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40 publications mentioning hsa-mir-671

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-671. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 455
Other miRNAs from this paper: hsa-mir-200b, hsa-mir-638
We further found that forced expression of miR-671-5p in breast cancer cell lines resulted in FOXM1 down-regulation and significant proliferation and invasion inhibition, which implicates a tumor suppressor function of miR-671-5p by targeting FOXM1. [score:12]
We showed that miR-671-5p: 1) was downregulated in breast cancer; 2) suppressed proliferation and invasion of breast cells by targeting FOXM1; 3) inhibited EMT and induced S-phase arrest; and 4) sensitized breast cancer cells to cisplatin, 5-FU and epirubicin treatment by impairing DNA repair capability. [score:10]
Thus, we reasoned that the inhibited proliferation and invasion by miR-671-5p is due to suppressed FOXM1 expression and/or its downstream target genes (Figure 7). [score:9]
In our present work, we found that miR-671-5p was downregulated in breast cancer progression, and forced expression of miR-671-5p inhibited cell proliferation and invasion in breast cancer cell lines. [score:8]
We showed that FOXM1 is a novel target of miR-671-5p and that overexpression of miR-671-5p can downregulate FOXM1. [score:8]
In our study, we observed that miR-671-5p transfected MDA-MB-231 cells showed an epithelioid appearance and expressed epithelial cell marker E-cadherin, while mock transfected cells displayed elongated, irregular fibroblastoid morphology and expressed typical mesenchymal marker vimentin, suggesting a tumor suppressive effect of miR-671-5p in EMT. [score:7]
Using the BD Matrigel, we found that miR-671-5p overexpression exhibited significant inhibition of invasion in MDA-MB-231 cells (60%) and moderate inhibition in Hs578T and SKBR3 cells (40%) compared to the mock (Figure 4C). [score:6]
We detected significant downregulation of CDK2 expression in miR-671-5p transfected cells. [score:6]
Our data, for the first time, defined a role for miR-671-5p as a tumor suppressor miRNA in breast cancer, involving cell proliferation, invasion, cell cycle arrest, EMT, and chemotherapeutic sensitivity by directly targeting FOXM1 and its downstream genes. [score:6]
These results suggest that miR-671-5p functions as a tumor suppressor by directly targeting FOXM1. [score:6]
Based on our data, we reasoned that overexpression of miR-671-5p could sensitize cells to chemotherapeutic agents or UV treatment by downregulating FOXM1. [score:6]
We found that miR-671-5p overexpression resulted in downregulated FOXM1, and further demonstrated miR-671-5p can sensitize breast cancer to anticancer drugs. [score:6]
miR-671-5p expression was assayed by the Taqman MiRNA Reverse Transcript Kit (Applied Biosystems), and target gene expression was analyzed using the ABI 7300 System as described previously [3]. [score:6]
Overexpression of miR-671-5p inhibited breast cancer cell proliferation and invasion. [score:5]
We have demonstrated that miR-671-5p suppressed FOXM1 expression on both the mRNA and protein levels. [score:5]
miR-671-5p serves as a tumor suppressor in human breast cancer progression by targeting FOXM1. [score:5]
Notably, silencing FOXM1 expression by miR-671-5p in SKBR3 and MCF-7 cells inhibited their proliferation and invasion, but not as significantly as in MDA-MB-231cells. [score:5]
Figure 4(A) FOXM1 protein expression was examined by Western blot after transfection of miR-671-5p mimic and inhibitor. [score:5]
In addition, miR-671-5p has been showed to silence the SMARCB1 expression in epithelioid sarcoma [26] and to repress BCL2L12 expression in melanoma [24]. [score:5]
We first established the stable miR-671-5p or mock transfected cells, and then those cells were further transient -transfected with miR-671-5p inhibitor or inhibitor mock. [score:5]
Repression of miR-671-5p expression by miR-671-5p inhibitor resulted in a converse effect. [score:5]
After overnight incubation, cells reached 30%–50% confluence, were transiently transfected with miR-671-5p mimic (Cat# 4464066), mock (mirVana™ miRNA Mimic, Negative Control, Cat# 4464059), inhibitor (Cat# 4464084), and mock (mirVana™ miRNA Inhibitor, Negative Control, Cat# 4464077) (Lifetechnologies) by Lipofectamine RNAiMAX (Life Technologies) using the Opti-MEM Reduced Serum Medium (Life Technologies). [score:5]
Here, we identified miR-671-5p as a tumor-suppressor miRNA by targeting Forkhead Box M1 (FOXM1), an oncogenic transcription factor, in breast tumorigenesis. [score:5]
Consistent with the luciferase assay results, significant down-regulation of FOXM1 mRNA was observed in MDA-MB-231, Hs578T, and SKBR3 cells after overexpression of miR-671-5p. [score:5]
These results suggest that miR-671-5p might be able to reverse anticancer resistance through inhibition of FOXM1 as a new therapeutic target for breast cancer. [score:5]
To confirm miR-671-5p inhibits proliferation, invasion and EMT by directly regulating FOXM1, miR-671-5p/mock-stable -transfected MDA-MB-231 cell lines were transiently transfected with pcDNA3.1-FOXM1 or pcDNA3.1 control. [score:5]
The converse E-cadherin and vimentin expression was observed with the transfection of miR-671-5p inhibitor in the stable transfected cells. [score:5]
Interestingly, we found that overexpression of miR-671-5p resulted in not only reduced expression of FOXM1, but also the MCM10 gene (Figure 7 and Supplementary Figure 1A). [score:5]
FOXM1 expression was decreased more significantly in MDA-MB-231 (71%) and MCF-7 (60%) cells in comparison with SKBR3 (23%) cells when miR-671-5p was overexpressed. [score:5]
These results suggest that miR-671-5p directly regulates FOXM1 expression by binding to its 3′UTR in breast cancer. [score:5]
Thus, reduced CCNB1 expression could explain the ability of miR-671-5p for S-phase arrest and inhibition of G [2]-phase entry. [score:5]
To validate the computational predictions and the biological effects of miR-671-5p targeting FOXM1, we first examined the expression of miR-671-5p and FOXM1 in breast cancer cell lines. [score:5]
Our data indicates that miR-671-5p may regulate cell cycle via FOXM1 mediated CCNB1 and/or CDK2 downregulation (Supplementary Figure 1). [score:5]
Down-regulation of miR-671-5p expression was present in 21 of 30 (70%) of IDC compared with their adjacent normal tissue (p < 0.05). [score:5]
Figure 2(A) Inverse correlated expression of miR-671-5p and its target FOXM1 in breast cancer cell lines. [score:5]
miR-671-5p overexpression induces global gene expression profile changes. [score:5]
Downregulation of miR-671-5p expression was present in 21 of 30 (70%) IDCs compared with their adjacent tissues (p < 0.05), which includes 8 of 10 TNBCs (80%) and 11 of 20 (60%) non-TNBCs (Figure 1). [score:5]
Overexpression of miR-671-5p resulted in significantly reduced FOXM1 expression in protein level (Figure 4A) and decreased proliferation (Figure 4B) compared with the mock control. [score:4]
Consistent with this notion, immunofluorescence (Figure 5C, middle) and Western blot (Figure 5C, bottom) analyses revealed an upregulation of the epithelial marker E-cadherin and a concomitant reduction in the EMT marker vimentin in miR-671-5p transfected MDA-MB-231 cells. [score:4]
On the contrary, a converse result was observed after miR-671-5p knockdown by transfection of miR-671-5p inhibitor in the stable transfected cells (Figure 5C, top). [score:4]
In our previous work miR-671-5p was observed to be downregulated in FFPE tissues during breast cancer progression. [score:4]
In addition, genes associated with cell proliferation, invasion, cell cycle, and EMT were detected to be downregulated in miR-671-5p transfected MDA-MB-231 cells, such as GINS Complex Subunit 2 (GINS2), cyclin -dependent kinase 2 (CDK2), and minichromosome maintenance complex component 10 (MCM10) gene. [score:4]
Figure 7 miR-671-5p directly targets FOXM1. [score:4]
To fully examine the effect of miR-671-5p on global gene regulation, we performed microarray analyses to identify targets experimentally by comparing miR-671-5p transfected and mock transfected breast cancer cell lines, MDA-MB-231, SKBR3 and MCF-7. The data was deposited in GEO database (Acc# GSE62411). [score:4]
In our study, we observed that the S-phase arrest in miR-671-5p transfected cells is associated with downregulation of FOXM1 and CCNB1. [score:4]
miR-671-5p directly targets FOXM1. [score:4]
Our data indicate that the shift from EMT to MET is due to miR-671-5p mediated downregulation of FOXM1 and MCM10. [score:4]
