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75 publications mentioning hsa-mir-455

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-455. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 264
Other miRNAs from this paper: hsa-mir-640, mmu-mir-455
We identified for the first time that upregulation of miR-455-3p expression could promote the migration of HUVECs while downregulation of miR-455-3p could inhibit the migration. [score:11]
Our results also showed that there is no change in iNOS expression either in miR-455-3p overexpressed cells or in downregulated ones (Supplementary Figure S1a and 1b). [score:8]
DNAJB12, DNAJB14, HERPUD1 mRNA expression did not change either in miR-455-3p overexpressed or in miR-455-3p downregulated HUVECs (Fig. 4a,b). [score:8]
Secondly, inhibiting expression of miR-455-3p to 50% (Fig. 2d) leaded to decreased expression of eNOS protein and NO content (Fig. 2e,f). [score:7]
H [2]S induced increasing expression of miR-455-3p were blocked when the expression of miR-455-3p were inhibited. [score:7]
Inhibiting expression of miR-455-3p not only leaded to increased expression of CUL3 but also blocked the effects of NaHS on CUL3 production (Fig. 4e,f). [score:7]
CUL3 could associate with other proteins to form ubiquitin ligase complex 18. and Western blot results showed thatHydrogen sulfide increases miR-455-3p, thus downregulates CUL3 and inhibits the proteasome degradation of eNOS protein. [score:6]
HUVECs were transfected with 0.05 nM, 0.5 nM, 5 nM has-miR-455-3p agomir to overexpress miR-455-3p and 150 nM has-miR-455-3p antagomir to downregulate it. [score:6]
However, neither overexpression nor downregulation of miR-455-3p has any effect on phosphorylation or dimerization of eNOS. [score:6]
Moreover, downregulation of miR-455-3p attenuated eNOS expression and NO content in HUVECs. [score:6]
We also found that the promoting effect of H [2]S on eNOS expression was abolished by the inhibition of miR-455-3p. [score:5]
Interestingly, we found that HUVECs with overexpressed miR-455-3p have decreased CUL3 expression both in mRNA and protein levels (Fig. 4c,d). [score:5]
Conversely, when endogenous miR-455-3p expression was inhibited by miR-455-3p antagomir, cell migration was blunted (Fig. 5c,f). [score:5]
The effects of exogenous H [2]S on the expression of eNOS, miR-455-3p and NO production in mice, and comparison of miR-455-3p expression and H [2]S production between atherosclerosis patients and chronic venous insufficiency patients. [score:5]
Ubiquitin-proteasome pathway inhibitor MG-132 blocked the effects of H [2]S and miR-455-3p on eNOS expression. [score:5]
We also found that increased expression of miR-455-3p was involved in NaHS induced eNOS expression, NO production, and HUVEC migration. [score:5]
To explore the mechanism of miR-455-3p on eNOS expression, we first identified potential targets for miR-455-3p by employing database miRecords (http://c1. [score:5]
H [2]S promotes miR-455-3p and eNOS expression in HUVECsCultured HUVECs were harvested after treated with vehicle or NaHS for 24 h. Then total RNA was extracted and real-time PCR experiments were performed to determine the expression of miR-455-3p. [score:5]
Figure 2i,j showed that inhibiting expression of miR-455-3p has no effects on phosphorylation or coupling levels of eNOS. [score:5]
Interestingly, the effects of H [2]S on eNOS expression and NO production were blocked by miR-455-3p inhibition (Fig. 2e,f). [score:5]
miR-455-3p mediates H [2]S induced eNOS expressionAs shown in Fig. 2a, HUVECs transfected with 5 nM miR-455-3p agomir showed an increased expression of miR-455-3p for nearly 200-folds. [score:5]
HUVECs with all three dosages of miR-455-3p overexpression have elevated eNOS expression (Fig. 2b). [score:5]
H [2]S and miR-455-3p downregulate the proteasome degradation pathway of eNOS protein. [score:4]
How to cite this article: Li, X. -H. et al. H [2]S regulates endothelial nitric oxide synthase protein stability by promoting microRNA-455-3p expression. [score:4]
Inhibition of miR-455-3p also blocked the pro-migration effect of H [2]S. These results indicate that miR-455-3p played an important role in H [2]S and eNOS mediated migration of HUVECs, and involves in the regulation of NO production. [score:4]
H [2]S and miR-455-3p downregulate the proteasome degradation pathway of eNOS proteinThe mRNA levels of eNOS were detected by and the results showed that there was no significant change either by NaHS treatment or miR-455-3p agomir transfection (Fig. 3a). [score:4]
No significant change was observed in kidney miR-455-3p expression. [score:3]
As shown in Fig. 2g,h, overexpression of miR-455-3p (5 nM) has no effects on phosphorylation or coupling levels of eNOS. [score:3]
Western blots and results showed that NaHS administration increased the expression of miR-455-3p and eNOS protein levels in skeletal muscle, heart and aorta. [score:3]
5 nM miR-455-3p agomir was chosen to perform the following experiments since it caused highest eNOS expression. [score:3]
Proteasome inhibitor MG-132 was used to detect whether miR-455-3p is involved in the ubiquitination and degradation of eNOS or not. [score:3]
As shown in Fig. 2a, HUVECs transfected with 5 nM miR-455-3p agomir showed an increased expression of miR-455-3p for nearly 200-folds. [score:3]
H [2]S promotes migration of HUVECs through increased expression of eNOS and miR-455-3p. [score:3]
eNOS and miR-455-3p expression increased in mice tissues after H [2]S administrationTo investigate if H [2]S could influence miR-455-3p and eNOS expression in vivo, 8-week-old mice were injected intraperitoneally with normal saline or 50 μmol/kg/day NaHS for one week. [score:3]
The effects of miR-455-3p on eNOS expression, NO production and eNOS coupling. [score:3]
CUL3 is the target gene of miR-455-3p in HUVECs. [score:3]
As shown by our results, overexpression of miR-455-3p dramatically elevated the protein levels of eNOS and NO content in HUVECs. [score:3]
When we decreased the dosage of miR-455-3p agomir to 0.5 nM or 0.05 nM, the expression level of miR-455-3p increased 8 or 2 folds respectively. [score:3]
Changes in miR-455-3p expression is more profound than NO content. [score:3]
miR-455-3p mediates H [2]S induced eNOS expression. [score:3]
To further investigate in vivo effects of H [2]S on miR-455-3p and their potential effects on the pathogenesis of diseases, we detected the expression of miR-455-3p in mouse healthy tissues. [score:3]
miRecords predicted several target genes of miR-455-3p such as DNAJB12, DNAJB14, HERPUD1 as well as CUL3 which are all related to proteasome degradation (Supplementary Table S1). [score:3]
While the increase range of NO content is only 10 to 30 percent, miR-455-3p expression increased in heart tissues for 2-fold, muscle tissues for 1.5-fold and aorta tissues for nearly 6-folds (Fig. 6a,b). [score:3]
Nevertheless, exogenous H [2]S remarkably increased both NO content (Fig. 6a) and miR-455-3p expression (Fig. 6b) in heart, muscle and aorta tissues. [score:3]
The has-miR-455-3p agomir oligonucleotide (5′-GCAGUCCAUGGGCAUAUACAC-3′), the has-miR-455-3p antagomir oligonucleotide (target sequence 5′-GUGUAUAUGCCCAUGGACUGC-3′), the agomir negative control and the antagomir negative control were synthesized by Biotend (Shanghai, China). [score:3]
Both H [2]S and miR-455-3p induced eNOS expression (Fig. 3b,c) and NO production (Fig. 3d,e) were blocked with the presence of MG-132 (1 μM). [score:3]
CUL3 is the target gene of miR-455-3p. [score:3]
After adding MG-132 to HUVECs, we found that the promoting effect of H [2]S and miR-455-3p on eNOS expression was abolished. [score:3]
Firstly, we examined NO production after miR-455-3p overexpression. [score:3]
The effects of exogenous H [2]S on miR-455-3p, eNOS and iNOS expression in HUVECs. [score:3]
eNOS and miR-455-3p expression increased in mice tissues after H [2]S administration. [score:3]
Our results indicate that H [2]S and miR-455-3p may participate in the compensation mechanism of eNOS expression in atherosclerotic plaque. [score:3]
Cultured HUVECs were harvested after treated with vehicle or NaHS for 24 h. Then total RNA was extracted and real-time PCR experiments were performed to determine the expression of miR-455-3p. [score:3]
Several predicted target genes of miR-455-3p such as DNAJB12, DNAJB14, HERPUD1 as well as CUL3 are related to proteasome degradation (Supplementary Table S1). [score:3]
H [2]S promotes miR-455-3p and eNOS expression in HUVECs. [score:3]
So that, we speculated that the stability of eNOS might be regulated by miR-455-3p. [score:2]
We found that proteasome degradation pathway of eNOS is regulated by H [2]S and miR-455-3p. [score:2]
As demonstrated in Fig. 5b,e, HUVECs overexpressing miR-455-3p showed a remarkable increase of migration when compared to the control groups. [score:2]
We also detected the expression of miR-455-3p in those patients and found that miR-455-3p levels increased in atherosclerotic plaques when compared with normal arterioles (Fig. 6f). [score:2]
Our results indicate the post-transcriptional regulation of NO production by H [2]S and miR-455-3p. [score:2]
As shown in Fig. 1a compared with vehicle group, the expression of miR-455-3p was increased with NaHS administration. [score:2]
In heart, muscle and aorta, miR-455-3p seems to play a vital role in eNOS regulation, while in kidney and liver, it does not play a decisive role. [score:2]
To investigate the mechanism of NO production regulation, we transfected agomir or antagomir of miR-455-3p in HUVECs to study its effect on eNOS expression, phosphorylation as well as the coupling of eNOS. [score:2]
However, the number of human samples is small in our experiments, more clinical samples and animal studies are needed to further investigate whether the compensation effect on NO production during atherosclerotic plaque formation is caused by increased H [2]S concentration and miR-455-3p expression. [score:1]
Taken together, the current work discovered for the first time that miR-455-3p was involved in the pro-migration effect of H [2]S on endothelial cells and mediates the effect of H [2]S on eNOS protein stability through ubiquitination pathway. [score:1]
However, eNOS protein level (Fig. 3b,c) and NO content (Fig. 3d,e) increased after H [2]S administration and miR-455-3p transfection. [score:1]
To investigate the role of miR-455-3p in HUVEC migration, miR-455-3p overexpression was achieved by agomir transfection. [score:1]
Synthesis and transfection of has-miR-455-3p agomir and antagomir. [score:1]
In liver, miR-455-3p levels increased while eNOS protein levels and NO production decreased. [score:1]
To investigate if H [2]S could influence miR-455-3p and eNOS expression in vivo, 8-week-old mice were injected intraperitoneally with normal saline or 50 μmol/kg/day NaHS for one week. [score:1]
Our results also showed that NO production and eNOS protein levels decreased in liver tissues (Fig. 6a,c) while miR-455-3p increased in liver tissues (Fig. 6b) after NaHS administration. [score:1]
Our results showed that eNOS protein levels, miR-455-3p levels as well as NO content did not change in kidney tissues (Fig. 6a–c). [score:1]
Elevated miR-455-3p caused increased NO production (Fig. 2c). [score:1]
miR-455-3p and eNOS protein levels in kidney did not change after NaHS administration. [score:1]
The mRNA levels of eNOS were detected by and the results showed that there was no significant change either by NaHS treatment or miR-455-3p agomir transfection (Fig. 3a). [score:1]
The role of eNOS and miR-455-3p during H [2]S -mediated migration of HUVECs. [score:1]
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2
[+] score: 225
Other miRNAs from this paper: hsa-mir-433
Importantly, patients with higher miR-455-3p expression experienced shorter overall and disease-free survival, whereas patients with lower miR-455-3p expression experienced longer overall and disease-free survival (P < 0.05; Fig. 4b). [score:9]
However, miR-455-3p is reportedly downregulated in prostate and colon cancer, and upregulation of miR-455-3p can inhibit the cancer proliferation [43, 44]. [score:9]
