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14 publications mentioning mmu-mir-505

Open access articles that are associated with the species Mus musculus and mention the gene name mir-505. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 141
Moreover, ectopic expression of miR-505-5p or miR-520c-3p decreased S100A4 mRNA and protein expression, whereas inhibition of the endogenous miRs by anti-miRs increased S100A4 expression. [score:9]
miR-505-5p and miR-520c-3p target the S100A4-3′UTR, and downregulate S100A4 expression. [score:8]
Here we demonstrate that loss of post-transcriptional regulation of S100A4 due to epigenetic silencing of miR-505-5p and miR-520c-3p expression could be one of the main causes for the induction of S100A4 expression in CRC and other cancer entities. [score:6]
miRNA mimic miR-505-5p (ID: MC12497), miR-520c-3p (ID: MC12719), miRNA inhibitor anti-miR-505-5p (ID: MH12497), anti-miR-520c-3p (ID: MH12719), miR -negative control (#4464058), siRNA targeting S100A4 (ID:12226) and scrambled control (#4390843) were purchased from Ambion, USA. [score:5]
In this study, we identified two miRs, miR-505-5p and miR-520c-3p, which post-transcriptionally inhibit the expression of S100A4, thereby hindering its mediated migration, invasion and formation of distant metastasis of CRC cells [34]. [score:5]
Further, loss or gain of function of miR-505-5p and miR-520c-3p along with S100A4 overexpression or knock-down clearly demonstrated that they mitigate the S100A4 mediated migration and invasion [35– 37]. [score:4]
S100A4 overexpression in combination with miR-505-5p or miR-520c-3p significantly increased migration (p = 0.006 and p = 0.02) and invasion (p = 0.006 and p = 0.03) of HCT116 cells compared to the miR overexpression in vector control cells, respectively. [score:4]
Western blotting confirmed the significant downregulation of S100A4 protein amounts in both cell lines, HCT116 and SW620, transfected with miR-505-5p (p = 0.01 and p = 0.04) and miR-520c-3p (p = 0.03 and p = 0.05). [score:4]
miR-505-5p and miR-520c-3p regulate the S100A4 gene expression. [score:4]
In order to explore further insights in the network of miR-505-5p and miR-520c-3p and their functional effects on S100A4 expression, we analyzed their epigenetic regulation. [score:4]
The endogenous expression of miR-505-5p and miR-520c-3p was lower in SW620 compared to HCT116 cells, whereas the S100A4 expression was higher (Supplementary Figure 3A; Supplementary Figure 2A, 2B; Supplementary Figure 4A). [score:4]
Taken together, these data suggest that the 3′-UTR of S100A4 is a direct functional target of miR-505-5p and miR-520c-3p. [score:4]
In conclusion, this study highlights a pivotal role of miR-505-5p and miR-520c-3p in various aspects of tumorigenesis such as migration, invasion, and in vivo metastasis formation in CRC through the post-transcriptional regulation of their novel target S100A4. [score:4]
The treatment with 5-Aza had no significant impact on the expression level of miR-505-5p (Supplementary Figure 6D) in HCT116 and SW620 cell lines. [score:3]
By co-transfecting miR mimics together with the S100A4-3′-UTR harboring either the wild type or mutated seed sequences of the predicted miRs, we identified S100A4 as a novel target of miR-505-5p and miR-520c-3p. [score:3]
The S100A4-3′-UTR was co -transfected along with control-miR, miR mimics or inhibitors (anti-miRs) of miR-505-5p and miR-520c-3p in HCT116 and SW620 cells. [score:3]
Given the results from the in silico analyses, we hypothesized that the S100A4-3′-UTR could be a functional target of miR-505-5p and miR-520c-3p. [score:3]