miR-671-5p negatively regulates FOXM1 expression in breast cancer cell lines. [score:4]
miR-671-5p regulates FOXM1 expression in breast cancer. [score:4]
miR-671-5p targets FOXM1 in breast cancer cell lines. [score:3]
Attenuated expression of miR-671-5p in breast cancer progression. [score:3]
miR-671-5p inhibits epithelial to mesenchymal transition (EMT). [score:3]
We next aimed to determine whether it was possible for the mesenchymal-like MDA-MB-231 breast cancer cells to undergo MET following expression of miR-671-5p. [score:3]
Human miR-671-5p overexpression and microarray analysis. [score:3]
Because CCNB1 is a downstream target of FOXM1, we investigated whether the G [2]-phase cyclin, CCNB1 [16], was affected by miR-671-5p expression. [score:3]
To further investigate expression of miR-671-5p in breast cancer progression, we analyzed miR-671-5p (Acc#: MIMAT00038800) expression in a separate cohort including 30 breast cancer samples microdissected into normal and cancer cells from the FFPE tissue by qRT-PCR. [score:3]
We proposed that both endogenous and exogenous FOXM1 was suppressed in miR-671-5p-stable -transfected MDA-MB-231 cells. [score:3]
Briefly, 4 μl (200 ng) of CsCl-purified pCMVLuc plasmids, damaged or non-damaged, were transfected with miR-671-5p overexpressing MDA-MB-231 cells using Lipofectamine 2000 (Invitrogen). [score:3]
miR-671-5p inhibits proliferation and decreases invasive ability of breast cancer cell lines. [score:3]
These results suggest the dynamic expression changes of miR-671-5p may be frequent events during the progression of breast cancer. [score:3]
Overexpression of miR-671-5p sensitizes MDA-MB-231 to chemotherapy and UV treatment. [score:3]
In addition to FOXM1, our microarray data (Supplementary Figure 1) showed reduced expression of cell proliferation associated genes such as CDK2, GINS2, and MCM10 (Figure 7 and Supplementary Figure 1A) in miR-671-5p transfected MDA-MB-231 cells. [score:3]
miR-671-5p induces S-phase arrest and inhibits EMT. [score:3]
Therefore, miR-671-5p may serve as a novel therapeutic target in the management of breast cancer, particularly for TNBC. [score:3]
We report a previously undescribed mechanism for the tumor suppressor role of miR-671-5p in breast cancer. [score:3]
FOXM1, a member of the FOX superfamily of transcription factors, was one of the 7304 predicted target genes of miR-671-5p by MICRORNA. [score:3]
Our results demonstrated that miR-671-5p is a potential tumor suppressor miRNA in breast oncogenesis. [score:3]
To date, aberrant expression of miR-671-5p has been detected in hepatocellular carcinoma [25], lung cancer [10], and epithelioid sarcoma [26]. [score:3]
Cells were plated (7 × 10 [5] cells/well) in 24 well plates and co -transfected with 100 ng of DNA with pEZX-FOXM1-3′UTR (wild type and mutant) expression clones inserted downstream of the firefly luciferase gene and 100 ng of DNA with pEZX-miR-671-5p or the pEZX-scrambled control (mock), using FuGENE Transfection Reagent (Promega). [score:3]
Overexpression of miR-671-5p significantly reduces cell invasion in MDA-MB-231, Hs578T and SKBR3, but only slightly in MCF-7 and T47D. [score:3]
Conversely, transfection of miR-671-5p inhibitor promoted cell growth in all cell lines except MCF-7 cells. [score:3]
Total RNA from cells with miR-671-5p overexpressing cells were converted to cDNA and amplified by Nugen WT Applause Plus kit (Nugen). [score:3]
miR-671-5p overexpression significantly increased cell sensitivity to cisplatin, 5-FU and epirubicin. [score:3]
Therefore miR-671-5p could be a therapeutic target for breast cancer metastasis. [score:3]
Our data suggest that miR-671-5p specifically targets the 3′UTR region at 828–848 nt of FOXM1 (Acc# XM_005253676.2). [score:3]
Decreased expression of FOXM1 mRNA was also observed in miR-671-5p transfected MCF-7 and T47D cells, although the change was not statistically significant (Figure 3A). [score:3]
Conversely, transfection of miR-671-5p inhibitor resulted in increased cell growth in all cell lines. [score:3]
The stable transfected MDA-MB-231 cell line was further transfected with miR-671-5p inhibitor or mock. [score:3]
This is consistent with our results above, where FOXM1 and CCNB1 were significantly downregulated in miR-671-5p transfected MDA-MB-231 cells compared with mock -transfected cells. [score:3]
Thus, miR-671-5p appears to be a novel therapeutic target for breast cancer treatment. [score:3]
Expression of miR-671-5p in IDC vs. [score:3]
miR-671-5p target gene prediction. [score:3]
miR-671-5p plays an essential role in tumor suppression by inducing a shift from EMT to MET. [score:3]
Figure 3(A) qRT-PCR analysis of miR-671-5p and FOXM1 mRNA expression in breast cancer cell lines transfected with miR-671-5p mimic or mock (** p < 0.01, * p < 0.05). [score:3]
miR-671-5p overexpression significantly reduced post-UV/drug host cell reactivation activity. [score:3]
In consistent with proliferation capability, revealed that restoration of FOXM1 abolished the inhibition of invasion capabilities of miR-671-5p in stable -transfected MDA-MB-231 cells (Supplementary Figure 1B). [score:3]
Briefly, prior to the start of each experiment, 500 μl of warm (37°C) serum-free DMEM medium was added to the upper and lower chambers and allowed to rehydrate for 2 h in a 37°C cell culture incubator while 8 × 10 [4] cells were transfected by either miR-671-5p and inhibitor or their mocks and seeded onto the top chamber of pre-wetted inserts. [score:3]
We observed that overexpression of miR-671-5p impaired DNA repair in breast cancer cell lines, suggesting that miR-671-5p might correspond to the cellular stress upon radiation and DNA damage agents. [score:3]
Forced expression of FOXM1 rescued cell proliferation, invasion and EMT in miR-671-5p-stable -transfected cells. [score:3]
Unsupervised clustering heat map was generated on the genes with fold change > = 1.5 fold and p < = 0.05. miR-671-5p expression in clinical samples was analyzed by the exact two-sided binomial test. [score:3]
We found that one of the miRNAs, miR-671-5p, was consistently down-regulated in ADH and IDC compared to normal [3]. [score:3]
Our results demonstrate that miR-671-5p plays an important role in DNA repair by targeting FOXM1, which enhances the sensitivity of anticancer drugs in breast cancer cells. [score:3]
Western blotting analysis showed that overexpression of FOXM1 can restore the EMT marker vimentin and decreased epithelial marker E-cadherin in protein level by miR-671-5p (Supplementary Figure 1C). [score:3]
Our data suggesting that restoration of FOXM1 abolished the inhibition of proliferation by miR-671-5p. [score:3]
We found that the level of miR-671-5p was inversely related to FOXM1 expression (Figure 2A). [score:3]
A schematic mo del for the regulation of miR-671-5p. [score:2]
These findings suggest that miR-671-5p regulates cell cycle via FXOM1 mediated CCNB1 repression. [score:2]
Due to the role of FOXM1 in cell cycle [12], we sought to examine the effects of miR-671-5p in cell cycle regulation. [score:2]
To confirm the specificity of miR-671-5p targeting FOXM1, we performed luciferase reporter assays with pEZX-MT05 vectors containing the miR-671-5p binding site (either wild type or mutant sequences) in the FOXM1 3′UTR region and DNA with pEZX-miR-671-5p or pEZX-scrambled control (Figure 2B). [score:2]
miR-671-5p regulates cell cycle progression in human breast cancer cells. [score:2]
To determine if overexpression of miR-671-5p affects cell proliferation, we transfected miR-671-5p mimic to breast cancer cell lines and examined proliferation via MTT assays. [score:2]
As such, we chose to focus on the regulatory role of miR-671-5p on FOXM1. [score:2]
Our present results implicate the potential effects of miR-671-5p on chemotherapy by regulating FOXM1. [score:2]
Proliferative activity was decreased after transfection of miR-671-5p mimic and increased after transfection of miR-671-5p inhibitor compared to the mock control in breast cancer cell lines. [score:2]
FFPE breast tissues from breast cancer patients were microdissected for the purpose of confirming the expression level of miRNA-671-5p in ADH, DCIS, and IDC as compared to normal tissue. [score:2]
miR-671-5p overexpression significantly increased cell sensitivity to cisplatin, 5-FU, and epirubicin in MDA-MB-231 cells compared to mock transfected lines. [score:2]
Immunofluorescence staining and Western blot analyses showed decreased FOXM1 protein expression in miR-671-5p transfected cells compared with the mock control in both MDA-MB-231 and MCF-7 cell lines (Figure 3B and 3C). [score:2]