Consistent with TCGA analysis, the results of which showed that miR-455-3p was markedly upregulated in ESCC and correlated with shorter overall and disease-free survival in patients with ESCC (Fig. 4a and Additional file 4: Figure S3A and B), real-time polymerase chain reaction (PCR) analysis showed that miR-455-3p was significantly upregulated in 207 ESCC specimens compared with 15 normal esophageal tissues, and that miR-455-3p levels were positively correlated with clinical stage (P < 0.001), TNM classification (P < 0.001), and histologic differentiation (P = 0.002) in patients with ESCC (Fig. 4a and Additional file 1: Table S2). [score:8]
Consistent with the GSEA findings that miR-455-3p levels were significantly correlated with gene signatures regulated by the Wnt/β-catenin and TGF-β/Smad pathways (Fig. 5a and Additional file 5: Figure S4A), overexpression of miR-455-3p significantly enhanced, but silencing of miR-455-3p reduced, luciferase reporter activities and levels of expression of nuclear β-catenin, phosphorylated (p)-Smad2, and downstream genes in their respective pathways (Fig. 5b and c and Additional file 5: Figure S4B), suggesting that miR-455-3p contributes to activation of the Wnt/β-catenin and TGF-β/Smad pathways in ESCC. [score:6]
Furthermore, we demonstrated that aberrantly expressed miR-455-3p in ESCC cells simultaneously activates Wnt/β-catenin and TGF-β/Smad signaling through concurrent suppression of multiple negative regulators of these pathways. [score:6]
Consistent with our finding that miR-455-3p is upregulated in ESCC and multiple distinct cancer types, miR-455-3p is also overexpressed in glioma, oral squamous cell cancer, and triple -negative breast cancer, where it contributes to cancer chemoresistance, proliferation, and invasion/migration [40– 42]. [score:6]
a Analysis of miR-455-3p expression in TCGA (n = 199; P = 0.008; left) and in collected clinical samples (n = 222; P < 0.001; right) indicating that miR-455-3p was significantly upregulated in primary ESCC. [score:6]
We found that silencing of miR-455-3p simultaneously deactivated multiple T-IC -associated pathways, resulting in functional inhibition of ESCC chemoresistance and tumor recurrence, suggesting that miR-455-3p may be a suitable therapeutic target for the treatment of ESCC. [score:5]
As shown in Fig. 4c and d and Additional file 4: Figure S3C, both in vitro and in vivo chemoresistance experiments indicated that PDEC2 cells with higher miR-455-3p expression exhibited greater resistance to chemotherapeutic drugs than PDEC1 cells with lower miR-455-3p expression. [score:5]
Meanwhile, the proportion of CD90 [+]/CD271 [+] cells and tumorsphere-forming capability of miR-455-3p-transduced cells decreased via inhibition of the Wnt/β-catenin and TGF-β/Smad pathways upon treatment with their respective inhibitors (Additional file 5: Figure S4D and E), demonstrating that these two pathways are required for the miR-455-3p -induced T-IC traits of ESCC. [score:5]
Inhibition of miR-455-3p chemosensitizes ESCC cells and reduces the subpopulations of CD90 [+] and CD271 [+] T-ICs via the suppression of multiple T-IC -associated pathways, including the Wnt/β-catenin and TGF-β pathways. [score:5]
d, e Predicted miR-455-3p targets (d) and RIP analysis of the association between miR-455-3p and the 3’UTR of the indicated targets (e). [score:5]
The inhibitory effects of miR-455-3p on the protein expression and 3’UTRs-activity of these transcripts were verified in ESCC cells and further confirmed in 10 freshly collected ESCC specimens. [score:5]
Strikingly, gene set enrichment analysis (GSEA) of The Cancer Genome Atlas (TCGA) datasets revealed that ESCC exhibiting high miR-455-3p expression was enriched in resistance gene sets for chemotherapeutic drugs such as CDDP, DOC, doxorubicin, gefitinib, dasatinib, cyclophosphamide, and vincristine, whereas ESCC exhibiting low miR-455-3p expression was enriched in chemotherapy sensitive gene sets (Fig. 2b and Additional file 2: Figure S1A), suggesting that miR-455-3p contributes to ESCC chemoresistance. [score:5]
We found that miR-455-3p overexpression significantly increased, but miR-455-3p inhibition reduced, the subpopulations of CD90 [+] and CD271 [+] T-ICs, suggesting that miR-455-3p functions in the interconversion between ESCC cells and ESCC T-IC subpopulations. [score:5]
b Kaplan–Meier analysis of overall and disease-free survival curves for patients with ESCC exhibiting low or high miR-455-3p expression. [score:5]
Importantly, miR-455-3p is aberrantly upregulated in numerous cancers and significantly associated with the decreased overall survival of cancer patients. [score:4]
Analysis of TCGA datasets indicated that miR-455-3p was also markedly upregulated in other human cancers, including gastric, lung, bladder, breast, cervical, kidney, and uterine cancers (Fig. 6a), suggesting that miR-455-3p may also function as an oncomiR in other human cancers. [score:4]
miRNA-455-3p targets a number of negative regulators. [score:4]
a GSEA analysis of TCGA indicating that miR-455-3p expression is significantly correlated with gene signatures regulated by the Wnt/β-catenin and transforming growth factor-β (TGF-β)/Smad pathways. [score:4]
a Analysis of TCGA datasets indicating that miR-455-3p is aberrantly upregulated in subsets of primary tumors, including gastric, lung, bladder, breast, cervical, head and neck, kidney, thyroid, and uterine cancers. [score:4]
Importantly, miR-455-3p exhibited aberrant upregulation in various human cancer types, and was significantly associated with decreased overall survival of cancer patients. [score:4]
Importantly, higher miR-455-3p expression was associated with shorter overall survival and significantly correlated with gene signatures regulated by the Wnt/β-catenin and TGF-β/Smad pathways in gastric, kidney, and lung cancers (Fig. 6b and Additional file 6: Figure S5). [score:4]
Our results suggest that the chemoresistant ESCC cells examined in our study possess T-IC-like traits, and that miR-455-3p represents a potential therapeutic target to achieve better clinical outcomes in cancer patients. [score:3]
miRNA-455-3p overexpression correlates with poor prognosis in ESCC patients. [score:3]
miR-455-3p overexpression activates T-IC -associated signaling pathways. [score:3]
f Hypothetical mo del illustrating that aberrant expression of miR-455-3p activates multiple cancer stem cell -associated signaling pathways, leading to cancer progression, chemotherapy failure, and poor clinical outcomes. [score:3]
These studies imply that miR-455-3p can act as either an oncomiR or a tumor-suppressive miRNA depending on the tumor type. [score:3]
We conducted miRNA profiling in EC-CR and EC-UT cells (GSE83362) and showed that miR-455-3p expression was significantly higher in EC-CR cells than in EC-UT cells (Fig. 2a). [score:3]
Altogether, these results imply that aberrant miR-455-3p expression activates T-IC -associated signaling pathways, leading to cancer progression, chemotherapy failure, and poor clinical outcomes (Fig. 6f). [score:3]
b Kaplan–Meier analysis of overall survival for the indicated cancer patients with low or high miR-455-3p expression. [score:3]
b GSEA of TCGA datasets indicating that miR-455-3p expression was significantly correlated with chemoresistance gene signatures. [score:3]
As predicted, overexpressing miR-455-3p conferred resistance to CDDP and DOC in EC-UT and Kyse30 cells, but silencing miR-455-3p enhanced the sensitivity of EC-CR and Eca109 cells to chemotherapeutic agents (Additional file 2: Figure S1B). [score:3]
Our results demonstrate that miR-455-3p functions as an oncomiR in ESCC progression and may provide a potential therapeutic target to achieve better clinical outcomes in cancer patients. [score:3]
Thus, both TCGA analysis and these results suggest a potential link between miR-455-3p overexpression and ESCC progression. [score:3]
These results suggest that miR-455-3p activates the Wnt/β-catenin and TGF-β/Smad pathways by directly binding to the 3′ UTRs of a number of negative regulators. [score:3]
Fig. 3Inhibition of miR-455-3p chemosensitizes ESCC cells and reduces stem cell-like traits. [score:3]
Aberrant miRNA-455-3p expression contributes to the progression of various cancers. [score:3]
To explore the molecular mechanism underlying the function of miR-455-3p in ESCC chemoresistance, we examined miR-455-3p expression in ESCC and found that miR-455-3p levels are significantly correlated with the clinical features and overall/relapse-free survival of patients with ESCC, suggesting that miR-455-3p may be associated with chemotherapy failure in these patients. [score:3]
Furthermore, we found that miR-455-3p levels in 207 ESCC specimens were positively correlated with the expression of nuclear β-catenin and p-Smad2 (Additional file 5: Figure S4C). [score:3]
Similarly, silencing of miR-455-3p drastically enhanced the inhibitory effect of CDDP on tumor growth in Eca109 cells and increased the apoptotic rate in Eca109 tumors (Additional file 3: Figure S2A and B). [score:3]
miR-455-3p overexpression correlates with poor prognosis in ESCC patient. [score:3]
Concordantly, silencing miR-455-3p in EC-CR and Eca109 cells significantly decreased the proportion of CD90 [+]/CD271 [+] and SP cells and reduced the expression of stemness -associated factors (Fig. 3d and e and Additional file 3: Figure S2D and F). [score:3]
We found that miR-455-3p levels are significantly correlated with poorer disease-free survival and overall survival in patients with primary ESCC. [score:3]
Right: The percentages of specimens showing low or high miR-455-3p expression relative to levels of nuclear β-catenin and p-Smad2 (Ser465/467). [score:3]
Stable cell lines expressing pMSCV-miR-455-3p or miRZip-455-3p was generated by retroviral infection using HEK293T cells, and selected with 0.5 μg/ml puromycin for 10 days. [score:3]
Additionally, miR-455-3p expression was recognized as an independent prognostic factor (P < 0.001; Additional file 1: Table S3). [score:3]
Moreover, in an in vivo chemoresistance assay, the tumors formed by miR-455-3p -overexpressing cells upon CDDP treatment were larger and contained fewer apoptotic cells than the control tumors (Fig. 2c and Additional file 2: Figure S1C). [score:2]
The point mutations in the tentative miR-455-3p -binding seed regions were created using the Strategene QuickChange Mutagenesis Kit (Stratagene, La Jolla, CA). [score:2]
The miR-455-3p anti-sense was cloned into miRZip plasmid purchased from System Biosciences (San Francisco, CA). [score:1]
miR-455-3p promotes chemoresistance and tumorigenesis of ESCC cells. [score:1]
Silencing miRNA-455-3p chemosensitizes ESCC cells and reduces T-ICs-like traits. [score:1]
In this study, we identified miR-455-3p as essential for ESCC chemoresistance both in vivo and in vitro. [score:1]
miR-455-3p enhances ESCC chemoresistance and promotes ESCC tumorgencity. [score:1]
Importantly, silencing miR-455-3p dramatically enhanced the sensitivity of PDEC2 cells to chemotherapeutic drugs, and reduced the percentages of CD90 [+]/CD271 [+] and SP cells and tumorsphere-forming capability of PDEC2 cells (Fig. 4d and f and Additional file 4: Figure S3D). [score:1]
Moreover, silencing miR-455-3p in gastric and bladder cancer cells dramatically decreased the transcriptional activities of the Wnt/β-catenin and TGF-β/Smad pathways and CDDP resistance (Fig. 6d and e). [score:1]
Fig. 4Silencing miR-455-3p chemosensitizes and reduces the tumorigenesis of PDEC cells. [score:1]
Together, these results support the contribution of miR-455-3p to the chemoresistance and tumorigenesis of ESCC. [score:1]
Collectively, these results suggest that miR-455-3p plays an important role in ESCC chemoresistance. [score:1]
The human miR-455-3p gene was PCR-amplified from genomic DNA and cloned into a pMSCV-puro retroviral vector. [score:1]
c RIP analysis of the association between miR-455-3p and the 3’UTR of the indicated genes. [score:1]
Strikingly, EC-CR-cell tumor growth recurred after the cessation of treatment with the miR-455-3p antagomir, despite continued CDDP treatment (Fig. 3c). [score:1]