Expression of mature miR-505-5p (MS00009849), miR-520c-3p (MS00007413) and U6-snRNA (RNUB6) (MS00033740) were determined by the miScript SYBR Green PCR Kit (Qiagen), and normalized using the 2 [–ΔΔCt] method relative to RNUB6. [score:3]
Taken together, these results suggest that miR-505-5p and miR-520c-3p significantly inhibit S100A4 -mediated migration and invasion in CRC cells. [score:3]
miR-505-5p and miR-520c-3p inhibit the S100A4 -mediated migration and invasion. [score:3]
Figure 2miR-505-5p and miR-520c-3p inhibit the S100A4 mediated migration and invasion in vitro(A) HCT116 cells were co -transfected with control-miR, miR-505-5p and miR-520c-3p along with either vector-control or -S100A4, respectively. [score:3]
The S100A4-3′-UTR is a target of miR-505-5p and miR-520c-3p. [score:3]
miR-505-5p and miR-520c-3p inhibit the S100A4 mediated migration and invasion in vitro. [score:3]
In this study, by in silico analyses we have identified miR-505-5p and miR-520c-3p as potential candidates targeting the 3′UTR of S100A4. [score:3]
Complementary target sequences were identified for miR-505-5p at nt 77–85, and for miR-520c-3p at nt 59–65 (Figure 1A). [score:3]
Additionally, we overexpressed miR-505-5p, miR-520c-3p or control-miR along with either si -RNA-S100A4 or si -RNA-control in SW620 cells. [score:3]
The ATP11C and miR-505-5p expression were positively correlated in CRC cell lines (R [2] =0.84, p = 0.05, Supplementary Figure 4B). [score:3]
miR-505 is located on chromosome Xq27.1 [–] as an intragenic miR of ATPase, Class VI, Type 11C (ATP11C) and may be expressed under the same promoter as its host gene. [score:3]
Ectopic overexpression of miR-505-5p and miR-520c-3p significantly reduced the migration (p = 0.01 and p = 0.05) and invasion (p = 0.01 and p = 0.02) in HCT116 as well as migration (p = 0.05 and p = 0.05) and invasion (p = 0.01 and p = 0.01) in SW620 cells (Figure 2A, 2B). [score:3]
Co-transfection of miR-505-5p or miR-520c-3p along with si -RNA-S100A4 significantly reduced migration (p = 0.001 and p = 0.04) and invasion (p = 0.05 and p = 0.007) compared to the miRs overexpression in the si -RNA-control cells (Figure 2B). [score:2]
On the other hand, cells that were transfected with the anti-miR inhibitor along with the S100A4-3′-UTR showed a significantly induced luciferase activity compared to the respective control (HCT116 cells anti-miR-505-5p (p = 0.01), anti-miR-520c-3p (p = 0.003); SW620 cells anti-miR-505-5p (p = 0.02), anti-miR-520c-3p (p = 0.005) Figure 1B). [score:2]
In addition, we also showed the S100A4 specific effects by overexpression of S100A4 in combination with control-miR, miR-505-5p or miR-520c-3p, compared to the respective vector controls in HCT116 cells. [score:2]
Although most human promoters are associated with CpG-islands, this might not be the case for miR-505, which suggests a different regulation [33]. [score:2]
Specific miR-505-5p and miR-520c-3p seed sequences were mutated using PCR based site directed mutagenesis kit (#210518, Agilent technologies, USA). [score:2]
Taken together, these results suggest that S100A4 is post-transcriptionally regulated by miR-505-5p and miR-520c-3p through binding to its 3′-UTR in CRC cell lines. [score:2]
Especially the miR-505-5p expression was higher in the noninvasive cell lines, Colo206f and Colo320DM, compared to the invasive SW620 and HCT116 cell lines (Supplementary Figure 4A) [30, 32]. [score:2]
Moreover, transfection of anti-miR-505-5p and anti-miR-520c-3p slightly induced protein expression of S100A4 compared to the control-miR (Figure 1D, Supplementary Figure 5B). [score:2]
The mRNA and protein expression analyses showed that miR-505-5p and miR-520c-3p reduced the S100A4-transcript levels in HCT116 (p = 0.01 and p = 0.01) and SW620 cells (p = 0.01 and p = 0.02), but no significant changes were observed in the anti-miR-505-5p and anti-miR-520c-3p conditions compared to the control-miR (Figure 1C). [score:2]