We then asked whether miR-671-5p enhanced the sensitivity of breast cancer cell lines to chemotherapy via DNA repair pathway. [score:1]
These results indicate an anti-proliferative effect of miR-671-5p in breast cancer cells. [score:1]
Top panel showing cell morphology was observed by microscopy in MDA-MB-231 cells transfected with mock and miR-671-5p. [score:1]
miR-671-5p/mock-stable -transfected MDA-MB-231 cell lines were transiently transfected with pcDNA3.1-FOXM1 and pcDNA3.1 empty vector. [score:1]
miR-671-5p sensitized breast cancer cells to anticancer drugs. [score:1]
Transfection of miR-671-5p into MDA-MB-231 cells (Figure 5A) caused an S-phase cell cycle arrest and a corresponding decrease in the G [1] phase of the cells (Figure 5B). [score:1]
miR-671-5p induced S-phase cell cycle arrest. [score:1]
To determine the drug effect after exposure, the miR-671-5p mimic or mock stable transfected MDA-MB-231 cells were seeded in 96-well tissue culture plates. [score:1]
These findings suggest that miR-671-5p reversed the EMT phenotype to a predominantly epithelial phenotype. [score:1]
Mock transfected MDA-MB-231 cells displayed elongated, irregular fibroblastoid morphology whereas miR-671-5p transfected cells showed a more epithelioid appearance. [score:1]
We observed that mock transfected MDA-MB-231 exhibits the same mesenchymal shape as the parental MDA-MB-231 cells (elongated, irregular fibroblastoid morphology), while miR-671-5p transfected MDA-MB-231 cells reversed to the epithelial shape (rounded). [score:1]
These results suggest that miR-671-5p might play a greater role in TNBC cell lines than in non-TNBC cell lines. [score:1]
A recent study has revealed that miR-671-5p was associated with chemoradiotherapy [46]. [score:1]
This suggests that miR-671-5p might play a greater role in TNBC than in non-TNBC cells (Figures 3 and 4). [score:1]
Effect of miR-671-5p on sensitivity of breast cancer cell lines to UVC/Chemosensitivity. [score:1]
miR-671-5p stable transfected MDA-MB-231 cells were labeled with PI and analyzed by DNA flow cytometry. [score:1]
We found that miR-671-5p transfected MDA-MB-231 cells have a significantly decreased number of invasive cells. [score:1]
Chattopadhyay et al. reported that MCM10 depletion by siRNA showed a similar cell morphological change to miR-671-5p transfected cells. [score:1]
pEZX-MR05-miR-671 containing the miR-671 precursor and pEZX-MR05-control with a scrambled sequence was obtained from GeneCopoeia (Rockville, Maryland, USA), and transfected into MDA-MB-231 cell lines using the standard FuGENE HD transfection reagent. [score:1]
miR-671-5p or mock was stable transfected into MDA-MB-231 cell line. [score:1]
Human miR-671-5p or scrambled mock oligos were purchased from LifeTechnologies. [score:1]
Decreased luciferase activity was also observed in miR-671-5p/FOXM1 3′UTR wild type cotransfected in Hs578T and MCF-7 cells, although the differences were not statistically significant (Figure 2C). [score:1]
Transfection of miR-671-5p and FOXM1 in human breast cancer cell lines. [score:1]
Permutation tests were performed for MTT assays between control and miR-671-5p mimic transfected groups. [score:1]
Dilutions of 90 pmol of miR-671-5p oligos or mocks and 5 μl of Lipofectamine 2000 (Invitrogen) in Opti-MEM serum-free medium were applied to 240,000 cells in a 6-well plate. [score:1]
miR-671-5p dysfunction is associated with a few human cancers [10], but there is no report in breast cancer. [score:1]
However, a significant sensitivity was detected only after 48 h of UV exposure in miR-671-5p transfected MDA-MB-231 cells. [score:1]
Stable transfected cells with miR-671-5p were plated at concentrations determined to yield 60–70% confluence within 24 h. Cells were harvested, and labeled with PI. [score:1]
Figure 5(A) Schematic diagram of miR-671-5p precursor sequence in pEZX-MR04. [score:1]
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2
[+] score: 164
Interestingly, literature mining and target analysis reveal that both miR-671-5p and SOX-2 may contribute to inhibiting the expression of common targets, like Solute Carrier Family 7 (Cationic Amino Acid Transporter, y+ System) member 1 (SLC7A1) or Fibronectin type III domain-containing 5 (FNDC5) [29, 30]. [score:9]
Its downregulation, mediated by increased expression of miR-671-5p and associated to downregulation of CDR1, paves the way to the study of new pathways involved in GBM pathogenesis. [score:9]
We also propose that CDR1 is an indirect target of miR-671-5p in the same biological context: its downregulation could be consequent to miR-671-5p -mediated degradation of CDR1-AS, as also suggested by literature [12]. [score:7]
We added CDR1 as further putative miR-671-5p target because its expression is known to be positively regulated by CDR1-AS (see Introduction and Discussion). [score:6]
Based on our in silico and experimental data, we further propose that CDR1-AS and VSNL1 are direct miR-671-5p targets, downexpressed in GBM (see Supplementary Figure 2). [score:6]
CDR1-AS is a validated miR-671-5p target with intriguing gene expression regulatory features (see Introduction on circRNAs). [score:6]
The list of predicted targets was further filtered by removing genes: (i) whose expression did not negatively correlate with that of miR-671-5p; (ii) had a miRanda-mirSVR score > - 0.5. [score:5]
Scatter plots showing correlation between expression of miR-671-5p and its targets. [score:5]
CHPF2 was overexpressed more than twofold in all GBM cell lines: similar to miR-671-5p, its overexpression appeared more pronounced in GBM cell lines than in other tissues (Figure 2B). [score:5]
We did not observe any other correlation between the expression of miR-671-5p or its targets and the clinical features of our GBM cohort. [score:5]
Ctrl (not transfected cells); NC Mim (Cells transfected with scramble molecules of miRNA mimics); 671–5p Mim (Cells transfected with miR-671-5p mimics); NC Inh (Cells transfected with scramble molecules of miRNA inhibitors); 671–5p Inh (Cells transfected with miR-671-5p inhibitors). [score:5]
Expression of CDR1-AS, CDR1, VSNL1 in DBTRG, SNB-19, U-87 MG cell lines after transfection with miR-671-5p mimics (miR-671-5p Mim) or inhibitors (miR-671-5p Inh). [score:5]
Final concentrations of miR-671-5p mimics and inhibitors were determined according to the best knock-in or knock-down efficiency, for each transfected cell line (see Supplementary Figure 3). [score:5]
Top 200 predicted targets of miR-671-5p were obtained through TargetScanHuman online algorithm, release 6.2 [41]. [score:5]
CDR1 downregulation (likely linked to miR-671-5p -dependent CDR1-AS degradation) may indeed contribute to loss of differentiation of neural cells, leading to neoplastic transformation [20]. [score:4]
Expression of miR-671-5p, miR-671-3p, miR-21 and miR-7 in GBM biopsies. [score:3]
MiR-671-5p mimics and inhibitors (anti-miR-671-5p) were purchased from Lifetechnologies™ (Carlsbad, CA, USA). [score:3]
Expression of miR-671-5p negatively correlated with that of CDR1-AS, CDR1, VSNL1 (r = −0.56, −0.57, −0.32, p = 1.33e-05, 1.91e-05, 0.021, respectively; n = 54, 51, 52, respectively, Spearman's Rank-Order Correlation test) (Figure 3). [score:3]
Hub nodes within miR-671-5p targets’ network. [score:3]
MiR-671-5p and miR-671-3p expression in GBM biopsies. [score:3]
miR-671-5p targets selection. [score:3]
DBTRG cells transfected with miR-671-5p mimics significantly increased their viability (16%) at 24 h after transfection; on the other hand, the same cells treated with miR-671-5p inhibitors significantly decreased their viability (12%) 72 h after transfection. [score:3]
Three out of the five GBM cell lines (A172, CAS-1, DBTRG) showed more than twofold miR-671-5p overexpression also respect to other two tumor cell lines (A375, HCT116) (Figure 1B). [score:3]
Negative correlation between expression of miR-671-5p and of CDR1-AS, CDR1 and VSNL1 in GBM biopsies and cell lines. [score:3]
The correlation between miR-671-5p and CHPF2 expression was not significant (r = 0.0077, p = 0.957, n = 51, Spearman's Rank-Order Correlation test) (Figure 3). [score:3]
Briefly, 10 [4] cells / well were reverse transfected with miR-671-5p mimics or inhibitors or scramble molecules, seeded into 96-well plates and incubated at 37°C for 24, 48, 72 h. At the end of each time point, cells were incubated for 3 h with 5 mg/ml of MTT solution (serum-free medium was used as solvent). [score:3]