We found that miR-455-3p played essential roles in ESCC chemoresistance and tumorigenesis. [score:1]
To establish the contribution of miR-455-3p, antagomir-455-3p treatment was stopped on Day 34, but CDDP treatment was continued (right). [score:1]
Cells were co -transfected with a plasmid that encodes HA-Ago1 and miR-455-3p (100 nM), followed by HA-Ago1 IP using an anti-HA antibody. [score:1]
miR-455-3p Chemoresistance Esophageal squamous cell carcinoma OncomiR Over the last two decades, accumulating evidence has implicated a minority population of cells within tumors, termed cancer stem cells (CSCs) or tumor-initiating cells (T-ICs), in cancer recurrence, metastasis, and conventional therapy resistance, which are the critical determinants of prognosis in human cancers [1– 4]. [score:1]
Furthermore, RIP assays indicated that miR-455-3p was associated with different negative regulators of the Wnt/β-catenin and TGF-β/Smad pathways in gastric and kidney cancer cells (Fig. 6c). [score:1]
Furthermore, we demonstrated that miR-455-3p plays essential roles in ESCC chemoresistance and tumorigenesis, and that treatment with a miR-455-3p antagomir chemosensitizes ESCC cells and reduces ESCC T-ICs subpopulations. [score:1]
Silencing miR-455-3p chemosensitizes ESCC cells and reduces stem cell-like traits of ESCC. [score:1]
GSEA analysis of TCGA datasets indicating that miR-455-3p levels are correlated with the gene signatures of the Wnt/β-catenin and TGF-β/Smad pathways in gastric and lung cancers. [score:1]
Treatment with a miR-455-3p antagomir dramatically chemosensitized ESCC cells and reduced the subpopulations of CD90 [+] and CD271 [+] T-ICs via deactivation of multiple stemness -associated pathways, including Wnt/β-catenin and TGF-β signaling. [score:1]
miRNA-455-3p activates the Wnt/β-catenin and TGF-β/Smad pathways. [score:1]
Silencing microRNA-455-3p chemosensitizes and reduces tumorigenesis of patient-derived esophageal squamous cell carcinoma cells. [score:1]
These results demonstrate that silencing miR-455-3p causes the chemosensitization of ESCC cells. [score:1]
Fig. 6Aberrant miR-455-3p contributes to the progression of various cancers. [score:1]
[1 to 20 of 75 sentences]
3
[+] score: 197
Other miRNAs from this paper: mmu-mir-122, hsa-mir-122, mmu-mir-455
Based on current findings, we cautiously propose that the upregulation of miR-455-3p—may be a compensatory to the amyloid beta toxicity in disease process. [score:6]
Expression of miR-455-3p was found to be significantly upregulated in AD serum samples,, AD mouse mo del, and AD cell lines (Kumar et al., 2017). [score:6]
miR-455-3p expression is upregulated in different AD mo dels and sources. [score:6]
Up-regulation of miR-455-5p by the TGF-β-SMAD signalling axis promotes the proliferation of oral squamous cancer cells by targeting UBE2B. [score:6]
To understand the roles of miR-455-3p in AD, expression of these genes needs to be studied by using miR-455-3p modulation approaches (mimics/inhibitors). [score:5]
MicroRNA-455-3p functions as a tumor suppressor by targeting eIF4E in prostate cancer. [score:4]
However, we don't know the exact reason for the upregulation of miR-455-3p in AD brains and further, we still do not know molecular mechanism(s) of its increased levels. [score:4]
However, we need further research to understand the nature of miR-455-3p upregulation, not only serum but also in affected tissues from AD patients and AD cell and mouse mo dels. [score:4]
MicroRNA-455 suppresses non-small cell lung cancer through targeting ZEB1. [score:4]
Upregulation of miR-455-3p in different cell and mouse mo dels of AD proven its biomarker potential for AD. [score:4]
We found miR-455-3p levels were upregulated in the fibroblasts and B-lymphocytes from AD patients relative to healthy control subjects. [score:4]
In this direction, next phase of our study is to determine the effect of miR-455-3p on its AD related target genes. [score:4]
Hence, upregulation of miR-455-3p in AD may be a “good” or “bad” signal for the cells. [score:4]
Up regulation of miR-455-3p expression in AD. [score:4]
To determine the diagnostic performance of miR-455-3p expression in AD patients, ROC curve was plotted using (ΔCT) values of miR-455-3p in AD patients and healthy controls. [score:3]
Interaction of miR-455-3p at these sites will influence the expression level of APP genes. [score:3]
Total RNA was extracted from the postmortem brains of healthy controls (n = 15) and AD patients (n = 27) and expression of hsa-miR-455-3p was quantified by real-time RT-PCR analysis. [score:3]
Alteration of miR-455-3p expression in AD cell lines indicates the strong molecular association of miR-455-3p with AD progression. [score:3]
showed a negative correlation r = −0.146 (with 95% confidence interval: −0.498 to 0.247; P = 0.466) between brains postmortem interval and miR-455-3p expression level (Figure 3A). [score:3]
As shown in Figures 3C,D, donors' age for fibroblasts (r = −0.396, 95% confidence interval: −0.821 to 0.310; P = 0.256), and B-lymphocytes (r = 0.235, 95% confidence interval: −0.391 to 0.713; P = 0.461), we did not find statistical significance, between donors age with miR-455-3p levels for fibroblasts and B-lymphocytes, indicating that donors age do not affect miR-455-3p expression levels. [score:3]
Our previous study reported the higher expression of miR-455-3p in patients with AD and other AD sources. [score:3]
We analyzed miR-455-3p expression levels in relation to (1) postmortem interval, (2) AD patients' age, and also (3) donors' age of fibroblasts, and (4) B-lymphocytes using Pearson correlation coefficients (r). [score:3]
Correlation of miR-455-3p expression with patients' demographic data. [score:3]
Figure 3Scattered plot diagrams showing the Pearson correlation coefficient (r) values of miR-455-3p expression with (A) autolysis time (B) Age of (C) Age of AD fibroblast cells and (D) Age of. [score:3]
MicroRNA-455 regulates migration and invasion of human hepatocellular carcinoma by targeting Runx2. [score:3]
Our study was the first to reveal the higher expression level of miR-455-3p in persons with AD. [score:3]
MiR-455-3p target genes were analyzed using various on-line miRNA algorithms (diana-microt, microrna. [score:3]
Each algorithm was run for miR-455-3p and validated/predictive target genes were analyzed. [score:3]
However, exact molecular link between miR-455-3p, AD, and target genes needs to be determined. [score:3]
Similarly, expression of miR-455-3p was quantified in the skin fibroblast cells generated form familial AD patients (n = 4), sporadic AD patients (n = 6), and healthy control subjects (n = 8). [score:3]
Current focus of our laboratory is to understand the role of miR-455-3p in APP processing and amyloid beta modulation, using miR-455-3p mimics and inhibitor treatments. [score:3]
Similarly, in B-lymphocytes, miR-455-3p level was significantly upregulated in sporadic AD cases compared to controls (P = 0.044). [score:3]
S. No Representative miRNA Ortholog of target gene Representative transcript Gene name 3P-seq tags + 5 Conserved sites total Cumulative weighted context++ score Total context++ score Aggregate PCT 1 hsa-miR-455-3p. [score:3]
Expression of miR-455-3p was quantified and its diagnostic potential was examined in different sources. [score:3]
ROC curve was analyzed for miR-455-3p expression in fibroblast cells form familial and sporadic AD patients vs. [score:3]
Figure 1Expression of hsa-miR-455-3p in AD patients. [score:3]
In-silico analysis for miR-455-3pMiR-455-3p target genes were analyzed using various on-line miRNA algorithms (diana-microt, microrna. [score:3]
Interestingly, fold-change analysis indicated the significantly higher expression of miR-455-3p in AD patients. [score:3]
Simultaneously, miR-455-3p target several key genes those are involved in the AD. [score:3]
MiR-455-5p acts as a novel tumor suppressor in gastric cancer by down -regulating RAB18. [score:3]
InROC curve was analyzed for miR-455-3p expression in fibroblast cells form familial and sporadic AD patients vs. [score:3]
MicroRNA-455-3p as a potential peripheral biomarker for Alzheimer's disease. [score:2]
MiR-455 has been implicated in various human diseases specially cancer and chondrogenesis (Chen et al., 2016). [score:2]
MicroRNA-455 (MiR-455) is identified as a member of broadly conserved family non-coding RNA and expressed in most of the phylum such as Eukaryota, Metazoa, Chordata, Craniata, Vertebrata, Euteleostomi; Mammalia, and Primates etc. [score:2]
MicroRNA-455-3p inhibits tumor cell proliferation and induces apoptosis in HCT116 human colon cancer cells. [score:2]
Figure 4 Schematic representation of miR-455-3p roles in AD pathogenesis. [score:1]
miR-455-3p having at least one or two binding site at 3′UTR of the genes and total context [++] score ranges from −0.1 to −0.46. [score:1]
However, in neurodegenerative diseases, role of miR-455-3p is barely investigated. [score:1]
Our current study on AD postmortem findings revealed that miR-455-3p levels are significantly increased in a large number (n = 27) of AD brains and a significant AUC value also strengthen its biomarker potential. [score:1]
These observations strongly suggest that miR-455-3p is a potential biomarker for sporadic AD. [score:1]
We also predict that two potential binding sites of miR-455-3p at the 3′UTR of APP gene may be involved in the modulation of full-length APP. [score:1]
Current findings is the continuation of our past study to elaborate the biomarker potential of miR-455-3p in more details. [score:1]
For e. g., miR-455-3p binds at the two sequence sites of 3′ UTR of APP gene at sequence position 522–528 and 3,139–3,145. [score:1]
A total of 323 predicted transcripts/human genes were identified with conserved miR-455-3p. [score:1]
Further, we also predict that miR-455-3p affects the APP processing and amyloid beta production. [score:1]
Many other reports identified the role of miR-455-3p in several cancers and chondrogenic differentiation (Chen et al., 2016; Cheng et al., 2016; Li et al., 2016; Liu et al., 2016; Qin et al., 2016; Zheng et al., 2016; Zhao et al., 2017). [score:1]
However, data from postmortem AD brains and cells showed significant ROC curve data further confirmed that the miR-455-3p as a valuable molecule capable of discriminating the patients with AD from healthy individuals. [score:1]
One of the most suitable identified candidate in our study was microRNA-455-3p. [score:1]
The curve was plotted based on the ΔCT value of miR-455-3p in AD patients and control samples. [score:1]
As mentioned above, our recent lab study on AD serum samples and other AD sources/AD mouse mo del unveiled the miR-455-3p as potential biomarker candidate for AD (Kumar et al., 2017; Figure 4). [score:1]
1 and hsa-miR-455-3p. [score:1]
Hence, results obtained from, AD fibroblast, and AD B-lymphocyte were conclusively confirmed the decisive role of miR-455-3p in AD assessment. [score:1]
Whereas a positive correlation r = 0.355 (with 95% confidence interval: −0.029 to 0.647; P = 0.069) was observed between the age of and miR-455-3p level (Figure 3B). [score:1]
MicroRNA-455-3p modulates cartilage development and degeneration through modification of histone H3 acetylation. [score:1]
In-silico analysis for miR-455-3p function in AD In-silico analysis was performed to understand the functions of miR-455-3p and its possible role in AD pathogenesis. [score:1]
In order to expose the roles and functions of miR-455-3p in AD, in-silico analysis provides the valuable information. [score:1]
In-silico analysis for miR-455-3p. [score:1]
Hence, these analyses indicated the possible way the miR-455-3p involved in AD pathogenesis. [score:1]
InSimilarly ROC curve for miR-455-3p was analyzed in B-lymphocytes of AD patients. [score:1]
Both cell types showed the significantly higher levels of miR-455-3p, especially in sporadic AD cases but not in familial AD. [score:1]
Thus, results showed a trend of reduced levels of miR-455-3p with increased postmortem interval and increased trend of miR-455-3p with patients' age. [score:1]
In-silico analysis for miR-455-3p function in AD. [score:1]