The miR-505 upstream region was unmethylated, whereas the ATP11C upstream region was mostly methylated (Supplementary Figure 4C). [score:1]
Transfection efficiency of miR-505-5p or miR-520c-3p was determined by qRT-PCR (Supplementary Figure 1B, 1C). [score:1]
Briefly, cells were seeded in 6-well plates and transfected with 50 nM control, miR-505-5p, miR-520c-3p or anti-miR-505-5p, miR-520c-3p (Thermo Fisher Scientific) using Lipofectamine RNAiMAX Reagent (Thermo Fisher Scientific) according to the manufacturer's instructions. [score:1]
Both, miR-505 and its host gene ATP11C, had no CpG-island in their upstream promoter region. [score:1]
Additionally, we analyzed the host gene of miR-505, ATP11C in this study. [score:1]
miR-505-5p was so far only shown to be dysregulated in cancer tissue compared to normal mucosa but no functional evidence was reported [54, 55]. [score:1]
Therefore, HCT116 cells were transfected with anti-miR-505-5p, anti-miR-520c-3p and control-miR. [score:1]
Figure 1(A) The seed sequences for miR-505-5p and miR-520c-3p in S100A4-3′-UTR (wild type) were detected by in silico predictions. [score:1]
Our study also identified S100A4 as the first cancer -associated target of miR-505-5p and its functional impact on metastasis -associated characteristics like migration and invasion. [score:1]
The minimum free energy predicted for hybridization of miR-505-5p or miR-520c-3p with the S100A4-3′-UTR at their site is ΔG = –26.2 kcal/mol and ΔG = –24.5 kcal/mol, respectively, determined by mFold analysis (Supplementary Figure 1A, 1B). [score:1]
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2
[+] score: 25
Time -dependent expression of miR-122, miR-192, miR-21, miR-29a, miR-34a, and miR-505 in study 1. Data were expressed as minus delta Ct with reference to spike-in control miRNA. [score:5]
MicroRNA profiling in two independent cohorts of animals validated the up-regulation of 6 microRNAs (miR-122, miR-192, miR-21, miR-29a, miR-34a and miR-505) in NASH mice, which was designated as the circulating microRNA signature for NASH. [score:4]
Notably, we detected significant up-regulation of liver miR-21, miR-34a and miR-505 in NASH mice compared to lean mice (data was not shown). [score:3]
The right panel depicted the expression level of miR-192 and miR-505 in mice having NAS > 3 compared with mice having NAS ≤ 3. c ROC curves of the microRNA signature in predicting mice having NAS > 3 (AUC = 0.897, 95% confidence interval: 0.75 - 1) in study 1. The confusion matrix was depicted in the inset (numbers in rows are actual classification, numbers in columns are predicted classification). [score:2]
MiR-505 was selected because of its high correlations with disease pathologies (NAS, r = 0.77), but relatively low associations with other microRNAs. [score:2]
a, b Univariate ROC analysis of miR-192 and miR-505, which was created by plotting the true positive rate (sensitivity) against false positive rate (1-specificity). [score:1]
c Principle component analysis (PCA) of miR-192, miR-122, miR-21, miR-29a, miR-34a, and miR-505 in study 2. Red dots represented NASH mice (mice on 3H diet for 7 months), and green dots represented lean mice. [score:1]
b, c ROC curves of the miR-192, miR-21, miR-505 and ALT in predicting mice having NAS > 3 in study 1 (AUC = 0.948, 95% confidence interval: 0.827 - 1) and study 3 (AUC = 0.931, 95% confidence interval: 0.845 - 1). [score:1]