Levels of CDR1-AS, CDR1 and VSNL1 transcripts significantly decreased or increased in DBTRG, SNB19 and U-87 MG following transfection with miR-671-5p mimics or inhibitors, respectively (Figure 4). [score:3]
U-87 MG significantly increased their viability (5%) 48 h after transfection with miR-671-5p mimics, while significantly decreased viability (19%) 48 h after transfection with miR-671-5p inhibitors (Figure 6). [score:3]
MiR-671-5p marked overexpression in GBM and its downstream effects on GBM cells migration and viability strongly suggest that this miRNA is a new oncomiR in GBM. [score:3]
Cerebellar Degeneration-Related Protein 1 (CDR1) antisense (CDR1-AS, a miR-7 sponge also known as ciRS-7) is the only circRNA known to be targeted and degraded by a microRNA (miR-671-5p) [11]. [score:3]
Negative correlation among putative targets and miR-671-5p was analyzed through miRGator v. 3.0 (http://mirgator. [score:3]
This circuitry may be upstream fostered by SOX2 (Sry-related box-2) in GBM cells: this transcription factor is known to promote malignancy in GBM and to positively control the expression of miR-671-5p [29, 30]. [score:3]
SNB-19 showed a significant increase of viability (9%) 48 h after transfection with miR-671-5p mimics and a significant reduction of viability (7%) 72 h after transfection with miR-671-5p inhibitors. [score:3]
We identified 46 validated and 61 predicted targets of miR-671-5p (see Supplementary Tables 1 and 2): among them, we selected CDR1-AS, CHPF2 and VSNL1 for further analysis. [score:3]
CHPF2 is the host gene of miR-671-5p and there is some experimental evidence that is targeted by the same miRNA. [score:3]
Validated targets of miR-671-5p were retrieved from miRTarbase, release 4.5 [40]. [score:3]
This molecular system is regulated by miR-671-5p, which under appropriate conditions leads to Argonaute RISC catalytic component 2 (AGO2) - mediated degradation of CDR1-AS [12]. [score:2]
MiR-671-5p expression in GBM cell lines. [score:2]
Spearman's nonparametric rank correlation coefficients were calculated using ΔCt values of miR-671-5p and its targets CDR1-AS A. CDR1 B. VSNL1 C. CHPF2 D. and ΔCt values of CDR1-AS and CDR1 E. See text for details. [score:1]
MiR-671-5p resulted significantly overexpressed in GBM biopsies compared to all reference tissues (average fold change = 13-fold, p-value < 0.001, Student's t-test). [score:1]
Involvement of miR-671-5p in DBTRG, SNB-19, U-87 MG migration. [score:1]
Figure 3Spearman's nonparametric rank correlation coefficients were calculated using ΔCt values of miR-671-5p and its targets CDR1-AS A. CDR1 B. VSNL1 C. CHPF2 D. and ΔCt values of CDR1-AS and CDR1 E. See text for details. [score:1]
Mir-671-5p resulted more than twofold overexpressed in A172, CAS-1, DBTRG, SNB-19 and U-87 MG GBM cells compared to whole brain, astrocytes and the neuroblastoma cell line SK-N-BE (Figure 1B). [score:1]
Based on our data, we propose that the axis miR-671-5p / CDR1-AS / CDR1 / Visinin-like 1 (VSNL1) is functionally altered in GBM and suggest that miR-671-5p is a novel oncomiR in GBM. [score:1]
CDR1-AS belongs to the recently discovered class of circRNAs: among them, it is the only one known to be degraded by a miRNA: miR-671-5p [12]. [score:1]
MiR-671-3p expression did not significantly differ compared to controls. [score:1]
The human gene encoding miR-671 maps at 7q36.1, a genomic region frequently amplified in GBM [13]. [score:1]
We sought to verify the involvement of miR-671 in GBM pathogenesis by applying the gene candidate approach. [score:1]
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[+] score: 142
Among the 77 miRNAs, 7 miRNAs, hsa-miR-33b-3p, hsa-miR-4284, hsa-miR-663a, hsa-miR-150-5p, hsa-miR-1233-3p, hsa-miR-671-3p, and hsa-miR-140-3p, were selected for further validation based on the fact that they were in the top 20 up- or downregulated miRNAs as found in microarray microRNA expression profiling presented in Fig.   1a, b. More specifically, miR-33b-3p and miR-4284 were among the top upregulated, and miR-663a, miR150-5p, miR-1233-3p, miR-671-3p, and miR-140-3p were downregulated. [score:12]
The expression levels of hsa-miR-33b-3p and hsa-miR-4284 coincided between the two methodologies, while hsa-miR-1233-3p, hsa-miR-140-3p, hsa-miR-150-5p, hsa-miR-663a, and hsa-miR-671-3p were marginally overexpressed in microarray analysis and appeared to be down-regulated with qRT-PCR Moreover, we found that hsa-miR-33b-3p and hsa-miR-4284 expression levels coincided between microarray analysis and qRT-PCR, exhibiting decreased expression in serum of OA samples compared to controls. [score:11]
The expression levels of hsa-miR-33b-3p and hsa-miR-4284 coincided between the two methodologies, while hsa-miR-1233-3p, hsa-miR-140-3p, hsa-miR-150-5p, hsa-miR-663a, and hsa-miR-671-3p were marginally overexpressed in microarray analysis and appeared to be down-regulated with qRT-PCR Moreover, we found that hsa-miR-33b-3p and hsa-miR-4284 expression levels coincided between microarray analysis and qRT-PCR, exhibiting decreased expression in serum of OA samples compared to controls. [score:11]
Hsa-miR-140-3p, hsa-miR-671-3p, and hsa-miR-150p were significantly downregulated in serum samples of OA patients compared to healthy individuals Among the 2549 miRNAs tested using the Agilent 8 × 60 K miRNA-array platform, a total of 279 miRNAs were found to be differentially expressed (205 upregulated and 74 downregulated) (FDR < 0.008, p < 0.05) in the serum of OA patients compared to healthy individuals (Fig.   1a, b ). [score:10]
Among these, INSR and IGF1R were targeted by all three miRNAs, while ADCY7, VANGL1, WNT5A, PPP3R2, TGFBR1, FZD4, BRAF, and CREB5 were co -targeted by hsa-miR-140-3p, and hsa-miR-671-3p, RPTOR, CDKN1A, PRKCB, ADCYA1, PDPK1, MAPK1, ADCY2, TCS1, Kras, CBL, CHRM3, SGL1, CREB1, KCNN3, PRKC1, PPP2R5E, and KCNJ11 were co -targeted by hsa-miR-33b-3p, and hsa-miR-140-3p and KCNN1 were co -targeted by hsa-miR-671-3p and hsa-miR-33b-3p. [score:9]
Regarding miR-671, besides its role in cancer cell migration [56], it was recently indicated that it regulates apoptotic genes such as caspase 8, p38, Myc -associated factor X (MAX), and Ras protein-specific guanine nucleotide releasing factor 1 (RASGRF1) in neurons of mice [56] and that it suppresses macrophage -mediated inflammation in orbital fat-derived stem cells by upregulating IL-IRA and TNFRII expressions [57, 58] highlighting its potential role in apoptosis and inflammation, both processes involved in OA. [score:9]
Hsa-miR-663a, hsa-miR-150-5p, hsa-miR-1233-3p, hsa-miR-140-3p, and hsa-miR-671-3p, which were marginally over-expressed in microarray analysis, appeared to be downregulated with qRT-PCR. [score:6]
Target-gene analysis of hsa-miR-140-3p, hsa-miR-33b-3p, and hsa-miR-671-3p revealed that InsR and IGFR1 were common targets of all three miRNAs, highlighting their involvement in regulation of metabolic processes that contribute to OA pathology. [score:6]
Fig. 4 Venn diagram of common target genes between miR-140-3p, miR-33b-3p and miR-671-3p Pathway enrichment analysis (Additional file  2: Table S2) revealed that the target genes of hsa-miR-140-3p, hsa-miR-33b-3p,and hsa-miR-671-3p are potentially involved in 48 common signaling pathways, including thyroid hormone synthesis, FoxO signaling pathway, insulin secretion, chemokine signaling pathway, MAPK signaling pathway, PI3K-Akt signaling pathway, estrogen signaling pathway, regulation of lipolysis in adipocytes, glucagon signaling pathway, and calcium signaling pathway, whereas 40 common pathways were predicted common between miR-140-3p and miR-33b-3p, such as mTOR signaling pathway, osteoclast differentiation, Ras signaling pathway, type II diabetes mellitus, adipocytokine signaling pathway, thyroid hormone signaling pathway, insulin signaling pathway, insulin resistance, sphingolipid signaling pathway, sphingolipid metabolism, and ErbB signaling pathway. [score:6]
Fig. 4 Venn diagram of common target genes between miR-140-3p, miR-33b-3p and miR-671-3p Pathway enrichment analysis (Additional file  2: Table S2) revealed that the target genes of hsa-miR-140-3p, hsa-miR-33b-3p,and hsa-miR-671-3p are potentially involved in 48 common signaling pathways, including thyroid hormone synthesis, FoxO signaling pathway, insulin secretion, chemokine signaling pathway, MAPK signaling pathway, PI3K-Akt signaling pathway, estrogen signaling pathway, regulation of lipolysis in adipocytes, glucagon signaling pathway, and calcium signaling pathway, whereas 40 common pathways were predicted common between miR-140-3p and miR-33b-3p, such as mTOR signaling pathway, osteoclast differentiation, Ras signaling pathway, type II diabetes mellitus, adipocytokine signaling pathway, thyroid hormone signaling pathway, insulin signaling pathway, insulin resistance, sphingolipid signaling pathway, sphingolipid metabolism, and ErbB signaling pathway. [score:6]