Similarly ROC curve for miR-455-3p was analyzed in B-lymphocytes of AD patients. [score:1]
Analysis showed the variations in miR-455-3p level among these groups, however significant difference (P = 0.044) in (–ΔCT) value was reported between sporadic AD cases (−13.98 ± 0.73) and controls (−15.50 ± 0.80; Figure 1C). [score:1]
Further, we checked the level of miR-455-3p in B-lymphocytes obtained from familial AD patients (n = 6), sporadic AD patients (n = 6), and healthy controls (n = 10). [score:1]
Analysis showed the significant area under ROC curve (AUROC) value of miR-455-3p (AUROC = 0.792) with the 95% confidence interval was 0.637–0.948 (P = 0.0018). [score:1]
As per miRbase database, a total of 3,102 reads of miR-455-3p has been detected by deep sequencing in 62 experiments (www. [score:1]
The reaction was set in the 7900HT Fast Real Time PCR System (Applied Biosystems, USA) using following reaction conditions: initial denaturation at 95°C for 5 min, denaturation at 95°C for 10 s, annealing at 60°C for 15 s, and extension at 72°C for 25 s. The relative levels of miR-455-3p in the AD patients vs. [score:1]
Further, in-silico analysis was performed to understand the roles and downstream application of miR-455-3p in AD. [score:1]
Thus, analysis showed that ROC analysis of miR-455-3p in B-lymphocytes was not significant. [score:1]
Figure 2ROC curve analysis of hsa-miR-455-3p in (A), (B) AD fibroblast cell lines, and in (C) B-lymphocytes cells from AD patients. [score:1]
In-silico analysis was performed to understand the functions of miR-455-3p and its possible role in AD pathogenesis. [score:1]
Role of miR-455 has been identified in Human Colon Cancer (Zheng et al., 2016), prostate cancer (Zhao et al., 2017), hepatocellular carcinoma (Qin et al., 2016), gastric cancer (Liu et al., 2016), oral squamous cancer cells (Cheng et al., 2016), and non-small cell lung cancer (Li et al., 2016). [score:1]
Beside brain tissues, we also investigated the and B-lymphocytes for miR-455-3p expression. [score:1]
Details about predictive and validated transcripts were obtained by searching hsa-miR-455-3p. [score:1]
Further, high level of miR-455-3p in and lymphoblasts indicate that increased levels of miR-455-3p is a typical feature of AD—both in the brain and peripheral cells. [score:1]
Findings from this study, will provide the valuable information about miR-455-3p role in AD and in search of pre-clinical biomarker for early AD detection. [score:1]
Therefore, current findings together with our recently published study in Human Molecular Genetics (Kumar et al., 2017), strongly suggest that miR-455-3p as a potential biomarker and a possible therapeutic candidate for AD. [score:1]
[1 to 20 of 88 sentences]
4
[+] score: 172
Other miRNAs from this paper: hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-141, hsa-mir-200a
These results suggest that expression of miR-455 targets and downregulates Cul3, causing Nrf2 protein stabilization. [score:8]
If miR-455 expression targets Cul3 to induce Nrf2 accumulation, Cul3 knockdown should also stabilize Nrf2. [score:6]
Notably, Cul3 downregulation (Figure 5B and 5C) and Nrf2 protein stabilization (Figure 5C) were observed in cells expressing miR-455 or. [score:6]
Cul3 knockdown by expressing miR-455 or targeted-shRNA protects hFOB1. [score:6]
Moreover, Cul3 protein was also downregulated in miR-455 -expressing cells (Figure 1D). [score:6]
19 cells, expressing Cul3 -expressing Vector [“Vec (1)”], or miR-455 anti-sense (“Anti-miR-455”) as well as the parental control cells (“PAR”) were treated with/out H [2]O [2] (250 μM) for 24 hours. [score:5]
The results above demonstrated that Cul3 depletion, by expressing miR-455 or targeted-shRNA, caused Nrf2 protein stabilization in hFOB1. [score:5]
Remarkably, Cul3 silencing by miR-455 expression or targeted-shRNA protected human osteoblasts from H [2]O [2]. [score:5]
More importantly, H [2]O [2] (250 μM) -induced cell death (Figure 5E) and apoptosis (Figure 5F) were largely inhibited in the primary cells expressing miR-455 or. [score:5]
Thus, we imply that Cul3 silence, by expressing miR-455 or targeted-shRNA, protects primary human osteoblasts from H [2]O [2]. [score:5]
19 cells from H [2]O [2]The results above demonstrated that Cul3 depletion, by expressing miR-455 or targeted-shRNA, caused Nrf2 protein stabilization in hFOB1. [score:5]
Remarkably, miR-455 expression dramatically decreased Cul3 mRNA expression in hFOB1. [score:5]
19 cells expressing Anti-miR-455 (Figure 3) and Cul3 -expressing construct (Figure 4A-4D), we then tested H [2]O [2] sensitivity in these cells. [score:5]
miR-455 anti-sense induces Cul3 upregulation and Nrf2 degradation. [score:4]
On the other hand, miR-455 depletion by miR-455 anti-sense led to Cul3 upregulation and Nrf2 protein degradation, which then exacerbated H [2]O [2] damages in human osteoblasts. [score:4]
Therefore, Anti-miR-455 depleted miR-455, causing Cul3 upregulation and Nrf2 degradation in hFOB1. [score:4]
19 cells (puromycin-selected), expressing miRNA-455 Vector [two lines, “Vec (1)/(2)”], microRNA-control (“miRC”) or the (“shCul3”), as well as the parental control hFOB1. [score:3]
miR-455 anti-sense expression. [score:3]
19 cell viability loss (MTT OD reduction, Figure 2C), cell death (Trypan blue increase, Figure 2D) and apoptosis (Histone DNA ELISA OD increase, Figure 2E) were also dramatically attenuated after expressing miR-455 or. [score:3]
Here, we identified microRNA-455 (miR-455) as a putative Cul3 -targeting miRNA. [score:3]
As shown in Figure 1B, miR-455 (-3p) expression level was significantly increased in the stable cells. [score:3]
Expressions of miR-455 and Cul3 in human osteoporosis and osteonecrosis tissues should also be tested in future studies. [score:3]
These results further confirm that miR-455 selectively targets Cul3 in hFOB1. [score:3]
Our results here demonstrated that miR-455 is a Cul3 -targeting miR in human osteoblasts. [score:3]
19 cells, mRNA expressions of NQO1, HO1 and GCLC were significantly increased in cells with miR-455 or (Figure 2A). [score:3]
miR-455 expression silences Cul3, causing Nrf2 protein stabilization in human osteoblastic cells. [score:3]
Primary-cultured human osteoblasts were constructed with miR-455 -expressing vector [“Vec (1)”] or the. [score:3]
19 osteoblastic cells (puromycin-selected), expressing miRNA-455 Vector [two lines, “Vec (1)/(2)”], microRNA-control (“miRC”) or the (“shCul3”), as well as the parental control hFOB1. [score:3]
Forced -expression of miR-455. [score:3]
miR-455 (-3p) level was only increased in cells expressing miR-455 vector, but not (Figure 5A). [score:3]
To further confirm that miR-455 selectively targets Cul3, the miR-455 anti-sense (“Anti-miR-455”) was introduced to hFOB1. [score:3]
Thereafter, a miR-455 -expressing vector (pSuper-GFP-puro) was constructed (See Method), which was introduced to hFOB1. [score:3]
Notably, Keap1 protein (Figure 1D) and mRNA (Figure 1F) were unchanged after miR-455 expression. [score:3]
These results together indicate that miR-455 expression could be a novel strategy to provoke Nrf2-ARE signaling activation in human osteoblasts. [score:3]
More importantly, forced -expression of miR-455 activated Nrf2 signaling possibly via silencing Cul3, which protected human osteoblasts from H [2]O [2]. [score:3]
Moreover, H [2]O [2] -induced ROS production was largely attenuated by either miR-455 expression or in hFOB1. [score:3]
miR-455 (3p) targets the 3-UTR of Cul3 mRNA at position 28-34 (A). [score:3]
The miR-455 precursor was purchased from RiboBio (Guangzhou, China), which was inserted to the pSuper-GFP-puro vector (Ambion, Shanghai, China) to establish the miR-455 -expression vector. [score:3]
miR-455 (3p) expression was always verified by the qRT-PCR assay. [score:2]
Expression of miR-455 in the stable cells was examined by qRT-PCR assay. [score:2]
As compared to the parental control cells (“PAR”), H [2]O [2] (250 μM) -induced cell death (Figure 4E) and apoptosis (Figure 4F) were dramatically exacerbated in cells expressing Anti-miR-455 or Cul3 vector. [score:2]
miR-455 (-3p) expression was tested via the TaqMan microRNA assay [52] (Applied Biosystems, Shanghai, China), from 5 ng of total RNA [53]. [score:2]
Figure 5miR-455 -induced Cul3 silence protects primary human osteoblasts from H [2]O [2]Puromycin-selected stable primary human osteoblasts, expressing miRNA-455 Vector [“Vec (1)”] or the (“shCul3”), as well as the parental control cells (“PAR”) were subjected to qRT-PCR assay (A, B and D) and (C) of listed microRNA or genes. [score:2]
Puromycin-selected stable primary human osteoblasts, expressing miRNA-455 Vector [“Vec (1)”] or the (“shCul3”), as well as the parental control cells (“PAR”) were subjected to qRT-PCR assay (A, B and D) and (C) of listed microRNA or genes. [score:2]
miR-455 -induced Cul3 silence protects primary human osteoblasts from H [2]O [2]. [score:1]
miR-455 -induced Cul3 silence protects primary human osteoblasts from H [2]O [2]The results above indicated that Cul3 silence could protect hFOB1. [score:1]
We discovered that miR-455 (“-3p. [score:1]
As shown in Figure 3A, Anti-miR-455 indeed depleted miR-455 in hFOB1. [score:1]
Together, our results suggest that miR-455 activates Nrf2 signaling via silencing Cul3, and protects human osteoblasts from oxidative stress. [score:1]
19 osteoblasticcells were transfected with 20 nM of miR-455 anti-sense (“Anti-miR-455”, Ambion, Shanghai, China) by Lipofectamine 2000 (Invitrogen). [score:1]
After two days, cells were split and were transfected with Anti-miR-455 again. [score:1]
19 cell lines with the construct, namely miR-455 Vec (1)/(2), were established. [score:1]
Human osteoblasts were transfected with the miR-455 construct or the scramble non-sense microRNA control (“miRC”, Genepharm, Shanghai, China) using the Lipofectamine 2000 reagent (Invitrogen). [score:1]
It will also be interesting to test the in vivo function of miR-455 against oxidative-damaged human osteoblasts. [score:1]
[1 to 20 of 54 sentences]
5
[+] score: 111
Other miRNAs from this paper: hsa-mir-210, hsa-mir-526b, hsa-mir-518b, hsa-mir-517a
48, 49, 50, 51 Whereas physiological target mRNAs of miR455-5P remain unknown, we have identified MUC1 mRNA as a bona fide miR455-3P target. [score:5]
To identify potential miR455 target mRNAs, we employed the miRNA target prediction software miRecords. [score:5]
Importantly, the reduced miR455 expression in PE samples is unlikely to be simply a consequence of low oxygen tension, because cultivation of BeWo cells under hypoxic conditions did not cause a significant change in miR455 expression (data not shown). [score:5]
In conclusion, PE patients display activated HIF2A -mediated hypoxia signaling in placenta, which may be caused by deregulated expression of miR455-3P. [score:4]
In conclusion, although the idea that reduced expression of miR455 is causally linked to the development of PE is intriguing, further experimental evidence to support this mo del is awaited. [score:4]
We observed RL/FL activity ratios that were not significantly different in control- and FSK -treated cells, demonstrating that luciferase activity is not affected by the syncytialization process or by FSK treatment per se, in the absence of an miR455 target sequence (Figure 3b). [score:3]
Whereas expression of miRNAs from the placenta-specific C19MC was not affected, miR455 miRNA levels were significantly lower in placenta from PE than control patients. [score:3]
Therefore, miR455 expression per se may already be irregular, early in the pregnancy of PE patients and thus contribute to pathogenesis. [score:3]
However, RL activity was significantly reduced by FSK treatment when the RL reporter was fused to a fully complementary miR455-3P target sequence (Figure 3c). [score:3]
Therefore, although increased precursor processing or miRNA stability cannot be ruled out, the observed elevation in mature miR455 upon FSK treatment of BeWo cells can be attributed to increased expression of the COL27A1 gene. [score:3]
Similarly, RL fused to a complementary miR455-5P target sequence was repressed upon FSK treatment (Figure 3d). [score:3]
