed the inverse downregulation of BCL2 with miR-34a-5p mimics and of ATP5G1 with miR-338-3p mimics. [score:4]
miR-338-3p has been found associated with axonal mitochondria where it regulates the expression of nuclear encoded mitochondrial mRNAs encoding subunits of the oxidative phosphorylation (OXPHOS) machinery 31, 41. [score:4]
Both AATK and miR-338 are highly conserved genes, mainly expressed in the central nervous system, where they play a role during differentiation, apoptosis and possibly neuronal degeneration [40]. [score:3]
Figure 2Relative expression levels of miR-34a-5p, miR-338-3p and miR-350 in brain (a), heart (b) and liver (c) tissues from PA mice at different ages. [score:3]
The analysis of miR-338-3p expression in different parts of the brain and in cultured neurons of the PA mouse mo del and the correlation with levels of APT5G1 and other components of the OXPHOS system are subject to future experimental examination. [score:3]
At a second stage, we examined the relative expression levels of miR-34a-5p and miR-338-3p in individual plasma samples in three different patient cohorts and their matched controls: 1) neonatal patients at diagnosis (<1 month old) (n = 8 per group); 2) 2–10 year-old patients at follow-up (n = 12 per group) and 3) 12–25 year-old patients at follow-up (n = 8 per group). [score:3]
However, the overall results are indicative of a regulatory effect of miR-34a-5p on BCL2, miR-338-3p on ATP5G1 and miR-350 on p38 in PA mice tissues. [score:2]
Of note, miR-34a-5p and miR-338-3p were included among these miRNAs, as well as others (miR-29a-5p, miR-31-3p, miR-326 and miR-335-3p) also found dysregulated in liver samples of the PA mouse mo del (Table  1). [score:2]
Kos, A. et al. MicroRNA-338 Attenuates Cortical Neuronal Outgrowth by Modulating the Expression of Axon Guidance Genes. [score:2]
Interestingly, plasma miR-34a-5p and miR-338-3p show a different profile in neonatal samples at diagnosis and in follow-up samples in older patients (Fig.   5). [score:1]
In addition, miR-338-3p modulates the expression of axon guidance genes [42], which should be evaluated in relation to PA pathology. [score:1]
miR-34a-5p and mir-338-3p mimics were transfected in Hep3B (a) and SH-SY5Y cells (b) and miR-350 mimics in Hl-1 (c) and N2A cells (d). [score:1]
miR-338 is encoded intronically within the apoptosis -associated tyrosine kinase (AATK) gene in mice and humans. [score:1]
We and other authors have reported that mitochondrial dysfunction and oxidative stress are probable key players in the pathophysiology of PA 24, 25, which led us to select three miRNAs for further studies, miR-34a-5p, miR-338-3p and miR-350, due to their involvement in these processes. [score:1]
Taken together, the results show a significant increase in miR-34a-5p plasma levels in neonatal PA samples and a decrease of both miR-34a-5p and miR-338-3p in older patients (Fig.   5). [score:1]
Thus, functional analysis was carried out in Hep3B and SH-SY5Y cells (for miR-34a-5p and miR-338-3p), or in HL-1 and N2A cells (for miR-350, a rodent specific miRNA), cell lines in which the miRNAs are readily detected. [score:1]
Figure 5Relative levels of miR-34a-5p and miR-338-3p in plasma samples from PA patients. [score:1]
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4
[+] score: 35
Taken together, our findings suggest that potential UCP1 -targeting miR-9 and miR-338-3p may be involved in the process of the browning of epididymal adipose tissue through posttranscriptional suppression of UCP1 gene expression. [score:7]
Compared with control group, as shown in Figure 3(b), the expression of miR-9 and miR-338-3p was significantly restrained in epididymal adipose tissue with CL316243 treatment (P < 0.05), and miR-let7g (not UCP1 -targeting miRNAs, as negative control) expression had no statistical differences (P > 0.05). [score:6]