We, next, validated with qRT-PCR, which offers high accuracy, sensitivity, and dynamic range [46] the expression levels of 7 selected out of the 77 DE miRNAs, which were among the top 20 up- or downregulated in the microarray screening, namely, hsa-miR-33b-3p, hsa-miR-4284, hsa-miR-663a, hsa-miR-150-5p, hsa-miR-1233-3p, hsa-miR-140-3p, and hsa-miR-671-3p, in serum and in OA and healthy articular cartilage samples. [score:6]
Hsa-miR-140-3p and hsa-miR-671-3p expression levels were consistently downregulated in articular cartilage of OA patients compared to healthy individuals. [score:5]
Target gene analysis of hsa-miR-140-3p, hsa-miR-33b-3p, and hsa-miR-671-3p revealed that 28 genes were co -targeted by at least two miRNAs. [score:5]
We found that three miRNAs, hsa-miR-140-3p, hsa-miR-671-3p, and hsa-miR-33b-3p, were significantly downregulated in the serum of OA patients compared to controls, and in addition, hsa-miR-140-3p and hsa-miR-671-3p were also significantly downregulated in OA compared to healthy articular cartilage (Figs.   3a, b and 6 ). [score:5]
qRT-PCR validation in seven selected out of the 77 miRNAs revealed 3 significantly downregulated miRNAs (hsa-miR-33b-3p, hsa-miR-671-3p, and hsa-miR-140-3p) in the serum of OA patients, which were in silico predicted to be enriched in pathways involved in metabolic processes. [score:4]
We identified a three-miRNA signature, including hsa-miR-140-3p, hsa-miR-671-3p, and hsa-miR-33b-3p, which was downregulated in the serum of OA patients compared to controls and in silico predicted to be involved in regulating metabolic factors. [score:4]
An interesting finding in the in silico prediction analysis was that InsR and IGFR1 were common targets of all three hsa-miR-140-3p, hsa-miR-33b-3p, and hsa-miR-671. [score:3]
Among these seven miRNAs, 3 miRNAs, hsa-miR-33b-3p, hsa-miR-671-3p, and hsa-miR-140-3p, were found significantly downregulated in OA serum samples compared to controls (p < 0.05) (Fig.   3a ). [score:3]
Hsa-miR-1233-3p (a), hsa-miR-140-3p (b), hsa-miR-150-5p (c), hsa-miR-33-3p (d), hsa-miR-4284 (e), hsa-miR-663a (f), and hsa-miR-671-3p (g) manifested an area under the curve (AUC) value > 0.8 (AUC > 0.8) and p < 0.01 We verified by qRT-PCR the expression levels of the seven selected miRNAs (hsa-miR-33b-3p, hsa-miR-4284, hsa-miR-663a, hsa-miR-150-5p, hsa-miR-1233-3p, hsa-miR-140-3p, and hsa-miR-671-3p) in all serum samples. [score:3]
Hsa-miR-140-3p, hsa-miR-671-3p, and hsa-miR-33b-3p were significantly downregulated in serum samples of OA patients compared to healthy individuals. [score:3]
Along the same thought process, another interesting finding in our study was that cAMP responsive element binding protein 5 (CREB5), co -targeted by hsa-miR-140-3p and hsa-miR-671-3p, was significantly enriched in insulin secretion and TNF signaling pathways. [score:3]
Hsa-miR-140-3p, hsa-miR-671-3p, and hsa-miR-150p were significantly downregulated in serum samples of OA patients compared to healthy individuals To our knowledge, this is the first study to establish a potential global serum miRNA signature in OA patients using a high-resolution microarray technology interrogating 2549 miRNAs. [score:3]
The expression levels of hsa-miR-140-3p, hsa-miR-150-5p, and hsa-miR-671-3p were significantly decreased in OA articular cartilage compared to healthy cartilage (p < 0.05) (Fig.   6 ). [score:2]
Furthemore, five pathways were predicted between miR-140-3p and miR-671-3p, including Wnt signaling pathway, endocrine and other factor-regulated, and calcium reabsorption (Fig.   5 ). [score:2]
All above suggest that the in silico predictions in the present study are highlighting the possible implication of circulating hsa-miR-140-3p, hsa-miR-33b-3p, and hsa-miR-671-3p as novel serum -based biomarkers for osteoarthritis prognosis and underlining their involvement in the regulation of metabolic processes that contribute to OA pathology. [score:2]
Fig. 5 Venn diagram of common signaling pathways between miR-140-3p, miR-33b-3p and miR-671-3p Based on the previous list of the revealed miRNAs, we further investigated their association with known diseases. [score:1]
Regarding hsa-miR-671-3p and hsa-miR-33b, there are no reports on their involvement in OA pathogenesis. [score:1]
The expression levels of 7 selected miRNAs screened with miRNA microarrays, as mature hsa-miR-33b-3p, hsa-miR-4284, hsa-miR-663a, hsa-miR-150-5p, hsa-miR-1233-3p, hsa-miR-140-3p, and hsa-miR-671-3p, were evaluated in serum samples from 12 OA patients and 12 healthy controls. [score:1]
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[+] score: 38
Together, these findings indicate that a similar approach might be applied in the context of Cutaneous Leishmaniasis, where the altered expression of miR-193b and miR-671 could be reverted in order to downregulate TNFR expression. [score:8]
We found only STAT3 as a potential target for miR-671 and 11 target genes for miR-193b considering both data sets (Figure 4A). [score:5]
It is tempting to speculate that the axis of miR-193b, miR-671, and TREM-1 is a potential candidate to the development of new tools to manage this disease and other inflammatory skin disorders. [score:4]
The statistical significance (p-value) of the correlations between miR-193b (Figure 4C) and miR-671 (Figure 4D) with their target genes reinforced the relevance of miRNAs in the regulation of inflammation. [score:4]
On the other hand, miR-671 showed a strong positive correlation with TNFR (Figure 4F), suggesting that miR-671 could indirectly enhance the expression of TNFR. [score:4]
From this analysis, only miR-193b and miR-671 had significant mRNA targets that matched these criteria. [score:3]
Furthermore, no reports in the literature have described altered expression of miR-193b and miR-671 in the same context. [score:3]
In this study, we identified both miR-193b and miR-671 as relevant regulators of the inflammatory response observed in human LCL patients. [score:2]
The most significant genes (CD40 and TNFR) were selected for detailed correlation analysis with miR-193b (Figure 4E) and miR-671 (Figure 4F). [score:1]
In addition, there was no correlation among miR-193b, miR-671, and TREM-1 in patients who required more than 90 days of treatment (Figure 4G), suggesting a role for miR-193b, miR-671, and TREM1 in better prognosis for LCL. [score:1]
Spearman correlations between (E) miR-193b/CD40 and (F) miR-671/TNFR. [score:1]
Only patients with a good response to treatment (0–59 days) presented negative correlations (red lines) among miR-193b, TREM-1, miR-671, and LFA-1. On the other hand, patients who needed more than 60 days to be cured presented only positive correlations (blue lines) between different molecules, such as GRB2 and STAT5. [score:1]
We observed that the axis of miR-193b, miR-671, and TREM-1 could be used as a predictive marker of prognosis for human LCL. [score:1]
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[+] score: 20
In vitro and in vivo CDR1as overexpression increases the oncogenic phenotype(47) Down Glioma Potentially anti-tumorigenic role, CDR1as is a target of miR-671-5p, and overexpressing miR-671-5p leads to downregulation of CDR1as, increasing cellular migration and proliferation(48) (Cir-ITCH) ITCH Down ESCCPotentially anti-tumorigenic role, by sponging miR-7 positively regulates ITCH, an inhibitor of WNT/beta-catenin. [score:13]
Because this miRNA can degrade CDR1as, it can be hypothesized that miR-671-5p directly controls the expression of a circular transcript in cancer (48). [score:4]
The expression of CDR1as negatively correlates with that of miR-671-5p in glioblastoma. [score:3]
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[+] score: 16
Furthermore, overexpression of miR-671-5p negatively correlated with the expression of ciRS-7, CDR1, and VSNL1, which implied that the miR-671-5p/CDR1as/CDR1/VSNL1 axis was functionally altered in GBM [94]. [score:5]
This suggests that miR-671 -mediated degradation of ciRS-7 may diminish the ciRS-7 -mediated miR-7 inhibition and enhance miR-7 levels in tumor cells [83]. [score:3]
It was also demonstrated that overexpression of miR-671-5p in glioblastoma multiforme (GBM) biopsies and cell lines increased the migration and proliferation rates of GBM cells [94]. [score:3]