In summary, the mature miRNAs miR455-3P and miR455-5P are expressed in human placenta. [score:3]
Importantly, we observed a very similar expression profile for the pri-miR455 precursor transcript upon FSK treatment, though not as high as the maximal level of the COL27A1 mRNA (Figure 1h). [score:3]
miR455 is differentially expressed during syncytialization. [score:3]
These results demonstrate that treatment of BeWo cells with FSK stimulates the expression of the COL27A1 gene and thus leads to increased production of pri-miR455. [score:3]
[39] Compiling lists of potential targets for miR455-3P and -5P, we noted at least eight genes that have been linked to hypoxia signaling (Figure 3a). [score:3]
MUC1 mRNA is a physiological target of miR455-3P. [score:3]
Thus, the two miR455 miRNAs are likely to be implicated in regulatory circuits that are important for placenta development and physiology. [score:3]
Thus, we conclude that MUC1 mRNA is a bona fide miR455-3P target that is strongly repressed during FSK -induced syncytialization of BeWo cells. [score:3]
[53] Our finding that miR455-3P causes a decrease in HIF2A protein levels indirectly by repressing MUC1 mRNA (Figure 5a) strongly suggests that miR455-3P may contribute to such buffering. [score:2]
To validate this observation, we assessed miR455-3P and miR455-5P expression by qRT-PCR using validated TaqMan assays. [score:2]
Corroborating our results, it has been shown recently that MUC1 is also regulated by miR455-3P in lung cells. [score:2]
To test whether miR455-3P and miR455-5P are part of functional miRISC and to verify predicted miR455 targets, we adopted a dual luciferase -based miRNA-activity reporter assay. [score:2]
Because miR455-3P and miR455-5P are relatively abundant in both BeWo cells and placenta samples, they might have an important role in regulating pathways relevant to placenta physiology. [score:2]
Because MUC1 is repressed by miR455-3P, miR210 levels are thus kept in check indirectly by miR455-3P (Figure 5c). [score:2]
Deregulation of miR455 in placentas from PE patients. [score:2]
Little is known about the possible regulatory activities of miR455. [score:2]
[32] To investigate whether miR455 is expressed in placenta and potentially misregulated in PE, we collected placenta samples from 15 PE cases and 14 healthy donor controls. [score:2]
To validate the predicted miR455-3P and -5P target mRNAs, we first performed dual luciferase miRNA reporter assays in BeWo cells. [score:2]
26, 27, 28, 29, 30, 36, 37 In contrast, miR455-3P and miR455-5P levels were significantly lower in PE than in control samples (Figure 2f). [score:1]
Importantly, we also detected miR455-3P and miR455-5P, which were both more abundant than U6 snRNA and miR210 in the control RNA samples (Figure 2c). [score:1]
Unlike most other miRNAs, the pre-miR455 hairpin produces two mature miRNAs, miR455-3P and miR455-5P. [score:1]
These results validate the predicted miR455-5P binding sites in the 3′UTR of ARNT and the miR455-3P binding sites in the 3′UTR of EGLN2, MUC1, and FIH1. [score:1]
[46] Notably, the presence of miR455-3P has been suggested in circulating blood. [score:1]
Prospective tests assessing miR210/miR455-3P and miR210/miR455-5P ratios may predict PE with high specificity (Supplementary Figure 5). [score:1]
The above results are consistent with the miR210 and miR455 levels that we found to be negatively correlated in placenta samples from PE and control patients (Figures 2e and f) and suggest that MUC1 and HIF2A levels are higher in PE than in control samples. [score:1]
We fused the complete 3′UTRs of the predicted mRNAs to the RL reporter and tested miR455 -mediated repression in FSK versus control conditions (Figure 3a). [score:1]
miR455 miRNAs are part of functional miRISC. [score:1]
48 h after FSK treatment, concomitant with a decline in pri-miR455 (Figure 1h). [score:1]
In contrast to the RL reporter fused to a fully complementary miR455 binding site (Figures 3c and d), FSK treatment did not result in significant repression of RL when fused to the 3′ UTR of either CUL3, EID1, SIRT1, or STEAP3 (Figures 3e and f). [score:1]
To confirm miR455-3P -mediated MUC1 mRNA repression independently of FSK treatment, we transfected BeWo cells with synthetic miR455 miRNAs. [score:1]
miR455-3P constrains HIF2A -mediated hypoxia signaling. [score:1]
As expected, MUC1 mRNA and protein levels were reduced by transfection of synthetic miR455-3P but not miR455-5P (Figures 3c and d). [score:1]
To test whether the endogenous EGLN2, MUC1, FIH1, and ARNT mRNAs are under negative control by the miR455 miRNAs, we assessed mRNA and protein levels by qRT-PCR and western blotting, respectively. [score:1]
However, elevated levels of the miRNAs miR455-3P and miR455-5P were observed consistently in FSK -treated cells. [score:1]
Besides miR210, we have identified miR455 as a further prognostic miRNA. [score:1]
Furthermore, increase in mature miR455-3P and miR455-5P miRNAs occurred later than the pri-miR455 precursor transcript. [score:1]
Importantly, in contrast to elevated miR210 levels, miR455-3P and miR455-5P levels were significantly lower in PE placenta than in controls. [score:1]
Thus, it is possible that miR455-3P acts as a rheostat restraining a hypoxia response that could otherwise prevent CT to SCT differentiation. [score:1]
We observed a maximal increase in mature miR455 ca. [score:1]
Consistent with the small RNA sequencing data, miR455-3P and miR455-5P levels were enhanced ca. [score:1]
The mature miR455-3P and miR455-5P miRNAs both derive from a pre-miRNA hairpin encoded in intron 10 of the collagen gene COL27A1 (Figure 1g and Supplementary Figure 2). [score:1]
The vector was digested using Asc1/Not1 enzymes and ciped (except for vectors containing perfect complementary sequences for miR455-3P and -5P). [score:1]
For control vectors, oligonucleotides containing perfect complementary sequences for miR455-3P or -5P (Supplementary Table S2) were annealed and ligated to unciped digested vector. [score:1]
Nonetheless, we believe that efforts to develop diagnostics using miRNAs as biomarkers to predict PE should be pursued, irrespective of further mechanistic insight into miR455 function. [score:1]
[1 to 20 of 55 sentences]
6
[+] score: 106
Other miRNAs from this paper: hsa-mir-21, hsa-mir-145
miR-455 directly targeted HDAC2 and its overexpression suppressed cell proliferation and induced cell apoptosis in CRC cells through HDAC2 repression. [score:8]
The data suggested that miR-455 overexpression inhibited HDAC2 expression. [score:7]
Ectopic expression of miR-455 inhibited cell proliferation and induced cell apoptosis of HCT116 cells. [score:5]
Therefore, we drew a conclusion that ectopic expression of miR-455 inhibited cell proliferation while inducing cell apoptosis of HCT116 cells. [score:5]
Ectopic expression of miR-455 reduced the expression of HDAC2 in HCT116 cells. [score:5]
The subsequent experiments on protein expression level of HDAC2 in HCT116 cells transfected with miR-NC or miR-455 mimics verified the effective repression of miR-455 on HDAC2 expression. [score:5]
miR-455, which locates at the protein-coding gene Col27a1, has been reported to be involved in early chondrogenic differentiation regulation (30), down-regulation of MMP-9 during exercise (31), hypoxia signaling (32) and acquired temozolomide resistance in glioblastoma cells (33). [score:5]
Also, the cell proliferation and apoptosis assays performed in cells transfected with miR-NC or miR-455 mimics successfully corroborated that the repression of HDAC2 expression induced by miR-455 obviously inhibited cell proliferation while promoted cell apoptosis in HCT116 cells. [score:4]
miR-455 directly targeted HDAC2 in HCT116 cells. [score:4]
Figure 3. miR-455 directly targeted HDAC2 in HCT116 cells. [score:4]
miR-455 reduced the expression of HDAC2. [score:3]
As of now, there is only one report that demonstrated the implication of miR-455 in cell proliferation and invasion of CRC cells by targeting RAF proto-oncogene serine/threonine-protein kinase (34). [score:3]
In other words, miR-455 could effectively repress cell proliferation while inducing cell apoptosis via targeting HDAC2. [score:3]
Figure 4. miR-455 reduced the expression of HDAC2. [score:3]
Figure 5. miR-455 inhibited proliferation and induced apoptosis of HCT116 cells. [score:3]
Finally, miR-455 was proved to effectively inhibit cell proliferation while inducing cell apoptosis in CRC cells. [score:3]
miR-455 inhibited proliferation and induced apoptosis of HCT116 cells. [score:3]
The protein expression level of HDAC2 was obviously reduced by transfection of miR-455 mimics in comparison with cells transfected with miR-NC (P<0.01, Figure 4A and B). [score:3]
The present study not only expanded the knowledge of miR-455 but also provided a novel therapeutic target for CRC. [score:3]
Screened by ScanTarget, miR-455 was predicted to bind to 3′UTR of HDAC2 (Figure 3A). [score:3]
HDAC2: histone deacetylase 2; 3′UTR: 3′-untranslated region; miR-455 mimics: microRNA-455 mimics; miR-NC: negative control of miR-455. [score:3]
Our observations suggested that miR-455 suppressed the oncogenic function of HDAC2 in human CRC. [score:3]
After prediction by TargetScan, the 3′UTR fragment of HDAC2 binds to miR-455. [score:3]
HDAC2 was validated as a target gene of miR-455 by luciferase assay in HCT116 cells co -transfected with HDAC2 3′UTR and miR-455 mimics or miR-NC. [score:2]
Screened by TargetScan, miR-455 was predicted to bind to 3′UTR of HDAC2 and the prediction was further confirmed by luciferase assay. [score:2]
By bioinformatics methods, we found the miR-455 might specifically bind to 3′UTR of HDAC2 gene. [score:1]
Besides, miR-455 might be practicable for treatment of CRC. [score:1]
HDAC2: histone deacetylase 2; miR-455 mimics: microRNA-455 mimics; miR-NC: negative control of miR-455. [score:1]
B, Luciferase activity of cells co -transfected with pmirGLO vector containing 3′UTR segment of the HDAC2 and miR-NC or miR-455 mimics. [score:1]
When the cells reached 70% confluence, 100 pmol of miR-455 mimics or its negative control (miR-NC; both from Genepharma) was added to each well accompanied by Lipofectamine 2000 (Invitrogen, USA). [score:1]
Thus, the 3′UTR segment of the HDAC2 gene, containing putative binding site for miR-455, was inserted into pmirGLO vector (Promega). [score:1]
miR-NC and miR-455 mimics were respectively transfected into HCT116 cells, followed by western blot analysis. [score:1]
A, Diagram showing miR-455 formed base-pair with the 3′ UTR of HDAC2. [score:1]
MTT: 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide; HDAC2: histone deacetylase 2; miR-455 mimics: microRNA-455 mimics; miR-NC: negative control of miR-455. [score:1]
After sequencing, the vector containing 3′UTR of HDAC2 was co -transfected with miR-455 mimics or miR-NC. [score:1]
Therefore, the study on associations between miR-455 and CRC might contribute to expand the current knowledge of miR-455. [score:1]
[1 to 20 of 36 sentences]
7
[+] score: 75
We showed that MAPK1 (ERK2, a potential target of miR-143), MAPK8 (JNK1, a demonstrated target of miR-455-3p), MAPK9 (JNK2, a demonstrated target of miR-17, miR-20b, and miR-106a), and p21 and RB (potential targets of miR-17 and miR-106a) were strongly upregulated at protein level upon inhibition of the miRNAs. [score:14]
Because the expression of the miR-17 family is directly controlled by the proto-oncogene MYC [32]– [34] and because we have recently demonstrated (7) that in human keratinocytes lacking p63, MYC expression is down regulated, the down-regulation of miR-17, miR-20, miR-106a, miR-143 and miR-455-3p genes we observed in keratinocytes lacking p63 could be due to MYC down-regulation. [score:13]
0045761.g005 Figure 5(A, B) Quantification of the expression of early differentiation markers K1 and K10 in double knockdowns of miR-143 and of its targets (A) and of miR-455-3p and its targets (B). [score:8]
Efficient knockdown of miR-455-3p was first verified (Figure 3E) and MAPK8 was up-regulated at protein level (1.96-fold) upon miR-455-3p silencing (Figure 3F) suggesting that MAPK8 could be a direct target of miR-455-3p. [score:8]