We then tested the performance of the new composite biomarker consisting of miR-192, miR-505, miR-21 and ALT in discriminating NASH animals (NAS > 3) from healthy mice (NAS ≤ 3) in study 1 and 3. As shown in Fig.   5b, the new biomarker outperformed the microRNA signature plus ALT mo del, and achieved AUROC of 0.958 with further reduction of one misclassified animal in study one. [score:1]
The top six common microRNAs including miR-21, miR-122, miR-192, miR-29a, miR-34a and miR-505, were designated as the circulating microRNA signature for NASH (Fig.   2b). [score:1]
Based on these findings, a microRNA -based composite biomarker consisting of miR-192, miR-21, miR-505 and ALT was proposed, which demonstrated great performance in distinguishing between lean and NASH mice (NAS > 3). [score:1]
To further improve the performance of microRNA -based biomarker, a new composite biomarker was proposed, which consists of miR-192, miR-21, miR-505 and ALT. [score:1]
Univariate ROC curve analysis showed that miR-192 and miR-505 achieved the greatest AUROC of 0.923 and 0.919 respectively in discriminating mice had NAS > 3, while miR-122, miR-29a, miR-34a and miR-21 had an AUROC of 0.88, 0.84, 0.80 and 0.79 (Fig.   4a and b). [score:1]
In view of the biological function of each feature, the new composite biomarker could potentially reflect the status of the liver from the following perspectives: miR-192 and ALT serve as independent indicator of hepatocyte function, miR-21 suggests of stellate cell activation and liver fibrosis, miR-505 implies for pathological manifestations. [score:1]
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3
[+] score: 16
Four out of the six miRNAs undergoing validation exhibited congruence between miRNA profiling and qRT-PCR results, ranging from ~2-fold down-regulation to ~2-fold up-regulation [Table 1 and Figure 3; miR27a: t [(10)] = 2.848, p = 0.0173; miR146b: t [(10)] = 3.448, p = 0.0063; miR505: t [(10)] = 10.471, p = 0.0001; miR202-5p: t [(10)] = 3.222, p = 0.0091]. [score:7]
miR name miR changemiR Log [2] value Gene miRSVR score mRNA change mmu-miR-146b ↓ −0.3362 Gripap1 −0.6473 ↓ ↓ Fstl1 −0.4896 ↓ ↓ Dlgap1 −0.4727 ↓ ↓ Vps26a −0.2555 ↓ ↓ Gosr2 −0.1763 ↓ ↓ Gprasp1 −0.1232 ↓ ↓ Zfand6 −0.1105 ↓ ↓ Serpini1 −0.1097 ↓ mmu-miR-27a ↓ −0.3670 ↓ Ppp1r9a −0.8020 ↓ ↓ Ubqln1 −0.7975 ↓ ↓ Rps6ka5 −0.7940 ↓ ↓ Gosr2 −0.7700 ↓ ↓ Canx −0.7310 ↓ ↓ AI593442 −0.5274 ↓ ↓ Nsf −0.4902 ↓ ↓ Dgkb −0.4384 ↓ ↓ Dlgap1 −0.3411 ↓ ↓ Atp2b2 −0.2743 ↓ ↓ Zfand6 −0.1456 ↓ ↓ Nufip1 −0.1278 ↓ mmu-miR-505 ↑ 1.1166 Sap25 −1.2974 ↑ ↑ Parp11 −1.0018 ↑ ↑ Srbd1 −0.6136 ↑ ↑ Dicer1 −0.3529 ↑ ↑ Txnip −0.2797 ↑ ↑ Phf17 −0.1855 ↑ ↑ Ccnf −0.1480 ↑ Green up arrow: up-regulated in morphine vs. [score:4]
At baseline (saline treated) expression level of miR27a and miR146b were significantly greater in D2 mice compared to the B6 mice while miR505 was equivalent and miR202-5p was significantly less than the B6 mice [miR27a: t [(8)] = 8.411, p = 0.0001; miR146b: t [(8)] = 3.448, p = 0.0007; miR505: t [(8)] = 0.261, ns; miR202-5p: t [(8)] = 3.000, p = 0.0171]. [score:2]
miR name miR changemiR Log [2] value mRNA miRSVR score mRNA change mmu-miR-146b ↓ −0.3362 Enpp5 −1.0510 ↑ ↓ Pet112l −1.0474 ↑ ↓ Afmid −1.0327 ↑ ↓ Ccna2 −0.6094 ↑ ↓ Baiap2l1 −0.3049 ↑ ↓ Phf17 −0.2832 ↑ ↓ Pcbp2 −0.1396 ↑ ↓ Dicer1 −0.1357 ↑ ↓ C86695 −0.1061 ↑ mmu-miR-202-5p ↑ 4.0723 Dlgap1 −1.2131 ↓ ↑ AI593442 −1.0566 ↓ ↑ Rps6ka5 −0.9715 ↓ ↑ Meis1 −0.7075 ↓ ↑ Fstl1 −0.6275 ↓ ↑ Atp2b2 −0.4273 ↓ ↑ Rab6b −0.2834 ↓ ↑ Ubqln1 −0.1476 ↓ ↑ Ppp1r9a −0.1379 ↓ ↑ Ralgps1 −0.1185 ↓ mmu-miR-27a ↓ −0.3690 Fmn2 −0.7565 ↑ ↓ Dicer1 −0.7044 ↑ ↓ Rufy3 −0.6805 ↑ ↓ Dusp9 −0.3455 ↑ ↓ Baiap2l1 −0.2262 ↑ mmu-miR-505 ↑ 1.1166 Meis1 −1.2283 ↓ ↑ Serpini1 −0.8085 ↓ ↑ Ralgps1 −0.4115 ↓ ↑ Canx −0. [score:1]
COA does not alter miRNA in these non-tolerant D2 providing increased support to these particular miRNA as high value candidates (miR27a; miR146b; miR505; miR202-5p, all ns). [score:1]