As a consequence, such miR-671 action may contribute to the increase in downstream target oncogenes (e. g., EGFR and XIAP) and promote vascularization, metastasis, and amplification of tumor cells [83]. [score:3]
The combination of ciRS-7 and miR-671 triggers the linearization and AGO2 -mediated cleavage of ciRS-7, which enables the release of the absorbed miR-7 molecules [42]. [score:1]
In addition to miR-7 binding sites, ciRS-7 contains an additional binding site for miR-671. [score:1]
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[+] score: 13
Predicted targets for the top 5 annotated miRNA in exosomes (miR-663, miR-503, miR-492, miR-498 and miR-671–5p) were searched using TargetScan and subsequently the target mRNAs were analysed by IPA software to determine predicted canonical pathways, networks and biofunctions regulated by the exosomal miRNAs (Fig. 5 and Additional Information, Table S6. [score:8]
TargetScanHuman 5.1 was applied to predict mRNA targets for the top 5 annotated microRNAs detected in exosomes (miR-663, miR-503, miR-492, miR-498 and miR-671–5p), which generated a list of 500 mRNA. [score:5]
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[+] score: 13
44 (−3.01) −0.48 (−3.05) −0.35 (−2.92) −0.27 (−2.84) hsa-miR-378c −0.8 (−1.44) −0.44 (−1.07) −0.69 (−1.33) −0.51 (−1.14) hsa-miR-378d −0.79 (−1.38) −0.56 (−1.14) −0.79 (−1.37) −0.73 (−1.31) hsa-miR-671-3p −0.51 (−1.86) −0.4 (−1.74) −0.89 (−2.23) −0.6 (−1.95) Candidate target genes for the 32 DE-miRNAs in BSS were predicted bioinformatically and compared with mRNAs identified as being differentially expressed in the analysis of the transcriptomes for the same samples (unpublished data). [score:4]
The five potential candidate miRNAs (hsa-miR-140-5p, hsa-miR-210, hsa-miR-362-5p, hsa-miR-590-3p, and hsa-miR-671-3p) may be important factors related to BSS in DM and can be used as biomarkers for diagnosis and drug targets for treating DM with BSS. [score:3]
were chosen from GO annotations in which target genes were significantly enriched (−log [10](P-value) > 5), which included hsa-miR-140-5p, hsa-miR-210, hsa-miR-362-5p, hsa-miR-590-3p, and hsa-miR-671-3p. [score:3]
Based on the analysis, it showed that five miRNAs were closely related to BSS in DM, including hsa-miR-140-5p, hsa-miR-210, hsa-miR-362-5p, hsa-miR-590-3p, and hsa-miR-671-3p. [score:1]
The current state of evidence for the relationship between miR-671-3p and DM has so far been unknown. [score:1]
Their miRNAs were selected as the potential candidate miRNAs of BSS in DM, which were hsa-miR-140-5p, hsa-miR-210, hsa-miR-362-5p, hsa-miR-590-3p, and hsa-miR-671-3p (Table 4). [score:1]
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[+] score: 11
Twelve radiation -suppressed miRNAs were identified, i. e. let-7d, miR-15a, miR-17, miR-30d, miR-92a, miR-197, miR-221, miR-320b, miR-342, miR-361, miR-501 and miR-671, and a significantly different expression between prostate cancer and the corresponding adjacent part was found, including 11 upregulated and 1 downregulated (Fig. 3B). [score:11]
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[+] score: 11
Out of 12 miRNA families that were predicted to target the PRKAG1 sense promoter in both human and mouse, nine (miR-718, miR-1224, miR-188, miR-346, miR-296, miR-671, miR-221, miR-1306, miR-506) can form highly stable duplex structures with their target sites (MFE ≤ −30 kcal/mol) in both organisms. [score:5]
In addition, six families (miR-34, miR-718, miR-346, miR-671, miR-340, miR-1306) target upstream sequences that contain previously reported AGO binding sites in both organisms. [score:3]
In this case, miR-671 and miR-1306 were good candidates for further testing of miRNA–PRKAG1 promoter interactions. [score:1]
Experimental evidence for the existence of nuclear miRNAs was also present for the three miRNA families, namely miR-188, miR-671 and miR-30. [score:1]
Some miRNAs in six families (miR-34, miR-188, miR-671, miR-340, miR-221, miR-1306) were shown by at least one experimental study to be nuclear dominant. [score:1]
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[+] score: 10
Tan et al reported that miR-671-5p is a tumor-suppressor miRNA in breast tumorigenesis by directly targeting FOXM1, and also demonstrated that overexpression of miR-671-5p in breast cancer cells attenuates cell proliferation and invasion, induces S-phase arrest, inhibits EMT and sensitizes cancer cells to cisplatin, 5-fluorouracil and epirubicin exposure [52]. [score:10]
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[+] score: 10
Experimental validation was done using quantitative RT-PCR for seven randomly chosen miRNAs (five upregulated and two downregulated) and we noticed significant induction in the levels of miR-503, -638, -663 and -744 while slight downregulation in miR-3175 and miR-671-5p (Figure 1b ). [score:10]
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[+] score: 10
control Expression in case group 1 hsa-mir-1290 0.26 down 2 hsa-mir-342-5p 0.22 down 3 hsa-mir-1224-5p 0.23 down 4 hsa-mir-345 0.38 down 5 hsa-mir-1228 0.38 down 6 hsa-mir-1249 0.32 down 7 hsa-mir-1826 0.26 down 8 hsa-miR-1306 0.38 down 9 hsa-miR-188-5p 0.43 down 10 hsa-miR-320a 0.48 down 11 hsa-miR-320c 0.26 down 12 hsa-miR-365 0.31 down 13 hsa-miR-423-5p 0.35 down 14 hsa-miR-483-5p 0.25 down 15 hsa-miR-634 0.31 down 16 hsa-miR-671-5p 0.23 down 17 hsa-miR-939 0.24 down 18 hsa-miR-1246 2.22 up 19 hsa-miR-150 10.41 up 20 hsa-miR-574-5p 8.04 up Table 3 MiRNAs Target Gene Symbol hsa-miR-345PUM2, PPP2R3A, BCAT1, ZFHX4, CHSY3, ARNT, SHE, SLC7A5, SOS1,. [score:5]
control Expression in case group 1 hsa-mir-1290 0.26 down 2 hsa-mir-342-5p 0.22 down 3 hsa-mir-1224-5p 0.23 down 4 hsa-mir-345 0.38 down 5 hsa-mir-1228 0.38 down 6 hsa-mir-1249 0.32 down 7 hsa-mir-1826 0.26 down 8 hsa-miR-1306 0.38 down 9 hsa-miR-188-5p 0.43 down 10 hsa-miR-320a 0.48 down 11 hsa-miR-320c 0.26 down 12 hsa-miR-365 0.31 down 13 hsa-miR-423-5p 0.35 down 14 hsa-miR-483-5p 0.25 down 15 hsa-miR-634 0.31 down 16 hsa-miR-671-5p 0.23 down 17 hsa-miR-939 0.24 down 18 hsa-miR-1246 2.22 up 19 hsa-miR-150 10.41 up 20 hsa-miR-574-5p 8.04 up Table 3 MiRNAs Target Gene Symbol hsa-miR-345PUM2, PPP2R3A, BCAT1, ZFHX4, CHSY3, ARNT, SHE, SLC7A5, SOS1,. [score:5]
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[+] score: 8
This suggests that miR-671 diminishes the inhibition of miR-7 expression through; improves the miR7 level in tumor cells; contributes to the increase of downstream target oncogenes, such as EGFR and XIAP; and promotes vascularization, metastasis and reproduction of tumor cells [41, 44]. [score:7]
miR-671 was found to be another binding site, and the combination of the two molecules mediates the Ago2 -mediated cleavage of to release the absorbed miR-7 [42, 43]. [score:1]
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[+] score: 8
Other miRNAs from this paper: hsa-mir-149, hsa-mir-3161
The number of targeted genes is similar between miRNAs bearing fixed mutations specific for H. s. n. and H. s. d. (Ensembl gene IDs): 1260 target genes for H. s. n. and 1547 for H. s. d. (excluding targets of hsa-mir-671-3p miRNA that possess specific variants common for H. s. d. and H. s. n. ). [score:8]
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16
[+] score: 8
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-24-1, hsa-mir-24-2, hsa-mir-25, mmu-let-7g, mmu-let-7i, mmu-mir-124-3, mmu-mir-9-2, mmu-mir-134, mmu-mir-137, mmu-mir-138-2, mmu-mir-145a, mmu-mir-24-1, hsa-mir-192, mmu-mir-194-1, mmu-mir-200b, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-215, hsa-mir-221, hsa-mir-200b, mmu-mir-296, mmu-let-7d, mmu-mir-106b, hsa-let-7g, hsa-let-7i, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-137, hsa-mir-138-2, hsa-mir-145, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-134, hsa-mir-138-1, hsa-mir-194-1, mmu-mir-192, 