MiR-455-3p is also under the regulation of p63 but act only on MAPK signaling and keratinocyte differentiation through the inhibition of its direct target MAPK8 (JNK1). [score:6]
We further confirmed that it was indeed the case with a luciferase::MAPK8 3′UTR reporter construct, since a LNA inhibitor of miR-455-3p increased luciferase activity (Figure 3G), while a miR-455-3p mimic strongly inhibited the reporter activity (Figure S1A). [score:5]
The following miRNA inhibitors (LNA) were obtained from Exiqon: hsa-miR-143 (138515-00), hsa-miR-455-3p (138667-00), hsa-miR-30a (138468-00), hsa-miR-17 (138461-00), hsa-miR-20b (138221-00), hsa-miR-106a (138477-00), and hsa-miR-18 (138462-00), and scramble miR (199002-04) was used as a negative control. [score:3]
Based on their level of expression in human primary keratinocytes in culture (data not shown) and their biological relevance, we chose several potential candidates from our list: miR-17, miR-18a, miR-20b, miR-30a, miR-106a, miR-143 and miR-455-3p. [score:3]
Among the putative in silico targets of miR-455-3p, we also identified MAPKs, and we focused on this signaling cascade by selecting MAPK8. [score:3]
Controls for miR-455-3p inhibition are in figure 3E. [score:3]
The expression of K1 and K10 was also rescued upon silencing of both miR-455-3p and MAPK8 (Figure 5B). [score:3]
miR-143 and miR-455-3p target several MAPKs. [score:3]
In this study, we have characterized multiple miRNAs, including the mir-17 family (miR-17, miR-20b, miR-106a) and miR-30a, miR-143 and miR-455-3p, which are downregulated in p63-silenced keratinocytes, suggesting that they act downstream of p63. [score:2]
Finally hsa-miR-455-3p mirVana® mimic and hsa-miR-17 mirVana® mimic were obtained from Qiagen. [score:1]
[1 to 20 of 14 sentences]
8
[+] score: 73
Previously, miR-455 is also recognized among a set of 6 miRNAs that are deregulated in a pancreatic ductal adenocarcinoma mo del of chemoresistant and a mesenchymal phenotype [36] as well in esophageal carcinoma cell lines [37] whereas the same is also reported to be up-regulated in CRC [38], which is similar with our findings, up-regulated miR 455 was down-regulated after the radiation and SN38 treatment. [score:11]
Colorectal cancer pathway with interaction between significant up-regulated miRNAs, let-7f-5p, miR-455-3p, miR-98, miR-155-5p, and down-regulated miRNAs, miR-1, miR-127-5p, miR-142-5p, miR-202-5p after radiation and SN38 treatments and their target genes. [score:9]
Contrary result, i. e. significant down-regulation of miR-455 is also reported in colon cancer along with its possible inhibitory role in proliferation and invasion of CRC by targeting RAF proto-oncogene serine/threonine-protein kinase [39]. [score:8]
Moreover, from EBarrays, we found miRNAs, such as let-7f-5p, miR-455-3p, miR-98, miR-155-5p, up-regulated to the highest degree and miRNAs, miR-1, miR-127-5p, miR-142-5p, miR-202-5p were down-regulated most, after the radiation and SN38 treatment. [score:7]
Heatmap of four most significant up-regulated miRNA, let-7f-5p, miR-455-3p, miR-98 and miR-155-5p, as well as four most down-regulated miRNA, miR-1, miR-127-5p, miR-142-5p and miR-202-5p after radiation and SN38 treatments, and different pathways by clustering from pathway union. [score:7]
Such as, let-7f-5p and miR-455-3p and miR-98 were up-regulated most after radiation and SN38 treatment in HCT116 [p53+/+] cells, whereas miR-155-5p was up-regulated mostly in HCT116 [p53−/−] cells after radiation and in HCT116 [p53+/+] cells after SN38 treatment. [score:7]
Based on our experimental results and EBarrays statistical analysis, let-7f-5p and miR-455-3p were up-regulated more than 12 times after radiation and SN38 treatment in HCT116 [p53+/+] cells compared to untreated cells, whereas they were down-regulated in HCT116 [p53+/−] cells and marginally increased (>3 times) in HCT116 [p53−/−] cells. [score:6]
We also found in KM12C and KM12L4a cells with p53 mutation, let-7f-5p, miR-455-3p, miR-98, miR-155-5p and miRNAs were up-regulated, whereas miR-1, miR-127-5p, miR-142-5p and miR-202-5p remained undetected after the radiation and SN38 treatment. [score:5]
In summary, after radiation and SN38 treatment, we found that most significant up- or down-regulation and interactions of 8 miRNAs (let-7f-5p, miR-455-3p, miR-98, miR-155-5p, miR-1, miR-127-5p, miR-142-5p, miR-202-5p), 7 cytokines (IL-1β, IL-4, IL-6, IL-10, IFN- γ, VEGF, TNF- α) and 2 chemokines (IL-8, MIP-1-α) were dependent on p53 status in colon cancer cells. [score:4]
The results showed that let-7f-5p, miR-455-3p, miR-98 and miR-155-5p were up-regulated in KM12C (Supplementary Figure S1) and KM12L4a (Supplementary Figure S2) cell lines after radiation and SN38 treatment, whereas miR-1, miR-127-5p, miR-142-5p and miR-202-5p were undetected in KM12C and KM12L4a cell lines after radiation and SN38 treatment. [score:4]
To validate our results found in HCT116 cells, we further examined the expression of miRNAs, let-7f-5p, miR-455-3p, miR-98, miR-155-5p, miR-1, miR-127-5p, miR-142-5p and miR-202-5p in KM12C and KM12L4a human colon cancer cell lines. [score:3]
PicTar reports possible interactions of has-miR-98 with IL-8. miR-455-3p: Direct interaction of miR-455-3p with IL-1β is predicted by DIANA-microT, PITA and RNA22 servers. [score:2]
[1 to 20 of 12 sentences]
9
[+] score: 48
The results showed that 5 miRNAs (miR-130b-5p (formerly designated as miR-130b*), miR-196a, miR-455-3p, miR-455-5p, and miR-801) or 2 miRNAs (miR-133b and miR-145) were significantly up-regulated or down-regulated, respectively in laryngeal cancers (Figure 1A). [score:7]
Interestingly, recent study have reported that decreased expression of miR-455-5p was correlated with vascular invasion, poor overall survival, and poor disease-free survival in endometrial serous adenocarcinoma suggesting the potential involvement of miR-455-5p in cancer progression [44]. [score:5]
One known target of miR-455-3p is TTK (also known as MPS1) protein kinase [59] which regulates mitotic spindle formation and cell proliferation [60] [61]. [score:4]
While miR-130b-5p, miR-455-3p, miR-455-5p, and miR-801 were up-regulated in laryngeal cancer in our study, much less study has been performed on these miRNAs before. [score:4]
Significant up-regulation of miR-455-5p and miR-196a in multiple laryngeal cancer samples. [score:4]
Significant up-regulation of miR-455-5p was observed in cancers compared with NCs and benign samples. [score:3]
Furthermore, expression levels of miR-196a and miR-455-5p were significantly higher in cancer tissues when compared with neighboring controls (miR-196a, p = 0.0460; miR-455-5p, p = 0.0286) (Figure 2A), while expression level of miR-133b was significantly lower in cancer samples compared with controls (p = 0.0274) (Figure 2B). [score:3]
Significant expressional differences between matched pairs were reproduced in miR-133b, miR-455-5p, and miR-196a, among which miR-196a being the most promising cancer biomarker as validated by qRT-PCR analyses on additional 84 tissue samples. [score:3]
Up-regulated miR-455-5p may have different roles in the biology of laryngeal cancer compared with endometrial carcinoma. [score:3]
Statistically significant differences of the expression levels of miR-196a, miR-455-5p, and miR-133b were observed between matched pairs. [score:3]
miR-455-3p has been reported to be differentially expressed in smokers compared to nonsmokers [59]. [score:2]
Thus, of these 4 miRNAs, 3 miRNAs (i. e., miR-196a, miR-455-5p and miR-133b) showed significantly different expression levels in cancer tissues when compared with their matched control tissues and further quantification of miRNAs was performed using 48 laryngeal samples. [score:2]
When 48 samples were studied, the expression level of miR-455-5p was significantly higher in cancers compared with adjacent noncancerous counterparts and benign laryngeal tissues (p = 0.0113). [score:2]
miR-455-5p instead of miR-455-3p was used in further studies, because miRNAs 3p and 5p are generated from either side of the same precursor stem to have similar sequences and recent report suggested the potential involvement of miR-455-5p in cancer progression [44]. [score:1]
0071480.g003 Figure 3(A) Expression levels of miR-455-5p and miR-196a were measured by TaqMan® qRT-PCR using 48 tissue samples. [score:1]
Thus, qRT-PCR analysis was performed on residual 4 miRNAs (i. e., miR-130b-5p, miR-196a, miR-455-5p, and miR-133b). [score:1]
[1 to 20 of 16 sentences]
10
[+] score: 47
Other miRNAs from this paper: hsa-mir-34a, hsa-mir-122, rno-mir-34a, rno-mir-122, rno-mir-455
However, the expression of miR-455-3p was significantly downregulated across the entire course of TAA treatments (except 28-d with high dose). [score:6]
While the expression of rno-miR-455-3p was decreased with an increase in the dose as well as followed a downregulation with almost all the time points (excluding high dose at 28-d). [score:6]
At the bottom of this figure, the higher expression values of rno-miR-455-3p in the control compared to treated samples, as a result, this miRNA is identified as significantly downregulated with all three doses and all four time points. [score:5]
Notably, rno-miR-34a-5p and rno-miR-455-3p were detected differentially expressed following all time-points and doses compared to the control group (Fig.   6), indicating the significant relevance of the expression of both miRNAs to the treatments. [score:4]
In a previous study, miR-455-3p has been observed as significantly downregulated in poorly differentiated HCC. [score:4]
On the other hand, rno-miR-455-3p, a downregulated DEM, was observed in 11 out of 12 treatment conditions (excluding high dose at 28-d). [score:4]
Expression of miR-34a-5p, miR-455-3p and miR-122. [score:3]
Importantly, the expression levels of two DEMs (i. e., rno-miR-34a-5p and rno-miR-455-3p) were found to be changed with almost all treatment conditions. [score:3]
Our pathway enrichment analysis of miR-455-3p targets also found several relevant biological signaling pathways including pathways in cancer, focal adhesion, pancreatic cancer, glioma, basal cell carcinoma, and Mapk-, Wnt- and mTOR-signaling, suggesting alteration of liver architecture. [score:3]
In case of miR-455-3p, the nuclear alteration and cellular loci classifiers cover the maximum AUC values (Figure  S1). [score:1]
In addition to miR-34a-5p, we found miR-455-3p which can potentially be used as an early and sensitive biomarker for the detection of liver injury and pre HCC. [score:1]
On the other hand, the nuclear alteration and cellular loci classifiers out of 6 histopathological features were found to obtain the maximum AUC values for miR-455-3p (Figure  S1). [score:1]
To further evaluate the correlation between these two DEMs and cancer progression, we carried out a regression analysis between the histopathological features and the expression patterns of miR-34a-5p, and miR-455-3p during TAA exposures. [score:1]
Information on two potential early and sensitive miRNA biomarkers (miR-34a-5p and miR-455-3p) and their associated signaling is given on the top two rows. [score:1]
Notably, miR-455-3p and miR-34a-5p were involved most of the cancer-related functional pathways. [score:1]
On the other hand, rno-miR-455-3p was comparatively higher in the controls than treated samples. [score:1]
Two potential biomarkers (miR-34a-5p and miR-455-3p) out of 48 overlapping DEMs are found common across all the treatments. [score:1]
The miR-34a-5p and miR-455-3p were selected to investigate their expression changes during TAA treatments. [score:1]
[1 to 20 of 18 sentences]
11
[+] score: 37
In this cohort of animals, only two miRNAs were differentially expressed compared to the baseline: bta-miR-150 and bta-miR-455-3p, which were down-regulated 1.65 and up-regulated 68.17 fold, respectively (Table  3). [score:8]
However, consistent with the speculation above, many of the target genes proposed for miR-455-3p were cell cycle regulators and zinc-finger containing proteins, from which it can be inferred that this single miRNA was regulating multiple cell survival pathways to facilitate the final stages of clearing FMDV infection. [score:5]