Clearly, we need to identify whether miR-9 and miR-338-3p are the potential candidates that target UCP1. [score:3]
Here we showed that miR-9 and miR-338-3p which possibly targeted UCP1 were dramatically decreased with CL316243 treatment. [score:3]
These results seemed to strictly correlate with an increase in UCP1 mRNA, confirming the hypothesis that CL316243 could reduce miR-9 and miR-338-3p expression leading to reducing the degradation of UCP1 messenger RNA. [score:3]
We proposed that β3-adrenergic stimulations might restrain expression of miR-9 and miR-338-3p in the epididymal adipose tissue in mice. [score:3]
A panel of 2 miRNAs, namely, miR-9 and miR-338-3p, was selected for its putative ability to target the 3′-UTRs of UCP1 mRNA (Figure 3(a)). [score:3]
Expressions of miR-9 and miR-338-3p in the Epididymal Adipose Tissue of Mice with CL316243 Treatment. [score:3]
Primers for miR-9, miR-338-3P, miR-let7g, and U6 were listed in Table 1. The relative expressions among the different genes and miRNAs were determined using the 2 [−ΔΔCT] method. [score:2]
Primers for miR-9, miR-338-3P, miR-let7g, and U6 were listed in Table 1. The relative expressions among the different genes and miRNAs were determined using the 2 [−ΔΔCT] method. [score:2]
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5
[+] score: 23
miR-338-3p, a microRNA with a similar developmental expression profile, was also downregulated. [score:7]
Thus, at least miR-138 and miR-338-3p expression resemble that of other key regulators in the network, displaying mirror image expression in differentiation versus dedifferentiation situations [20]. [score:6]
Indeed, the expression of some candidates, such as miR-338 and miR-146b, was reduced in the P5 Egr2 [−/−] sciatic nerve. [score:3]
Thus, EGR2 is either directly or indirectly upstream of miR-138, miR-338, and miR-146b in vivo. [score:3]
Thus, in addition to EGR2 repression of antecedent gene expression programs via NAB corepressors [46], EGR2 induction of miR-138, and potentially miR-338 and miR-146b, may be a second mechanism by which EGR2 carries out or reinforces the repression. [score:3]
Following up these studies, emerging literature points to roles for specific microRNAs in myelination, the best studied examples in mice being miR-219 and miR-338 in oligodendrocyte differentiation and let-7 in SC differentiation 15, 16, 37, 38. [score:1]
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[+] score: 15
Of the eight differentially expressed miRNAs found in both males and females exposed to O [3], a total of six miRNAs were upregulated exclusively in males: miR-338-5p (log fold change = 1.636), miR-222-3p (log fold change = 0.699), miR-130b-3p (log fold change = 0.646), let-7i-5p (log fold change = 0.552), miR-195a-5p (log fold change = 0.543), and miR-144-3p (log fold change = 0.427) (Fig.   2). [score:6]
Some miRNAs such as miR-338-5p, miR-106a-5p, and let-7a-5p (affected exclusively in males) were predicted to target the IL-6 family both directly and indirectly (Fig.   5). [score:5]
Several of these were also involved in inflammation (miR-130b-3p, miR-17-5p, miR-294a-3p, and miR-338-5p) and targeted key regulators of the immune response including IL-6, SMAD2/3, and TMEM9 (Table  1, Additional file  3: Figure S2B). [score:4]
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7
[+] score: 14
Other miRNAs from this paper: mmu-mir-128-1, mmu-mir-130b, mmu-mir-98, mmu-mir-128-2
Integrins have been shown to be downregulated by microRNAs in several studies in different types of cancer, some of which regulate ITGB3 translation, such as miR-128, which is upregulated in hypoxia [81, 82], miR-98 in hypoxia and miR-338, which inhibits migration by targeting HIF1α under low-oxygen conditions [83]. [score:14]