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-24-2, mmu-mir-346, hsa-mir-200c, mmu-mir-17, mmu-mir-25, mmu-mir-200c, mmu-mir-221, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-138-1, mmu-mir-7a-1, mmu-mir-7a-2, mmu-mir-7b, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-106b, hsa-mir-200a, hsa-mir-296, hsa-mir-369, hsa-mir-346, mmu-mir-215, gga-let-7i, gga-let-7a-3, gga-let-7b, gga-let-7c, gga-mir-221, gga-mir-17, gga-mir-138-1, gga-mir-124a, gga-mir-194, gga-mir-215, gga-mir-137, gga-mir-7-2, gga-mir-138-2, gga-let-7g, gga-let-7d, gga-let-7f, gga-let-7a-1, gga-mir-200a, gga-mir-200b, gga-mir-124b, gga-let-7a-2, gga-let-7j, gga-let-7k, gga-mir-7-3, gga-mir-7-1, gga-mir-24, gga-mir-7b, gga-mir-9-2, dre-mir-7b, dre-mir-7a-1, dre-mir-7a-2, dre-mir-192, dre-mir-221, dre-mir-430a-1, dre-mir-430b-1, dre-mir-430c-1, dre-let-7a-1, dre-let-7a-2, dre-let-7a-3, dre-let-7a-4, dre-let-7a-5, dre-let-7a-6, dre-let-7b, dre-let-7c-1, dre-let-7c-2, dre-let-7d-1, dre-let-7d-2, dre-let-7e, dre-let-7f, dre-let-7g-1, dre-let-7g-2, dre-let-7h, dre-let-7i, dre-mir-7a-3, dre-mir-9-1, dre-mir-9-2, dre-mir-9-4, dre-mir-9-3, dre-mir-9-5, dre-mir-9-6, dre-mir-9-7, dre-mir-17a-1, dre-mir-17a-2, dre-mir-24-4, dre-mir-24-2, dre-mir-24-3, dre-mir-24-1, dre-mir-25, dre-mir-92b, dre-mir-124-1, dre-mir-124-2, dre-mir-124-3, dre-mir-124-4, dre-mir-124-5, dre-mir-124-6, dre-mir-137-1, dre-mir-137-2, dre-mir-138-1, dre-mir-145, dre-mir-194a, dre-mir-194b, dre-mir-200a, dre-mir-200b, dre-mir-200c, dre-mir-430c-2, dre-mir-430c-3, dre-mir-430c-4, dre-mir-430c-5, dre-mir-430c-6, dre-mir-430c-7, dre-mir-430c-8, dre-mir-430c-9, dre-mir-430c-10, dre-mir-430c-11, dre-mir-430c-12, dre-mir-430c-13, dre-mir-430c-14, dre-mir-430c-15, dre-mir-430c-16, dre-mir-430c-17, dre-mir-430c-18, dre-mir-430a-2, dre-mir-430a-3, dre-mir-430a-4, dre-mir-430a-5, dre-mir-430a-6, dre-mir-430a-7, dre-mir-430a-8, dre-mir-430a-9, dre-mir-430a-10, dre-mir-430a-11, dre-mir-430a-12, dre-mir-430a-13, dre-mir-430a-14, dre-mir-430a-15, dre-mir-430a-16, dre-mir-430a-17, dre-mir-430a-18, dre-mir-430i-1, dre-mir-430i-2, dre-mir-430i-3, dre-mir-430b-2, dre-mir-430b-3, dre-mir-430b-4, dre-mir-430b-6, dre-mir-430b-7, dre-mir-430b-8, dre-mir-430b-9, dre-mir-430b-10, dre-mir-430b-11, dre-mir-430b-12, dre-mir-430b-13, dre-mir-430b-14, dre-mir-430b-15, dre-mir-430b-16, dre-mir-430b-17, dre-mir-430b-18, dre-mir-430b-5, dre-mir-430b-19, dre-mir-430b-20, mmu-mir-470, hsa-mir-485, hsa-mir-496, dre-let-7j, mmu-mir-485, mmu-mir-543, mmu-mir-369, hsa-mir-92b, gga-mir-9-1, mmu-mir-671, mmu-mir-496a, mmu-mir-92b, hsa-mir-543, gga-mir-124a-2, mmu-mir-145b, mmu-let-7j, mmu-mir-496b, mmu-let-7k, gga-mir-124c, gga-mir-9-3, gga-mir-145, dre-mir-138-2, dre-mir-24b, gga-mir-9-4, mmu-mir-9b-2, mmu-mir-124b, mmu-mir-9b-1, mmu-mir-9b-3, gga-mir-9b-1, gga-let-7l-1, gga-let-7l-2, gga-mir-9b-2
This observation suggest that miR-671 might function as an indirect regulator of miR-7 activity by targeting and reducing ciRS-7 levels; however, the exact function of the ciRS-7:miR-671 interaction during the development of the CNS is still unknown. [score:6]
An interesting finding is the miR-671-directed cleavage of ciRS-7 due to the perfect sequence complementarity that exists between both RNAs (Hansen et al., 2013). [score:2]
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17
[+] score: 7
Statistical significance enrichment analysis identified nine miRNAs as frequently targeted at detected spliced transcripts: hsa-miR-769-3p (predicted to target four transcripts), hsa-miR-378 (with six targets) as well as hsa-mir-320, hsa-miR-92b-5p, hsa-miR-16, hsa-miR-150, hsa-miR-671, hsa-miR-20a, and hsa-miR-18b (The full list and adjusted p-values are given under Table S10). [score:7]
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[+] score: 7
Seven over-expressed microRNAs that were altered at least four fold, including hsa-miR-671-5p, hsa-miR-542-5p, hsa-miR-542-3p, hsa-miR-1185, hsa-miR-539, hsa-miR-148a and hsa-miR-301a, (Figure 4A) and six over-expressed microRNAs that were highly expressed (normalized data ≥6), including hsa-miR-1290, hsa-miR-136, hsa-miR-424, hsa-miR-30a, hsa-miR-148a and hsa-miR-1246 (Figure 4B), were selected for further qRT-PCR analyses. [score:7]
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[+] score: 7
Except for miR-671-3p, all other miRNAs were found down-regulated in tumor tissues. [score:4]
Five miRNAs are newly found to be associated with PCa namely, miR-671-3p, miR-143-5p, miR-145-3p, miR-195-3p and miR-320b. [score:1]
We report here 4 miRNAs, which are associated with prostate cancer for the first time, namely miR-671-3p, miR-143-5p, miR-145-3p and miR-320b. [score:1]
Our findings, along with the report indicating a significant association of miR-671-3p with breast cancer [25], suggest that miR-671-3p could be an attractive marker for prostate cancer risk. [score:1]
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[+] score: 7
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-21, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-26a-1, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-99a, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-16-2, hsa-mir-192, hsa-mir-148a, hsa-mir-10b, hsa-mir-181a-2, hsa-mir-181a-1, hsa-mir-215, hsa-mir-223, hsa-mir-224, hsa-mir-200b, hsa-mir-15b, hsa-mir-27b, hsa-mir-125b-1, hsa-mir-141, hsa-mir-143, hsa-mir-152, hsa-mir-125b-2, hsa-mir-126, hsa-mir-146a, hsa-mir-184, hsa-mir-200c, hsa-mir-155, hsa-mir-29c, hsa-mir-200a, hsa-mir-99b, hsa-mir-296, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-378a, hsa-mir-342, hsa-mir-148b, hsa-mir-451a, ssc-mir-125b-2, ssc-mir-148a, ssc-mir-15b, ssc-mir-184, ssc-mir-224, ssc-mir-23a, ssc-mir-24-1, ssc-mir-26a, ssc-mir-29b-1, ssc-let-7f-1, ssc-mir-103-1, ssc-mir-21, ssc-mir-29c, hsa-mir-486-1, hsa-mir-499a, hsa-mir-378d-2, bta-mir-26a-2, bta-mir-29a, bta-let-7f-2, bta-mir-103-1, bta-mir-148a, bta-mir-16b, bta-mir-21, bta-mir-499, bta-mir-99a, bta-mir-125b-1, bta-mir-126, bta-mir-181a-2, bta-mir-27b, bta-mir-31, bta-mir-15b, bta-mir-215, bta-mir-30e, bta-mir-148b, bta-mir-192, bta-mir-200a, bta-mir-200c, bta-mir-23a, bta-mir-29b-2, bta-mir-29c, bta-mir-10b, bta-mir-24-2, bta-mir-30a, bta-mir-200b, bta-let-7a-1, bta-mir-342, bta-let-7f-1, bta-let-7a-2, bta-let-7a-3, bta-mir-103-2, bta-mir-125b-2, bta-mir-15a, bta-mir-99b, hsa-mir-664a, ssc-mir-99b, hsa-mir-103b-1, hsa-mir-103b-2, ssc-mir-15a, ssc-mir-16-2, ssc-mir-16-1, bta-mir-141, bta-mir-143, bta-mir-146a, bta-mir-152, bta-mir-155, bta-mir-16a, bta-mir-184, bta-mir-24-1, bta-mir-223, bta-mir-224, bta-mir-26a-1, bta-mir-296, bta-mir-29d, bta-mir-378-1, bta-mir-451, bta-mir-486, bta-mir-671, bta-mir-29e, bta-mir-29b-1, bta-mir-181a-1, ssc-mir-181a-1, ssc-mir-215, ssc-mir-30a, bta-mir-2318, bta-mir-2339, bta-mir-2430, bta-mir-664a, bta-mir-378-2, ssc-let-7a-1, ssc-mir-378-1, ssc-mir-29a, ssc-mir-30e, ssc-mir-499, ssc-mir-143, ssc-mir-10b, ssc-mir-486-1, ssc-mir-152, ssc-mir-103-2, ssc-mir-181a-2, ssc-mir-27b, ssc-mir-24-2, ssc-mir-99a, ssc-mir-148b, ssc-mir-664, ssc-mir-192, ssc-mir-342, ssc-mir-125b-1, oar-mir-21, oar-mir-29a, oar-mir-125b, oar-mir-181a-1, hsa-mir-378b, hsa-mir-378c, ssc-mir-296, ssc-mir-155, ssc-mir-146a, bta-mir-148c, ssc-mir-126, ssc-mir-378-2, ssc-mir-451, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, hsa-mir-451b, hsa-mir-499b, ssc-let-7a-2, ssc-mir-486-2, hsa-mir-664b, hsa-mir-378j, ssc-let-7f-2, ssc-mir-29b-2, ssc-mir-31, ssc-mir-671, bta-mir-378b, bta-mir-378c, hsa-mir-486-2, oar-let-7a, oar-let-7f, oar-mir-103, oar-mir-10b, oar-mir-143, oar-mir-148a, oar-mir-152, oar-mir-16b, oar-mir-181a-2, oar-mir-200a, oar-mir-200b, oar-mir-200c, oar-mir-23a, oar-mir-26a, oar-mir-29b-1, oar-mir-30a, oar-mir-99a, bta-mir-664b, chi-let-7a, chi-let-7f, chi-mir-103, chi-mir-10b, chi-mir-125b, chi-mir-126, chi-mir-141, chi-mir-143, chi-mir-146a, chi-mir-148a, chi-mir-148b, chi-mir-155, chi-mir-15a, chi-mir-15b, chi-mir-16a, chi-mir-16b, chi-mir-184, chi-mir-192, chi-mir-200a, chi-mir-200b, chi-mir-200c, chi-mir-215, chi-mir-21, chi-mir-223, chi-mir-224, chi-mir-2318, chi-mir-23a, chi-mir-24, chi-mir-26a, chi-mir-27b, chi-mir-296, chi-mir-29a, chi-mir-29b, chi-mir-29c, chi-mir-30a, chi-mir-30e, chi-mir-342, chi-mir-378, chi-mir-451, chi-mir-499, chi-mir-671, chi-mir-99a, chi-mir-99b, bta-mir-378d, ssc-mir-378b, oar-mir-29b-2, ssc-mir-141, ssc-mir-200b, ssc-mir-223, bta-mir-148d
Similarly, Naeem et al. (2012) demonstrated a differential regulation of four miRNAs (Bta-miR-181a, miR-16, miR-31, and miR223) in bovine mammary tissue infected with Streptococcus uberis as compared to healthy tissue while Hou et al. (2012) showed that bta-miR-296, miR-2430, and miR-671 were up-regulated and miR-2318 was down-regulated in mammary tissues of cows with mastitis. [score:7]
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[+] score: 6
Meanwhile, we obtained a list of miRNAs including miR-671, miR-615, miR-20a, miR-17 and miR-196a through the gene-miRNA targets function of miRWalk 2.0, which were predicted to regulate the expression of UBE2C. [score:6]
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[+] score: 6
A study has identified a highly expressed endogenous circular RNA (circRNA) in human brain and mouse brain and has demonstrated that the circRNA in Cerebellar Degeneration Related protein 1 (CDR1) locus can be endonucleolytically cleaved by miR-671 in an Ago2- dependent manner (Hansen et al., 2011, 2013a, b). [score:3]