MiR-505, -146b, and -202 are proposed to be involved in various adaptive processes such as angiogenesis (miR-505; Yang et al., 2014), dendritic cell apoptosis and cytokine production (146b; Park et al., 2015) and cell proliferation (Zhang et al., 2014). [score:1]
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4
[+] score: 13
Mmu-miR-505-5p was downregulated in Sca-1 [+]CD31 [−] compared to Sca-1 [+]CD31 [+] cells, with targets Cyp1b1, Dcbld2, Igf1, and Ppp1r14b,Txndc5 increased in expression; Igf1 was involved in mTOR and PI3K-Akt signaling and Cyp1b1by with microRNAs in cancer. [score:7]
In addition, we corroborated the expression in Sca-1 [+]CD31 [−] cells of differentiation promoting-miRNAs mmu-miR-322-5p, mmu-miR-505-5p, mmu-miR-18a-5p, and mmu-miR-139-5p. [score:3]
Mmu-miR-322-5p and mmu-miR-505-5p had more targeted and inversely associated genes and transcription factors (Table 3). [score:3]
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5
[+] 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-17, hsa-mir-18a, hsa-mir-20a, hsa-mir-21, hsa-mir-29a, hsa-mir-33a, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-107, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-29b-1, mmu-mir-124-3, mmu-mir-126a, mmu-mir-9-2, mmu-mir-132, mmu-mir-133a-1, mmu-mir-134, mmu-mir-138-2, mmu-mir-145a, mmu-mir-152, mmu-mir-10b, mmu-mir-181a-2, hsa-mir-192, mmu-mir-204, mmu-mir-206, hsa-mir-148a, mmu-mir-143, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-10b, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-204, hsa-mir-211, hsa-mir-212, hsa-mir-181a-1, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, mmu-mir-106b, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-138-2, hsa-mir-143, hsa-mir-145, hsa-mir-152, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-126, hsa-mir-134, hsa-mir-138-1, hsa-mir-206, mmu-mir-148a, mmu-mir-192, 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-20a, mmu-mir-21a, mmu-mir-29a, mmu-mir-29c, mmu-mir-34a, mmu-mir-330, hsa-mir-1-1, mmu-mir-1a-2, hsa-mir-181b-2, mmu-mir-107, mmu-mir-17, mmu-mir-212, mmu-mir-181a-1, mmu-mir-33, mmu-mir-211, mmu-mir-29b-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-7a-1, mmu-mir-7a-2, mmu-mir-7b, hsa-mir-106b, hsa-mir-29c, hsa-mir-34b, hsa-mir-34c, hsa-mir-330, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-181b-2, hsa-mir-181d, hsa-mir-505, hsa-mir-590, hsa-mir-33b, hsa-mir-454, mmu-mir-181d, mmu-mir-590, mmu-mir-1b, mmu-mir-145b, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-let-7k, mmu-mir-126b, mmu-mir-9b-2, mmu-mir-124b, mmu-mir-9b-1, mmu-mir-9b-3
MiR-505 acts as a tumor suppressor by inhibiting proliferation and inducing apoptosis of human breast cancer cells (Yamamoto et al., 2011). [score:4]
miRNA Gene targets miR-134Brain-derived neurotrophic factor (BDNF) and cAMP response element -binding factor (CREB) miR-204 BDNF and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) miR-211 BDNF and AMPA miR-505 BDNF and AMPA miR-590-3p BDNF and CREB MiR-134 has an important role in the brain, where it is essential for activity -dependent dendritic outgrowth, nerve growth cone guidance, and size of dendritic spines of hippocampal neurons (Schratt et al., 2006; Khudayberdiev et al., 2009; Han et al., 2011). [score:3]
miRNA Gene targets miR-134Brain-derived neurotrophic factor (BDNF) and cAMP response element -binding factor (CREB) miR-204 BDNF and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) miR-211 BDNF and AMPA miR-505 BDNF and AMPA miR-590-3p BDNF and CREBMiR-134 has an important role in the brain, where it is essential for activity -dependent dendritic outgrowth, nerve growth cone guidance, and size of dendritic spines of hippocampal neurons (Schratt et al., 2006; Khudayberdiev et al., 2009; Han et al., 2011). [score:3]