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8
[+] score: 14
For experimental validation in oral tumors, we narrowed down that candidate miRNAs to six (miR-137, miR-148a-3p, miR-30a-5p, miR-30b-5p, miR-338-3p and miR-22-3p) by reviewing the functional evidence present in the literature, analyzing their expression in HNSCC datasets from TCGA and correlating with OIP5-AS1 expression (Supplementary Table  S2). [score:5]
miR-30a-5p, miR-30b-5p, miR-338-3p and miR-22-3p shared maximum common downstream targets. [score:3]
Out of the 8 selected miRNAs, miR-137, miR-140–5p, miR-148a-3p, miR-30a-5p and miR-338-3p were significantly downregulated in the tumors compared with normal tissue (P < 0.001, <0.001, 0.001, 0.001 and 0.0003, respectively) (Fig.   3a). [score:3]
Six miRNAs miR-137, miR-148a-3p, miR-338-3p, miR-30a/b-5p and miR-22-3p known to be associated with several cancers were chosen to study the expression levels in oral tumors 20, 25, 26. [score:3]
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9
[+] score: 12
All miRNAs analyzed were significantly downregulated in Dicer [fl/fl] Dhh-Cre [+] nerves at p4: p≤0.0001 (miR-34a, miR-146b, miR-338-3p, miR-204, miR-27b, miR-140, miR-138, miR-30a), p = 0.0002 (miR-195). [score:4]
Furthermore, miRNAs were confirmed to be upregulated upon myelination: p≤0.0001 (miR-34a, miR-146b), p = 0.04 (miR-338-3p), p = 0.003 (miR-204), p = 0.0007 (miR-27b), p = 0.005 (miR-140), p = 0.0002 (miR-138), p = 0.01 (miR-195), p = 0.0004 (miR-30a). [score:4]
Some of the upregulated miRNAs are important for oligodendrocyte differentiation, e. g. miR-338 [11], [12] and miR-138 [11]. [score:4]
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10
[+] score: 10
Transfection of miR-323-5p (data not shown), miR-338-5p, and miR-370 plasmids did not affect the expression of luciferase reporter from constructs containing the respective target sequence in the 5′UTR (Fig S1A–B). [score:5]
miR-196b, miR-338-5p, miR-370 and miR-375 were previously reported to be expressed in adult mouse pancreas [22]. [score:3]
Additionally, transfection of miR-370 and miR-338-5p duplexes did not show any significant change in reporter activity when transfected with insulin1 and insulin2-S reporters, respectively (Fig. S1C,D). [score:1]
Four miRNAs (miR-196b, miR-323-5p, miR-338-5p and miR-370) with high complementarity to seed sequences (at least 5 base pairs between nucleotide position 2–8 of the miRNA) and a free energy of less than −22 kCal/Mole were selected (Table 1) for further analysis. [score:1]
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[+] score: 8
Other miRNAs from this paper: mmu-mir-34a, mmu-mir-320
The miRNAs miR-338 and miR-320 are amongst the miRNAs that have been shown to downregulate NRP1 expression, and their endothelial expression is associated with reduced angiogenesis in vitro and in tumour xenograft mo dels (Peng et al., 2014, Wu et al., 2014). [score:8]
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[+] score: 8
MiR-338-3p suppresses epithelial-mesenchymal transition in gastric cancer cells by targeting MACC1/Met/Akt pathway (Huang et al., 2015a). [score:4]
MiR-338–3p inhibits epithelial-mesenchymal transition in gastric cancer cells by targeting ZEB2 and MACC1/Met/Akt signaling. [score:4]
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[+] score: 8
Mir-29a, miR-219, miR-338 and miR-132 were the miRNAs undergoing the strongest upregulation during development, a result confirmed by reverse transcription PCR (Supplementary Fig. 1) and in agreement with previous data 8, whereas miR-298, miR-149 and miR-331 were the top downregulated miRNAs. [score:8]