The fact that circular RNAs are targeted by endogenous miRNAs was reported by Hansen et al. The authors outlined a circRNA destruction mechanism in which miR-671 binds CDR1as/ciRS-7 with greater complementarities than miR-7 and induces cleavage of this circRNA mediated by Ago [the catalytic component of RNA induced silencing complex (RISC) which is a central component of RNA interference (RNAi) machinery] (Hansen et al., 2011). [score:3]
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[+] score: 6
In an intriguing elaboration of this regulatory pathway, the activity of the mammalian miR-7 miRNA can be inhibited by CDR1as/ciRS-7, which is in turn targeted by another miRNA, miR-671, which shows near-perfect complementarity and triggers endonucleolytic cleavage of CDR1as [8– 10]. [score:6]
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24
[+] score: 5
Nuclear miRNA may also influence non-coding RNA activity by targeting endogenous anti-sense and sense transcripts, such as miR-671-directed cleavage of CDR1 anti-sense transcripts by Ago2 (Hansen et al., 2011); while various co-regulatory transcriptional relationships between intronic miRNA and their host genes have been described (Ballarino et al., 2009; Janas et al., 2011). [score:5]
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25
[+] score: 4
Such included some of the most upregulated miRNA in the array data, such as miR-379, miR-671-5p and miR-708 (Figure S4). [score:4]
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26
[+] score: 4
A large number of overexpressed IR-responsive miRNAs that we identified in our work were found to be deregulated in human cancers, such as hsa-mir-513 [55], hsa-mir-744 [56], hsa-mir-92a [57], [58], hsa-mir-1228* [59], hsa-mir-671-5p [60], hsa-mir-638 [38], hsa-mir-370 [61], and hsa-mir-675 [62]. [score:4]
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27
[+] score: 3
Only two of them, miR-671-3p and miR-487b-3p showed a tendency of differential expression, albeit not reaching significance levels (Additional file 2: Table S15). [score:3]
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[+] score: 3
Next, to further explore the functions of these miRNAs in HCC, we selected miRNAs with a fold change >5, namely hsa-miR-636, hsa-miR-671, hsa-miR-489, hsa-miR-26a, hsa-miR-320, hsa-miR-628, hsa-miR-505, hsa-miR-100, hsa-miR-664, hsa-miR-942, hsa-miR-192, hsa-miR-99b, hsa-miR-125b, hsa-miR-10b, hsa-miR-30b, and hsa-miR-145, for GO (Gene Ontology) enrichment analysis [21] of their target genes using the web -based software WebGestalt 2.0 [22]. [score:3]
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[+] score: 3
The resistant haplotypes had differentially expressed miR-21-3p, miR-134-5p, miR-542-5p, and miR-671 these miRs were found to be associated with NFκβ pathway and increased resistance to infection suggesting their role in inflammation, though further functional analysis needs to be undertaken (Jiang et al., 2016). [score:3]
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[+] score: 3
To add an additional level of regulation, miR-671 via near-perfect complementarity has been shown to cause RISC -induced endonucleolytic ciRS-7 degradation [38]. [score:2]
Therefore, miR-671 could possibly be considered a positive regulator of miR-7 either by release of ciRS-7 bound miR-7 or by reducing the number of available ciRS-7 molecules for miR-7 sequestration [12]. [score:1]
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[+] score: 3
In addition, the interaction of Cdr1as with miR-7 could be targeted by another miRNA, miR-671, which triggers endonucleolytic cleavage of Cdr1as 25. [score:3]
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[+] score: 3
neuroglioma circRNA unknown miR-671-5p↑/CDR1-AS↓/CDR1↓/VSNL1↓-migration↑, migration↑Barbagallo, D [56]. [score:1]
carcinoma circ-CDR1 unknown CDR1↓-miR-671-CDR1 mRNA ↓Hansen, T. B [60]. [score:1]
Circ-Sry ↑ Sry-miR-138 lead -induced neuronal cell apoptosis circ-Rar1 unknown circRar1-miR-671- apoptosis -associated caspase8/p38Nan, A. [46]. [score:1]
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[+] 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-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-22, hsa-mir-26a-1, hsa-mir-29a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-99a, hsa-mir-101-1, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-106a, hsa-mir-16-2, hsa-mir-197, hsa-mir-199a-1, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-10a, hsa-mir-34a, hsa-mir-182, hsa-mir-199a-2, hsa-mir-205, hsa-mir-210, hsa-mir-221, hsa-mir-223, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-23b, hsa-mir-122, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-140, hsa-mir-142, hsa-mir-143, hsa-mir-125b-2, hsa-mir-134, hsa-mir-146a, hsa-mir-150, hsa-mir-206, hsa-mir-155, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-101-2, hsa-mir-130b, hsa-mir-26a-2, hsa-mir-361, hsa-mir-362, hsa-mir-363, hsa-mir-376c, hsa-mir-371a, hsa-mir-375, hsa-mir-376a-1, hsa-mir-378a, hsa-mir-342, hsa-mir-151a, hsa-mir-324, hsa-mir-335, hsa-mir-345, hsa-mir-423, hsa-mir-483, hsa-mir-486-1, hsa-mir-146b, hsa-mir-202, hsa-mir-432, hsa-mir-494, hsa-mir-495, hsa-mir-193b, hsa-mir-497, hsa-mir-455, hsa-mir-545, hsa-mir-376a-2, hsa-mir-487b, hsa-mir-551a, hsa-mir-571, hsa-mir-574, hsa-mir-576, hsa-mir-606, hsa-mir-628, hsa-mir-629, hsa-mir-411, hsa-mir-320b-1, hsa-mir-320c-1, hsa-mir-320b-2, hsa-mir-378d-2, hsa-mir-889, hsa-mir-876, hsa-mir-744, hsa-mir-885, hsa-mir-920, hsa-mir-937, hsa-mir-297, hsa-mir-1233-1, hsa-mir-1260a, hsa-mir-664a, hsa-mir-320c-2, hsa-mir-2861, hsa-mir-378b, hsa-mir-1260b, hsa-mir-378c, hsa-mir-1233-2, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, hsa-mir-664b, hsa-mir-378j, hsa-mir-486-2
Circulating exosomal miRNAs (miR-671-5p, miR-16-5p, and miR-150-3p) have also been observed to be differentially expressed in serum samples from both mild and extremely severe cases of HFMD when compared to that from healthy individuals (216). [score:2]
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[+] score: 2
miR-671 directs cleavage of an antisense transcript of the cerebellar degeneration-related protein 1, 34 kDa (CDR1), leading to a concomitant decrease in CDR1 [37]. [score:2]
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35
[+] 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, mmu-mir-216b, mmu-mir-671, mmu-mir-497a, mmu-mir-495, mmu-mir-146b, mmu-mir-708, mmu-mir-505, 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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36
[+] score: 1
EpCAM-Exos was identified to contain MIR671 and another 8 novel miRNAs (for a detailed list of identified pri-miRNAs, see). [score:1]
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37
[+] score: 1
Additionally, miR-202 miR-423-5p miR-503 miR-184 and miR-922 bind also to the conserved binding region chromosome 15 positions 58889443–5889473 and miR-330-5p (chr15:58889149–58889178), miR-671-5p (chr15:58889720–58889745) and miR-432 (chr15:58889688–58889718) bind to a region with good conservation also to the far related species zebra fish, but these eight miRNAs have no indication to be involved in AD (Table  1). [score:1]
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38
[+] score: 1
For example, computational analysis indicated that miRNAs that interact with the CD44 3′-UTR also have binding sites in other matrix encoding mRNA 3′-UTRs, including collagen type 1α1 (Col1α1) repressed by miR-328 and fibronectin type 1 (FN1) repressed by miR-512-3p, miR-491 and miR-671 [19]. [score:1]
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39
[+] score: 1
In another study, they indicated that the CD44 3′UTR is also the ceRNA for collagen type 1α1 (Col1α1) mediated by hsa-miR-328-5p and the ceRNA for fibronectin type 1 (FN1) mediated by hsa-miR-512-3p, hsa-miR-491-5p, and hsa-miR-671-5p [40]. [score:1]
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40
[+] score: 1
In the 67 APAP-early patients, miR-122-5p identified subsequent liver injury when normalized by any of the 6 endogenous miRNA normalizers described above (miR-122-5p area under ROC curve normalized by miR-1913, 0.97 (95% CI 0.92–1.01); miR-671, 0.96 (0.92–1.01); miR-1287, 0.95 (0.90–1.00); let7-d, 0.94 (0.89–1.00); miR-1260, 0.93 (0.88–1.00); miR-324, 0.93 (0.87–1.00) miR-122-5p ROC-AUC significantly larger than all other miRNAs – P < 0.05). [score:1]
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