Notably, bta-miR-455-3p was the highest up-regulated miRNA detected in the entire proof-of-concept study; see outlying miRNA in the far right of the volcano plot for array plate 2 (Fig.   2b). [score:4]
In strong contrast, bta-miR-455-3p was the most up-regulated miRNA in all of the data sets examined in this study. [score:4]
Since one of the cellular mechanism for combating a viral infection is the induction of apoptosis in infected cells, thereby also increasing cellular turn-over, the augmentation in bta-miR-455-3p expression may be reflective of the animal reversing those effects and shutting down those pathways now that FMDV infection has been eliminated. [score:3]
As with the bioinformatics analysis conducted to identify prospective gene targets for miR-17-5p and miR-1281, a consensus target gene for miR-455-3p was not found to further investigate (Additional file 2: Table S1). [score:3]
It would be expected that the serum miRNAs of an animal that cleared FMDV would return to a basal level similar to an uninfected animal, and consistent with that, the samples obtained from convalescent cattle exhibited only two dysregulated miRNAs: one that is immune modulatory (bta-miR-150) and one that promotes cellular proliferation (bta-miR-455-3p). [score:2]
A survey of published findings on miR-455-3p point toward it being a potent upstream regulator of multiple signaling pathways associated with induced cellular proliferation [61– 63]. [score:2]
Of the differentially regulated miRNAs, 16 (bta-miR-23b-5p, let-7 g, bta-miR-22-5p, bta-miR-1224, bta-miR-144, bta-miR-497, bta-miR-455-3p, bta-miR-154a, bta-miR-369-3p, bta-miR-26b, bta-miR-34a, bta-miR-205, bta-miR-181b, bta-miR-146a, bta-miR-17-5p, and bta-miR-31) have previously been described to play a role in cellular proliferation or apoptosis (Fig.   6b, orange circle). [score:2]
The non-clustered miRNAs included: let-7 g, bta-miR-26b, bta-miR-150, bta-miR-34a, bta-miR-146a, bta-miR-147, bta-miR-205, bta-miR-455-3p, bta-miR-1224, bta-miR-1281, and bta-miR-31. [score:1]
The remaining 8 miRNAs are encoded within intronic regions: bta-miR-26b, bta-miR-455-3p, bta-miR-23b-5p, bta-let-7 g, bta-miR-22-5p, bta-miR-147, bta-miR-369-3p, and bta-miR-1224. [score:1]
The only chromosomes in the Bos taurus genome that were associated with more than one of the identified miRNAs were: chromosome #8 with bta-miR-23b-5p, bta-miR-31, and bta-miR-455-3p; chromosome #16 with bta-miR-34a, bta-miR-181b, and bta-miR-205; chromosome #19 with bta-miR-22-5p, bta-miR-144, and bta-miR-497; and finally chromosome #21 with bta-miR-154a and bta-miR-369-3p. [score:1]
It is interesting to note that six of the 19 miRNAs described in this study are considerably abundant in cattle liver: bta-miR-22-5p, bta-miR-150, bta-miR-17-5p, bta-miR-455-3p, bta-miR-146, and let 7-g [64]; an organ in which FMDV does not establish infection. [score:1]
[1 to 20 of 13 sentences]
12
[+] score: 30
We observed a significant reduction of luciferase expression upon miR-24, miR-186, and miR-455 expression (Figure 1A) compared to a scrambled miRNA (SCR) negative control. [score:4]
It is interesting to note that both miR-186 and miR-455 have previously been shown to have an altered expression level in AD cerebrospinal fluid (CSF) samples, which further underscores the possible association between these miRNAs and AD development. [score:4]
In order to determine the functional consequences of miR-24, miR-186, and miR-455 expression on Aβ production, we performed using HEK293-APPSwe cells. [score:3]
In conclusion, we identified NCSTN -targeting miRNAs (miR-24, miR-186, and miR-455) that could decrease Aβ secretion. [score:3]
FIGURE 2 miR-24, miR-186, and miR-455 expression results in decreased Aβ secretion. [score:3]
This analysis resulted in a list of 22 miRNAs (Table 1), which we narrowed down to six (i. e., miR-24, miR-186, miR-340, miR-455, miR-656, and miR-1301) based on our previous expression profiling studies in the human cerebral neocortex (45 raw reads cut-off; Hébert et al., 2013). [score:3]
We thus identified miR-24, miR-186, and miR-455 as endogenous regulators of human NCSTN. [score:2]
MiR-186 and miR-455 were previously shown to be altered in AD CSF samples, and we demonstrated that the miRNA -mediated repression of NSCTN mRNA is altered by the presence of SNPs rs113810300 and rs141849450. [score:1]
Both miR-186 and miR-455 decreased (soluble) Aβ40 and Aβ42 levels, while miR-24 had a small, nonetheless significant effect on Aβ42 (Figure 2). [score:1]
SNPID Position in 3′UTR Polymorphism Predicted microRNA Seed region Number of raw reads Ts10059 18 C/T hsa-miR-31 Y 0 Ts41266889 196 C/T hsa-miR-3153 Y 0 Ts180769907 360 A/T hsa-miR-1226* Y 0 hsa-miR-608 N 0 hsa-miR-92a* N 0 Ts1043230 367 C/A hsa-miR-92a-2* Y 0 hsa-miR-4298 N 0 Ts1043329 460 C/T hsa-miR-24 N 150 Ts141849450 515–516 delCA hsa-miR-455-5p Y 95 Ts34629439 582 delT hsa-miR-1301 N 45 hsa-miR-590-5p N 11 hsa-miR-27b* N 23 hsa-miR-582-5p N 15 hsa-miR-656 N 107 Ts113810300 623 T/G hsa-miR-1252 Y 0 hsa-miR-3125 Y 0 hsa-miR-340 Y 1708 hsa-miR-142-5p Y 20 hsa-miR-186 Y 1209 hsa-miR-3121 N 0 hsa-miR-4311 N 0 Ts71719087 638/639 delAT hsa-miR-3145 Y 0The SNP ID and the nature of the polymorphism are indicated. [score:1]
On the other hand, both seed region SNPs T623G and delCA515–516 reduced miR-186 and miR-455 -mediated repression, respectively (Figures 3B–D). [score:1]
Taken together, we identified miR-186 and miR-455, which are functionally affected by polymorphisms. [score:1]
FIGURE 3 SNP delCA 515–516 and SNP T623G reduce miR-455- and miR-186 -mediated NCSTN repression. [score:1]
Our data provide additional proof of principle that polymiRTS could contribute to neurodegenerative disorders, and that miR-186 and miR-455 could be important players in AD pathology. [score:1]
Notably, only miR-186 and miR-455 decreased both the mature and immature forms of NCSTN (Edbauer et al., 2002). [score:1]
[1 to 20 of 15 sentences]
13
[+] score: 27
Upregulation of miR-455-3p and miR-33a was found to be associated with chemosensitivity while upregulation of miR-224, miR-1236, and miR-520d-3p was associated with chemoresistance [21]. [score:7]
Interestingly, among the 736 miRNAs analyzed in the first study, upregulation of miR-455-3p and miR-33a was associated with chemosensitivity while upregulation of miR-224, miR-1236, and miR-520d-3p was associated with chemoresistance [21]. [score:7]
In addition, a predictor score based on a signature of five miRNAs, among which high expression of miR-224, miR-1236, and miR-520d-3p and low expression of miR-455-3p and miR-33a were individually associated with unfavorable outcome, has been proposed to predict the clinical outcome of DLBCL patients, independent from the IPI score [21]. [score:5]
On the other hand, high expression of miR-224, miR-1236, and miR-520d-3p and low expression of miR-455-3p and miR-33a were found to be individually associated with unfavorable outcome and a score based on this five-miRNAs was proposed to predict the clinical outcome of DLBCL patients treated with R-CHOP regimen, independent from the IPI score [21]. [score:5]
Five miRNAs were differentially expressed between both groups (miR-224, miR-1236, miR-520d-3p, miR-33a, and miR-455-3p) and were validated in an independent group of 133 patients. [score:3]
[1 to 20 of 5 sentences]
14
[+] score: 24
In accordance with our results, miR-21, miR-100, and miR-125b were upregulated, whereas miR-455-3p and miR-378 were downregulated in chemoresistant BxPC-3. In addition, miR-330-5p could be detected by Tréhoux et al. as a tumor suppressor in PDAC in vitro and in vivo, sensitizing pancreatic cancer cells to gemcitabine [19]. [score:9]
RT-PCR validation of mostly dysregulated miRs confirmed that miR-138, miR-147b, miR-148a, miR-99a, miR-455-3p and miR-125b were significantly upregulated and miR-31-star, miR-422a, miR-330-3p, mir-330-5p and miR-378d were downregulated in PANC-1-GR cell clones vs. [score:8]
In MIA-PaCa-2-GR cell clones miR-125b, miR-210, miR-21, miR-100, miR-148a, miR-99a and miR-455-3p were significantly upregulated, whereas miR-330-3p, miR-330-5p, miR-486-5p, miR-422a and miR-31-star were significantly downregulated (Fig 6B). [score:7]
[1 to 20 of 3 sentences]
15
[+] score: 21
To understand the molecular mechanism of miR-29b deregulation, we analyzed the co -expression profiles of two important upstream suppressors (miR-152 and miR-455) [71]. [score:6]
In SKBR3, along with the over -expression of miR-29b, miR-455 was also up-regulated whereas miR-152 did not show any significant change. [score:6]
Both of miR-29b suppressors, miR-152 and miR-455, were over-expressed in MDA-MB231 cell line. [score:5]
These data suggest a prominent inhibitory effect of miR-152 rather than miR-455 on the regulation of miR-29b emphasizing the controlling effect of miRNAs in certain types of cancer. [score:4]
[1 to 20 of 4 sentences]
16
[+] score: 17
Other miRNAs from this paper: hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-382
The effects of miR-455 are thought to be mediated by activation of AMPK α1 through targeting of hypoxia inducible factor 1 α subunit inhibitor (HIF1an) as AMPK promotes the brown adipogenic program and mitochondrial biogenesis. [score:5]
Concomitantly, miR-455 also targets the adipogenic suppressors Runx1t1 and Necdin, initiating adipogenic differentiation [64]. [score:5]
miR-455 exhibits a BAT-specific expression pattern and can be induced by cold exposure and the browning regulator BMP7. [score:4]
With regard to BAT, miR-455 is a potential microRNA target which has been demonstrated to play a role in brown adipogenesis. [score:3]
[1 to 20 of 4 sentences]
17
[+] score: 16
The expression of miR-221, miR-18a, miR-18b, and miR-423-5p in poorly differentiated HCC were significantly higher than in well differentiated HCC, and 8 miRNAs (miR-455-3p, miR-1914*, miR-100, miR-215, miR-122*, let-7b, miR-22 and miR-99a) in poorly differentiated HCC had significantly lower expression levels than in well differentiated HCC (p < 0.05) (Table  2). [score:5]
14.0 and showed that the expression of miR-221, miR-18a, miR-18b, and miR-423-5p in poorly differentiated HCC were significantly higher than in well differentiated HCC, and 8 miRNAs (miR-455-3p, miR-1914*, miR-100, miR-215, miR-122*, let-7b, miR-22 and miR-99a) in poorly differentiated HCC were expressed significantly lower than in well differentiated HCC. [score:5]
Homo sapiens trinucleotide repeat containing 6B (TNRC6B) was a common hypothetical target gene in miR-221, miR-18a, miR-18b, miR-423-5p, miR-455-3p, miR-1914*, miR-215, miR-122*, let-7b, and miR-22 using miRanda algorithm. [score:3]
miR-455-3p and let-7b were used as negative controls. [score:1]
Ago2-IP fractionated cell lysates were prepared by transfecting 293FT cells with mature double strand of miR-18b, miR-22, miR-455-3p, let-7b, or a non-specific siRNA which was used as a control RNA. [score:1]
The concentration of TNRC6B IP -RNA treated with miR-18b was higher than those treated with the control RNA or double strand of miR-22, miR-455-3p, and let-7b (Figure  1D). [score:1]
[1 to 20 of 6 sentences]
18
[+] score: 15
Bone morphogenetic protein receptor 2 (BMPR2) is known to be targeted by miR-19a, −20a and miR-25 [28] and predicted to be targeted by miR-455. [score:5]
Of these miRNAs, 145 were expressed in both human and mouse BAT (Additional file 4), including 23 miRNAs that had the same name but their sequences differed by few nucleotides between the species (i. e. miR-155, miR-193b, miR-455). [score:3]
The miR-193b-365 cluster and miR-455 are known to regulate mouse brown fat development and were identified in our selection of 25 BAT-enriched miRNAs common to mice and humans. [score:3]
miR-455 expression levels are also increased in mature murine brown adipocytes and positively correlate with uncoupling protein 1 (UCP1) levels suggesting a potential metabolic role in brown adipocytes [10]. [score:3]
miR-193b null mice have elevated levels of miR-455 suggesting a compensatory effect in the absence of the miR-193b-365 cluster. [score:1]