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14
[+] score: 7
Other miRNAs from this paper: mmu-mir-138-2, mmu-mir-140, mmu-mir-138-1, mmu-mir-146b, mmu-mir-709
For instance, during development, miR-138 and miR-338 lead to the repression of Sox-2, c-Jun and other anti-myelinating factors to initiate differentiation of glial cells [19], [23] while these transcripts are translated following peripheral nerve injury despite having sites for other upregulated miRNAs (Fig. 2). [score:7]
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[+] score: 7
This deficit is caused by the haploinsufficiency of Dgcr8 that depletes levels of the thalamus-enriched microRNA miR-338-3p, which negatively regulates Drd2 in the auditory thalamus (Chun et al., 2017). [score:2]
The generation of Df(16)1/+, Dgcr8 floxed, and miR338 [−/−] mouse lines has been reported previously (Chun et al., 2017, Lindsay et al., 1999, Yi et al., 2009). [score:1]
Our previous study indicated that Dgcr8 haploinsufficiency in 22q11DS mice leads to increased Drd2 levels in the auditory thalamus via depletion of the thalamus-enriched microRNA miR-338 (Chun et al., 2017). [score:1]
However, miR338 [−/−] mice were deficient in active avoidance (Figure S7B). [score:1]
However, in contrast to TC deficits, thalamo-LA–related behaviors are not solely dependent on miR-338. [score:1]
In miR-338 KO mice, active avoidance behavior, but not fear conditioning behavior, was impaired, suggesting that, in addition to miR-338, other microRNAs mediate the Dgcr8–Drd2 mechanism in fear memory circuits of 22q11DS. [score:1]
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[+] score: 6
microRNAs (miRNAs) are endogenous non-coding RNAs that facilitate sequence -dependent posttranscriptional silencing, playing pivotal roles in brain development and neuronal function 1– 3. miRNA activity is required for motor neuron survival [4] and broad dysregulation of miRNA biogenesis is associated with Amyotrophic Lateral Sclerosis (ALS) 4– 8. Several miRNA genes have already been suggested to play critical roles in motor neurons, including miR-155 [5], miR-206 [6], miR-338 [9], miR-9 [4] and miR-218 10– 12. [score:3]
Aschrafi, A. et al. MicroRNA-338 regulates the axonal expression of multiple nuclear-encoded mitochondrial mRNAs encoding subunits of the oxidative phosphorylation machinery. [score:3]
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[+] score: 6
Zhao et al. showed that miR-219 and miR-338 functioned in part by directly repressing negative regulators of oligodendrocyte differentiation, and that these miRNAs were important regulators of oligodendrocyte differentiation, possibly providing new targets for myelin repair [40]. [score:6]
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[+] score: 6
Specifically, miR-153in the Udown group microRNA and five microRNAs in the Uup group, miR-148a/b, miR-101a/b, and miR-338-3p, targeted the same mRNA, Robo2. [score:3]
Also, Robo2 was targeted by miR-153 in the Udown group and miR-148a/b, miR-338-3p, and miR-101a/b in the Uup group (Fig 6A). [score:3]
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19
[+] score: 5
Next, we validated the microarray results by analyzing the aberrant expressed microRNA level (miR-7-1-3p, miR- 196a, miR-196b, miR-744-3p, let-7a-3p, miR-34a- 3p, miR-338-5p and miR-365a-5p) in a cohort of 47 LSCC tissues using QPCR and compared with the paired normal tissues (Figure 1). [score:2]
MiR- 7-1-3p, miR-338-5p and miR-365a-5p were detected in the LSCC tissues and the paired normal epithelia. [score:1]
In comparison, let-7a-3p, miR-34a-3p, miR-338-5p and miR-365a- 5p could only be detected in normal epithelial culture. [score:1]