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6
[+] score: 6
TargetScan analyses also revealed specific miRNAs highly involved in targeting relevant gene functions in repair such as miR-290 and miR-505 at 7 dpi; and let-7, miR-21 and miR-30 at 15 dpi. [score:5]
These additional criteria narrowed the selection down to 3 miRNAs at 7 dpi (miR-290, miR-1940, miR-505) which were marked to be crucial in the early repair phase. [score:1]
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7
[+] score: 6
Besides the metabolic pathways, recent studies have shown that micro RNAs, such as miR-122, miR-192, miR-21, miR-29a, miR-34a, and miR-505, are up or down regulated at disease state of NASH and may play a role in the disease progression (Liu et al., 2018). [score:6]
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8
[+] score: 6
Other miRNAs from this paper: mmu-mir-16-1, mmu-mir-16-2, mmu-mir-503
T3 down-regulates miR-424 and miR-505 targets. [score:6]
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9
[+] score: 4
Differential expression of six miRNAs (miR-142-3p, miR-505*, miR-1248, miR-181a-2*, miR-25* and miR-340*) was found to accurately discriminate between tumors from BRCA1/2 mutation carriers and noncarriers [12]. [score:4]
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10
[+] score: 4
Three miRNAs associated with human basal-type tumors (miR-135b, miR-505 and miR-155), and seven miRNAs associated with human luminal type tumors (let-7a, let-7f, miR-100, miR-130a, miR-152, miR-214 and miR-29b) are similarly expressed in mouse basal-like and luminal-type tumors, respectively. [score:3]
miR-135b, miR-505 and miR-155 are expressed in both basal human and mouse mammary tumors and many basal -associated miRNAs have not been previously characterized. [score:1]
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11
[+] score: 3
On the other hand, miR-143-3p, miR-141, and miR-505 are potential tumor suppressors [12– 14]. [score:3]
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12
[+] score: 3
Other miRNAs from this paper: hsa-mir-25, hsa-mir-28, hsa-mir-95, mmu-mir-151, mmu-mir-290a, mmu-mir-297a-1, mmu-mir-297a-2, mmu-mir-130b, mmu-mir-340, mmu-mir-25, mmu-mir-28a, hsa-mir-130b, hsa-mir-367, hsa-mir-372, hsa-mir-378a, mmu-mir-378a, hsa-mir-340, hsa-mir-151a, mmu-mir-466a, mmu-mir-467a-1, hsa-mir-505, hsa-mir-506, mmu-mir-367, hsa-mir-92b, hsa-mir-548a-1, hsa-mir-548b, hsa-mir-548a-2, hsa-mir-548a-3, hsa-mir-548c, hsa-mir-648, hsa-mir-548d-1, hsa-mir-548d-2, hsa-mir-659, hsa-mir-421, hsa-mir-151b, hsa-mir-1271, hsa-mir-378d-2, mmu-mir-467b, mmu-mir-297b, mmu-mir-297a-3, mmu-mir-297a-4, mmu-mir-297c, mmu-mir-421, 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-467c, mmu-mir-467d, mmu-mir-92b, mmu-mir-466d, hsa-mir-297, mmu-mir-467e, mmu-mir-466l, mmu-mir-669g, mmu-mir-466i, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-467f, mmu-mir-466j, mmu-mir-467g, mmu-mir-467h, mmu-mir-1195, hsa-mir-548e, hsa-mir-548j, hsa-mir-1285-1, hsa-mir-1285-2, hsa-mir-1289-1, hsa-mir-1289-2, hsa-mir-548k, hsa-mir-1299, hsa-mir-548l, hsa-mir-1302-1, hsa-mir-1302-2, hsa-mir-1302-3, hsa-mir-1302-4, hsa-mir-1302-5, hsa-mir-1302-6, hsa-mir-1302-7, hsa-mir-1302-8, 