In comparison, let-7a-3p, miR-34a-3p, miR-338-5p and miR-365a-5p could only be detected in normal epithelial culture. [score:1]
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20
[+] score: 5
Preferential expression in the retina was also observed for miR-376a, miR-138, miR-338, and miR-136 as compared with the mouse platform; it is notable, however, that these miRs are expressed at higher levels in brain than in retina. [score:4]
Indeed miR-136, miR-138, and miR-338 were previously cloned from the hippocampus and cerebral cortex [19]. [score:1]
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[+] score: 4
Fig. 6 Tst 3′UTR variation within predicted target site for miRNA mmu-miR-338-5p. [score:3]
Amongst potential miRNA species, miRNA mmu-miR-338-5p is predicted to bind to the 3′UTR Lean line allele with no mismatches and with a mismatch to the Fat line allele (Fig.   6). [score:1]
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[+] score: 4
From the set of the 87 Aire -dependent miRNAs identified in this study, we identified 6 miRNAs (miR-10, miR-30e*, miR142-3p, miR-425, miR-338-3p, and miR-297) that were shared with the set of Aire -dependent miRNAs identified by in vitro Aire-knockdown of an mTEC cell line (35) and 4 miRNAs (miR-206, miR-10b, miR-181c, and miR-363) whose expression was previously detected in TECs. [score:4]
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23
[+] score: 4
In particular, miR-142 and miR-338 are known to be down-regulated in AD patients [21]. [score:4]
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24
[+] score: 3
Down regulation of miR-16-2-3p and -1294, up regulation of miR-338-3p, -30e-3p, and -30a-3p were found in the plasma or CSF of PD patients [29, 30]. [score:3]
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25
[+] score: 3
In addition, we also identified some miRNAs, which were not previously reported to regulate ESC derived endoderm differentiation, such as mir-338-5p and mir-340-3p. [score:2]
Red: mir-338-5p binding site; Yellow: mir-181c binding site; Blue: mir-196 a/mir-196b binding site. [score:1]
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[+] score: 3
Other miRNAs from this paper: mmu-mir-219a-1, mmu-mir-219a-2, mmu-mir-219b, mmu-mir-219c
miRNA 219 and miR-338 have been shown to inhibit Sox6 and block oligodendrocyte differentiation [36]. [score:3]
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[+] score: 3
It is also possible that the action of other miRNAs, such as miR-9, miR-124, miR-137, miR-338 or let-7, could compensate for miR-219 inhibition in NSCs. [score:3]
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[+] score: 3
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-21, hsa-mir-23a, hsa-mir-30a, hsa-mir-98, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-15b, mmu-mir-30a, mmu-mir-30b, mmu-mir-101a, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-9-2, mmu-mir-132, mmu-mir-133a-1, mmu-mir-135a-1, mmu-mir-150, mmu-mir-155, mmu-mir-204, mmu-mir-205, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-30e, hsa-mir-34a, hsa-mir-204, hsa-mir-205, hsa-mir-217, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-30b, hsa-mir-125b-1, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-150, mmu-mir-19b-2, 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-18a, mmu-mir-21a, mmu-mir-23a, mmu-mir-34a, mmu-mir-98, mmu-mir-322, hsa-mir-155, mmu-mir-17, mmu-mir-19a, mmu-mir-135a-2, mmu-mir-19b-1, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-125b-1, mmu-mir-217, hsa-mir-30c-1, hsa-mir-34b, hsa-mir-34c, hsa-mir-30e, hsa-mir-338, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, hsa-mir-18b, hsa-mir-503, mmu-mir-541, mmu-mir-503, mmu-mir-744, mmu-mir-18b, hsa-mir-541, hsa-mir-744, mmu-mir-133c, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-mir-30f, mmu-let-7k, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