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-1255b-1, hsa-mir-1255b-2, mmu-mir-1906-1, hsa-mir-1972-1, hsa-mir-548q, mmu-mir-466m, mmu-mir-466o, mmu-mir-467a-2, mmu-mir-467a-3, mmu-mir-466c-2, mmu-mir-467a-4, mmu-mir-466b-4, mmu-mir-467a-5, mmu-mir-466b-5, mmu-mir-467a-6, mmu-mir-466b-6, mmu-mir-467a-7, mmu-mir-466b-7, mmu-mir-467a-8, mmu-mir-467a-9, mmu-mir-467a-10, mmu-mir-466p, mmu-mir-466n, mmu-mir-466b-8, hsa-mir-3116-1, hsa-mir-3116-2, hsa-mir-3118-1, hsa-mir-3118-2, hsa-mir-3118-3, hsa-mir-548s, hsa-mir-378b, hsa-mir-466, hsa-mir-548t, hsa-mir-548u, hsa-mir-548v, hsa-mir-3156-1, hsa-mir-3118-4, hsa-mir-3174, hsa-mir-3179-1, hsa-mir-3179-2, hsa-mir-3179-3, hsa-mir-548w, hsa-mir-3156-2, hsa-mir-3156-3, hsa-mir-548x, mmu-mir-3470a, mmu-mir-3470b, mmu-mir-3471-1, mmu-mir-3471-2, hsa-mir-378c, hsa-mir-1972-2, hsa-mir-1302-9, hsa-mir-1302-10, hsa-mir-1302-11, mmu-mir-1906-2, hsa-mir-3683, hsa-mir-3690-1, hsa-mir-548y, hsa-mir-548z, hsa-mir-548aa-1, hsa-mir-548aa-2, hsa-mir-548o-2, hsa-mir-1268b, 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, mmu-mir-28c, mmu-mir-378b, mmu-mir-28b, 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, hsa-mir-378j, mmu-mir-378c, mmu-mir-378d, hsa-mir-548ay, hsa-mir-548az, hsa-mir-3690-2, mmu-mir-290b, hsa-mir-548ba, hsa-mir-548bb, hsa-mir-3179-4, mmu-mir-466c-3, hsa-mir-548bc, mmu-mir-1271
In the miR-28 network (Figure 8C), ASF/SF2 expression is modulated by miR-28 and miR-505 (not show here) which are negatively controlled by LRF to influence the proliferation and survival of mouse embryonic fibroblasts [75]. [score:3]
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13
[+] 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-17, hsa-mir-18a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-21, hsa-mir-23a, hsa-mir-31, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-96, hsa-mir-98, hsa-mir-99a, hsa-mir-106a, mmu-let-7g, mmu-let-7i, mmu-mir-23b, mmu-mir-99a, mmu-mir-127, mmu-mir-128-1, mmu-mir-136, mmu-mir-142a, mmu-mir-145a, mmu-mir-10b, mmu-mir-182, mmu-mir-183, mmu-mir-187, mmu-mir-193a, mmu-mir-195a, mmu-mir-200b, mmu-mir-206, mmu-mir-143, hsa-mir-139, hsa-mir-10b, hsa-mir-182, hsa-mir-183, hsa-mir-187, hsa-mir-210, hsa-mir-216a, hsa-mir-217, hsa-mir-219a-1, hsa-mir-221, hsa-mir-222, hsa-mir-224, hsa-mir-200b, mmu-mir-302a, mmu-let-7d, mmu-mir-106a, hsa-let-7g, hsa-let-7i, hsa-mir-23b, hsa-mir-128-1, hsa-mir-142, hsa-mir-143, hsa-mir-145, hsa-mir-127, hsa-mir-136, hsa-mir-193a, hsa-mir-195, hsa-mir-206, mmu-mir-19b-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-18a, mmu-mir-21a, mmu-mir-23a, mmu-mir-31, mmu-mir-92a-2, mmu-mir-96, mmu-mir-98, hsa-mir-200c, mmu-mir-17, mmu-mir-139, mmu-mir-200c, mmu-mir-210, mmu-mir-216a, mmu-mir-219a-1, mmu-mir-221, mmu-mir-222, mmu-mir-224, mmu-mir-19b-1, mmu-mir-92a-1, mmu-mir-128-2, hsa-mir-128-2, mmu-mir-217, hsa-mir-200a, hsa-mir-302a, hsa-mir-219a-2, mmu-mir-219a-2, hsa-mir-363, mmu-mir-363, hsa-mir-302b, hsa-mir-302c, hsa-mir-302d, hsa-mir-371a, hsa-mir-18b, hsa-mir-20b, hsa-mir-452, mmu-mir-452, ssc-mir-106a, ssc-mir-145, ssc-mir-216-1, ssc-mir-217-1, ssc-mir-224, ssc-mir-23a, ssc-mir-183, ssc-let-7c, ssc-let-7f-1, ssc-let-7i, ssc-mir-128-1, ssc-mir-136, ssc-mir-139, ssc-mir-18a, ssc-mir-21, hsa-mir-146b, hsa-mir-493, hsa-mir-495, hsa-mir-497, hsa-mir-505, mmu-mir-20b, hsa-mir-92b, mmu-mir-302b, mmu-mir-302c, mmu-mir-302d, hsa-mir-671, mmu-mir-216b, mmu-mir-671, mmu-mir-497a, mmu-mir-495, mmu-mir-146b, mmu-mir-708, mmu-mir-18b, mmu-mir-493, mmu-mir-92b, hsa-mir-708, hsa-mir-216b, hsa-mir-935, hsa-mir-302e, hsa-mir-302f, ssc-mir-17, ssc-mir-210, ssc-mir-221, mmu-mir-1839, ssc-mir-146b, ssc-mir-206, ssc-let-7a-1, ssc-let-7e, ssc-let-7g, ssc-mir-128-2, ssc-mir-143, ssc-mir-10b, ssc-mir-23b, ssc-mir-193a, ssc-mir-99a, ssc-mir-98, ssc-mir-92a-2, ssc-mir-92a-1, ssc-mir-92b, ssc-mir-142, ssc-mir-497, ssc-mir-195, ssc-mir-127, ssc-mir-222, ssc-mir-708, ssc-mir-935, ssc-mir-19b-2, ssc-mir-19b-1, ssc-mir-1839, ssc-mir-505, ssc-mir-363-1, hsa-mir-219b, hsa-mir-371b, ssc-let-7a-2, ssc-mir-18b, ssc-mir-187, ssc-mir-218b, ssc-mir-219a, mmu-mir-195b, mmu-mir-145b, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, ssc-let-7d, ssc-let-7f-2, ssc-mir-20b-1, ssc-mir-20b-2, ssc-mir-31, ssc-mir-182, ssc-mir-216-2, ssc-mir-217-2, ssc-mir-363-2, ssc-mir-452, ssc-mir-493, ssc-mir-671, mmu-let-7k, ssc-mir-7138, mmu-mir-219b, mmu-mir-216c, mmu-mir-142b, mmu-mir-497b, mmu-mir-935, ssc-mir-9843, ssc-mir-371, ssc-mir-219b, ssc-mir-96, ssc-mir-200b