A previous study showed that runx2 is a target of miR-30c, miR-135a, miR-204, miR-133a, miR-217, miR-205, miR-34, miR-23a and miR-338 [34]. [score:3]
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[+] score: 3
Other miRNAs from this paper: mmu-mir-138-2, mmu-mir-212, mmu-mir-138-1
Examples of negatively correlated interactions include miR-212-3p, miR-338-3p and miR-138-5p and their potential targets involved in neural functions, Arc, Fos and Ntrk1 respectively. [score:3]
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S7 7. Nrf2 -dependent effect of 5 mg / kg PQ Nrf2(+/+) PQ5—Nrf2(–/–) PQ5 miR-135a, miR-376c, miR-31, miR-let-7i*, miR-669b*, miR-344, miR-15b, miR-700*, miR-3099, miR-377, miR-338-5p, miR-382, miR-219-3p and miR-310a S8 8. Nrf2 -dependent effect of 10 mg / kg PQ Nrf2(+/+) PQ10—Nrf2(–/–) PQ10 miR-495*, miR-154*, miR-let-7b, miR-1983, miR-103 and miR-26a S9 The miR-380-3p / Sp3 mRNA pathway is worth to mention here. [score:1]
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For instance, miR-338-3p is reportedly decreased in β cells of pregnant or obese rats (Jacovetti et al., 2012). [score:1]
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Other miRNAs from this paper: hsa-mir-16-1, hsa-mir-17, hsa-mir-20a, hsa-mir-21, hsa-mir-23a, hsa-mir-100, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-107, hsa-mir-16-2, mmu-mir-1a-1, mmu-mir-23b, mmu-mir-125b-2, mmu-mir-130a, mmu-mir-9-2, mmu-mir-145a, mmu-mir-181a-2, mmu-mir-184, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-205, mmu-mir-206, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-199a-2, hsa-mir-205, hsa-mir-181a-1, hsa-mir-214, hsa-mir-219a-1, hsa-mir-223, mmu-mir-302a, hsa-mir-1-2, hsa-mir-23b, hsa-mir-125b-1, hsa-mir-130a, hsa-mir-145, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125b-2, hsa-mir-184, hsa-mir-206, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-20a, mmu-mir-21a, mmu-mir-23a, mmu-mir-103-1, mmu-mir-103-2, rno-mir-338, rno-mir-20a, hsa-mir-1-1, mmu-mir-1a-2, hsa-mir-181b-2, mmu-mir-107, mmu-mir-17, mmu-mir-100, mmu-mir-181a-1, mmu-mir-214, mmu-mir-219a-1, mmu-mir-223, mmu-mir-199a-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-181b-1, mmu-mir-125b-1, hsa-mir-302a, hsa-mir-219a-2, mmu-mir-219a-2, hsa-mir-302b, hsa-mir-302c, hsa-mir-302d, hsa-mir-367, hsa-mir-372, hsa-mir-338, mmu-mir-181b-2, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-16, rno-mir-17-1, rno-mir-21, rno-mir-23a, rno-mir-23b, rno-mir-100, rno-mir-103-2, rno-mir-103-1, rno-mir-107, rno-mir-125b-1, rno-mir-125b-2, rno-mir-130a, rno-mir-145, rno-mir-181a-2, rno-mir-181b-1, rno-mir-181b-2, rno-mir-184, rno-mir-199a, rno-mir-205, rno-mir-206, rno-mir-181a-1, rno-mir-214, rno-mir-219a-1, rno-mir-219a-2, rno-mir-223, hsa-mir-512-1, hsa-mir-512-2, rno-mir-1, mmu-mir-367, mmu-mir-302b, mmu-mir-302c, mmu-mir-302d, rno-mir-17-2, hsa-mir-1183, mmu-mir-1b, hsa-mir-302e, hsa-mir-302f, hsa-mir-103b-1, hsa-mir-103b-2, rno-mir-9b-3, rno-mir-9b-1, rno-mir-9b-2, rno-mir-219b, hsa-mir-23c, hsa-mir-219b, mmu-mir-145b, mmu-mir-21b, mmu-mir-21c, mmu-mir-219b, mmu-mir-219c, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
Similarly, recent rodent studies demonstrated the roles of miR-219 [56], [57] and miR-338 [57] in controlling oligodendrocyte differentiation. [score:1]
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Other microRNAs, including miR-101, miR-101*, miR-181a, miR-30b and miR-338-3p, demonstrated correlation with the differentiation status of the tumours (Supplementary Figures 2a and b). [score:1]
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