adj ssc-miR-21 -1.1788 1.45E-02 1.68E-02 -2.4642 2.07E-04 3.85E-04 ssc-miR-143-3p -1.1940 1.40E-02 1.67E-02 -2.7004 2.27E-05 5.34E-05 ssc-miR-145-3p -1.2289 2.47E-02 2.68E-02 -2.6837 6.34E-04 1.10E-03 ssc-miR-505 -1.3657 2.68E-02 2.82E-02 -2.1577 4.16E-02 4.16E-02 ssc-miR-98 -1.5185 3.46E-03 5.15E-03 -2.8061 7.55E-05 1.55E-04 ssc-miR-139-3p -1.6685 2. 54E-02 2.71E-02 -2.5158 1.69E-02 1.93E-02 ssc-miR-23b -1.7157 3.70E-03 5.42E-03 -2.3687 8.39E-03 1.10E-02 ssc-miR-224 -1.8515 1.41E-02 1.67E-02 -2.5778 1.95E-02 2.19E-02 ssc-miR-23a -1.8753 3.40E-03 5.15E-03 -2.4676 1.00E-02 1.24E-02 ssc-miR-143-5p -1.9243 1.15E-04 2.60E-04 -3.9943 1.25E-09 5.88E-09 ssc-miR-139-5p -2.1198 2.01E-02 2.24E-02 -3. 2644 1.01E-02 1.24E-02 ssc-miR-222 -2.2666 2.58E-07 1.02E-06 -2.6019 2.34E-05 5.35E-05 ssc-miR-671-5p -2.3068 1.15E-02 1.47E-02 -2.7986 3.86E-02 3.92E-02 ssc-miR-9843-3p -2.3507 9.68E-04 1.87E-03 -4.7281 5.90E-05 1.31E-04 ssc-miR-145-5p -2.7059 2.08E-03 3.50E-03 -4.3459 7.18E-05 1.51E-04 ssc-miR-221-5p -2.7136 3.21E-07 1.21E-06 -1.9513 3.02E-02 3. 22E-02 ssc-miR-221-3p -2.9643 8.31E-11 5.47E-10 -2.1967 1.74E-03 2.90E-03 ssc-miR-708-5p -4.0615 2.31E-06 7.60E-06 -2.8238 6.43E-03 8.72E-03 ssc-miR-193a-3p -4.1933 2.39E-07 1.02E-06 -4.3848 2.87E-07 9.18E-07 ssc-miR-193a-5p -4.1933 2.39E-07 1.02E-06 -7.1423 2.32E-12 1.33E-11 ssc-miR-452 -4.3025 5.55E-11 3.99E-10 -2.2057 1.53E-02 1.77E-02 ssc-miR-206 -5.3001 6. 39E-09 3.37E-08 -6.2200 3.10E-09 1.38E-08 10.1371/journal. [score:1]
adj ssc-miR-21 -1.1788 1.45E-02 1.68E-02 -2.4642 2.07E-04 3.85E-04 ssc-miR-143-3p -1.1940 1.40E-02 1.67E-02 -2.7004 2.27E-05 5.34E-05 ssc-miR-145-3p -1.2289 2.47E-02 2.68E-02 -2.6837 6.34E-04 1.10E-03 ssc-miR-505 -1.3657 2.68E-02 2.82E-02 -2.1577 4.16E-02 4.16E-02 ssc-miR-98 -1.5185 3.46E-03 5.15E-03 -2.8061 7.55E-05 1.55E-04 ssc-miR-139-3p -1.6685 2. 54E-02 2.71E-02 -2.5158 1.69E-02 1.93E-02 ssc-miR-23b -1.7157 3.70E-03 5.42E-03 -2.3687 8.39E-03 1.10E-02 ssc-miR-224 -1.8515 1.41E-02 1.67E-02 -2.5778 1.95E-02 2.19E-02 ssc-miR-23a -1.8753 3.40E-03 5.15E-03 -2.4676 1.00E-02 1.24E-02 ssc-miR-143-5p -1.9243 1.15E-04 2.60E-04 -3.9943 1.25E-09 5.88E-09 ssc-miR-139-5p -2.1198 2.01E-02 2.24E-02 -3. 2644 1.01E-02 1.24E-02 ssc-miR-222 -2.2666 2.58E-07 1.02E-06 -2.6019 2.34E-05 5.35E-05 ssc-miR-671-5p -2.3068 1.15E-02 1.47E-02 -2.7986 3.86E-02 3.92E-02 ssc-miR-9843-3p -2.3507 9.68E-04 1.87E-03 -4.7281 5.90E-05 1.31E-04 ssc-miR-145-5p -2.7059 2.08E-03 3.50E-03 -4.3459 7.18E-05 1.51E-04 ssc-miR-221-5p -2.7136 3.21E-07 1.21E-06 -1.9513 3.02E-02 3. 22E-02 ssc-miR-221-3p -2.9643 8.31E-11 5.47E-10 -2.1967 1.74E-03 2.90E-03 ssc-miR-708-5p -4.0615 2.31E-06 7.60E-06 -2.8238 6.43E-03 8.72E-03 ssc-miR-193a-3p -4.1933 2.39E-07 1.02E-06 -4.3848 2.87E-07 9.18E-07 ssc-miR-193a-5p -4.1933 2.39E-07 1.02E-06 -7.1423 2.32E-12 1.33E-11 ssc-miR-452 -4.3025 5.55E-11 3.99E-10 -2.2057 1.53E-02 1.77E-02 ssc-miR-206 -5.3001 6. 39E-09 3.37E-08 -6.2200 3.10E-09 1.38E-08 10.1371/journal. [score:1]
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14
[+] score: 2
We previously identified three microRNAs (miR- 148a, miR-505 and miR-1207-5p) that provide feedback regulation of epithelial-mesenchymal transition (EMT) induced by growth factors such as EGF and TGF-β. [score:2]
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