[1 to 20 of 5 sentences]
19
[+] score: 15
, High Wycombe, UK) analysis of 1733 human microRNAs and validation by qRT-PCR showed microRNA-21, microRNA-99a, microRNA-100, microRNA-125b, microRNA-138, microRNA-147b, microRNA-148a, microRNA-210, microRNA-376a, and microRNA-455-3p to be significantly upregulated, whereas microRNA-31-star, microRNA-330-3p, microRNA-330-5p, microRNA-378d, microRNA-422a, and microRNA-486-5p were significantly downregulated. [score:7]
p < 0.05 indicates significance Expression of in vitro dysregulated microRNA-376a, microRNA-330-3p, microRNA-330-5p, microRNA-378d, microRNA-422a, microRNA-455-3p, and microRNA-486-5p did not differ between PDAC and control. [score:4]
p < 0.05 indicates significance Expression of in vitro dysregulated microRNA-376a, microRNA-330-3p, microRNA-330-5p, microRNA-378d, microRNA-422a, microRNA-455-3p, and microRNA-486-5p did not differ between PDAC and control. [score:4]
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20
[+] score: 12
Previous studies have shown that miR-155, miR-146a, miR-146b, miR-125a and miR-455 can be up-regulated by heat killed C. albicans in Bone marrow derived macrophages [21]. [score:4]
However, in contrast to their results, the up-regulation of miR-455, miR-125 and miR-155 was not be detected in our study. [score:4]
Monk et al. reported that miR-455, miR-125, miR-146 and miR-155 were up-regulated in murine bone marrow derived macrophages (BMDMs) stimulated with heat killed C. albicans [21]. [score:4]
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[+] score: 12
For example, the unedited pri-miR-455-5p promotes melanoma by silencing the expression of the tumor suppressor CPEB1 in metastatic melanoma, gastric, thyroid and lung cancers, while editing is tumor-suppressive (Figure 3A). [score:7]
Bioinformatics studies revealed that other potential target sites of miR-455-5p include the transcripts of RHOC, MDM4 and integrin α-2 [104], all of which facilitate tumor growth. [score:3]
Shoshan E. Mobley A. K. Braeuer R. R. Kamiya T. Huang L. Vasquez M. E. Salameh A. Lee H. J. Kim S. J. Ivan C. Reduced adenosine-to-inosine miR-455–5p editing promotes melanoma growth and metastasis Nat. [score:1]
However, ADAR1 may also be physically involved in the complex formation between miR-455 and Drosha or Dicer. [score:1]
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[+] score: 12
Overall, we identified four miRNAs that are both edited and differentially expressed by ADAR2 (shown in bold in Table  1), 14 miRNAs that are edited but not significantly modulated by ADAR2 (Table  1) and 89 miRNAs that are modulated (either up-regulated or down-regulated) by ADAR2 but not edited within their mature sequence (Additional file 3; excluding the edited miR-138-1* and miR-455). [score:9]
Comparing miRNA editing (Table  1) and expression (Additional file 2 and Additional file 3), we observed that relatively few miRNAs were both edited and significantly modulated by ADAR2 (shown in bold in Table  1): miR-22, miR-503 (Additional file 2), miR-138-1* and miR-455 (Additional file 3). [score:3]
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[+] score: 11
Interestingly, miR-455-3p and miR-455-5p were highly expressed in both the F100 cerebellum and the adult cortex, which suggests that the same miRNAs are expressed in both regions, but seem to reach a maximum level of expression at different time points during development. [score:8]
Therefore, miRNAs found to be over-expressed in the cortex (e. g. miR-455-3p, miR-455-5p) might be responsible for growth and neuron formation. [score:3]
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[+] score: 11
Smad2, Chordin-Like 1 (CHRDL1), and Activin Receptor Type IIB (ACVR2B) have been identified as direct miRNA-455-3p targets, which are related with the TGF-β pathway [110]. [score:4]
Another study demonstrated that in OA a prominent feature is the altered expression of two miRNAs, miRNA-140-5p and miRNA-455-3p [110]. [score:3]
A reciprocal regulation among miRNA-455-3p and TGF-β pathways—TGF-β influences miRNA-455-3p levels, while miRNA-455-3p dampens Smad2/3 -mediated signaling, thereby possibly contributing to cartilage erosion—has been reported. [score:2]
Intriguingly, both miRNA-455-3p and miRNA-140-5p are derived from intronic miRNA precursors that reside within collagen type XXVII alpha 1 (COL27A1) and WW domain containing E3 ubiquitin protein ligase 2 (WWP2) locus), respectively [110, 111]. [score:1]
Certain OA-related miRNAs, i. e., miRNA-33a, miRNA-455-3p, miRNA-140, and miRNA-335-5p, are actually embedded within the intronic regions of human SREBP-2, COL27A1, WWP2, and MEST, respectively. [score:1]
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[+] score: 10
In addition to this, miR-455 is downregulated in old mice [146] and upregulated in the liver of HFD-fed mice [147]. [score:7]
In adipose-specific miR-455 transgenic mice, it has been found that miR-455 activates AMPK in brown adipose tissue (BAT), suggesting the importance of this miRNA in BAT adipogenesis through the regulation of the AMPK/Sirtuins/PGC1-1α pathway [145]. [score:2]
Zhang H. Guan M. Townsend K. L. Huang T. L. An D. Yan X. Xue R. Schulz T. J. Winnay J. Mori M. MicroRNA-455 regulates brown adipogenesis via a novel HIF1an-AMPK-PGC1α signaling networkEMBO Rep. [score:1]
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[+] 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-21, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-98, hsa-mir-101-1, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-106a, hsa-mir-107, hsa-mir-16-2, hsa-mir-198, hsa-mir-148a, hsa-mir-30d, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181c, hsa-mir-182, hsa-mir-183, hsa-mir-205, hsa-mir-210, hsa-mir-181a-1, hsa-mir-222, hsa-mir-224, hsa-mir-200b, hsa-let-7g, hsa-let-7i, hsa-mir-23b, hsa-mir-27b, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-128-1, hsa-mir-132, hsa-mir-137, hsa-mir-140, hsa-mir-141, hsa-mir-142, hsa-mir-143, hsa-mir-144, hsa-mir-153-1, hsa-mir-153-2, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-134, hsa-mir-136, hsa-mir-146a, hsa-mir-150, hsa-mir-184, hsa-mir-185, hsa-mir-186, hsa-mir-206, hsa-mir-320a, hsa-mir-200c, hsa-mir-128-2, hsa-mir-200a, hsa-mir-101-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-299, hsa-mir-26a-2, hsa-mir-373, hsa-mir-376a-1, hsa-mir-342, hsa-mir-133b, hsa-mir-424, hsa-mir-429, hsa-mir-433, hsa-mir-451a, hsa-mir-146b, hsa-mir-494, hsa-mir-193b, hsa-mir-376a-2, hsa-mir-33b, hsa-mir-644a, hsa-mir-548d-1, hsa-mir-548d-2, hsa-mir-320b-1, hsa-mir-320c-1, hsa-mir-320b-2, hsa-mir-301b, hsa-mir-320d-1, hsa-mir-320c-2, hsa-mir-320d-2, hsa-mir-320e, hsa-mir-3613, hsa-mir-4668, hsa-mir-4674, hsa-mir-6722
Kumar et al. (2017) demonstrated that upregulation of miRNA-455-3p, miRNA-4668-5p, miRNA-3613-3p, and miRNA-4674, while downregulation of miRNA-6722 in 10 AD positive brain samples. [score:7]
MicroRNA-455-3p as a potential peripheral biomarker for Alzheimer’s disease. [score:2]
Furthermore, the amyloid protein fragment amyloid beta (Aβ), is also influenced by miRNA-24, miRNA-186, miRNA-455, miRNA-146a, and miRNA-98 (Delay et al., 2011; Li Y. Y. et al., 2011; Hu et al., 2013). [score:1]
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[+] score: 10
Other miRNAs from this paper: hsa-mir-31, hsa-mir-372, hsa-mir-574
Among the differentially expressed ceRNAs, one mRNA (PLAU), two miRNAs (miR-31-5p and miR-455-3p), and three lncRNAs (FAM83A-AS1, MIR31HG, and MIR99AHG) were found to be associated with the overall survival of patients with LUSC by univariate Cox regression analysis. [score:3]
Using these results, we constructed a ceRNA network and studied the significance of the expression pattern of LUSC-specific ceRNAs (PLAU, miR-31-5p, miR-455-3p, FAM83A-AS1, MIR31HG, and MIR99AHG) for overall survival of patients with LUSC. [score:3]
MiR-455-3p was found to play a role in acquired temozolomide resistance and may be a novel therapeutic target in recurrent glioblastoma multiforme (Ujifuku et al., 2010). [score:2]
Kaplan–Meier survival curves indicated that the lncRNA MIR99AHG positively correlated with overall survival, whereas PLAU, miR-31-5p, miR-455-3p, FAM83A-AS1, and MIR31HG were negatively associated with overall survival (Fig. 8). [score:1]
Kaplan–Meier survival curves for six ceRNA (PLAU, miR-31-5p, miR-455-3p, FAM83A-AS1, MIR31HG, and MIR99AHG) associated with overall survival. [score:1]
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[+] score: 9
Ujifuku et al. (2010) also identified three miRNAs (miR-195, miR-455-3p, and miR-10a*) overexpressed in the induced TMZ-resistant cell line, and demonstrated that miR-195 inhibition enhanced TMZ -induced cell death. [score:5]
In fact, recent miRNA studies have revealed that aberrant miRNA expression could affect chemosensitivity, and have also identified several miRNAs (i. e., miR-21, miR-125b-2, miR-195, miR-455-3p, miR-10a) associated with TMZ resistance (Shi et al., 2010; Ujifuku et al., 2010; Zhang et al., 2012). [score:3]
miR-195, miR-455-3p and miR-10a(*) are implicated in acquired temozolomide resistance in glioblastoma multiforme cells. [score:1]
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[+] score: 9
Secondly, in most of miRNAs we identified (miR-196b, miR-4299, miR-324-5p, miR-455-3p and miR-939), the potential linkage between their expression and chemoresistance was already established; then some of them were identified for the first time. [score:3]
A validation study was done to corroborate a subset of the results, including expression levels of miR-4299, miR-196b, miR-324-5p, miR-455-3p and miR-939, through analyzing stage IV colon adenocarcinoma tissues (not responding and responding to the chemotherapy) with laser capture microdissection and quantitative real-time PCR. [score:3]
Fig.  2 Dots indicate of the relative quantification (RQ) values of miRNA expression levels (a miR-4299, b miR-196b, c miR-324-5p, d miR-455-3p, e miR-939), normalized by U6. [score:3]
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[+] score: 9
Down -expression was observed only for miR-21, whereas over -expression was observed in 12 miRNA (miR-143, miR-145, miR-151-5p, miR-155*, miR-199a-5p, miR-23a, miR-30a, miR,30c, miR-21, miR-455-3p, miR-708 and miR-let-7i) and only two were not deregulated in a statistically significant way (miR-30a and miR-30c) (Table 3). [score:6]
The remaining 8 miRNAs (miR-151-5p, miR-155*, miR-17, miR-199a-5p, miR-23a, miR-30a-5p, miR-455-3p, and miR-let-7i) did not exhibit significantly altered expression. [score:3]
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[+] score: 8
The discovery of dysregulated miRNAs, e. g., miR-210, miR-376c, and miR-455, and their gene-regulatory roles in placental development has provided a new avenue for elucidating the underlying mechanisms of pregnancy-specific diseases, such as PE 17– 19. [score:6]
Lalevee S Lapaire O Buhler M miR455 is linked to hypoxia signaling and is deregulated in preeclampsiaCell Death Dis. [score:2]
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[+] score: 8
84uphsa-miR-574-3p1.77down   hsa-miR-19a2.32downhsa-miR-5722.92uphsa-miR-574-5p2.41down   hsa-miR-21*3.23downhsa-miR-574-3p3.75up      hsa-miR-301a2.32downhsa-miR-574-5p2.083up      hsa-miR-30e2.24downhsa-miR-629*2.85up      hsa-miR-7203.39downhsa-miR-6382.19up         hsa-miR-6634.52up         hsa-miR-9392.32up         hsa-miR-100*3.47down         hsa-miR-12603.09down         hsa-miR-12803.01down         hsa-miR-1414.5down         hsa-miR-21*4down         hsa-miR-2212.72down                   hsa-miR-455-3p 2.16 down Among the listed profiles of differentially down-regulated miRNA as compared with non-infected control cells, it was found that miR-574-5p was down regulated (>2-fold, p<0.05) in H5N1 infected cells at 3-hour post-infection. [score:4]
84uphsa-miR-574-3p1.77down   hsa-miR-19a2.32downhsa-miR-5722.92uphsa-miR-574-5p2.41down   hsa-miR-21*3.23downhsa-miR-574-3p3.75up      hsa-miR-301a2.32downhsa-miR-574-5p2.083up      hsa-miR-30e2.24downhsa-miR-629*2.85up      hsa-miR-7203.39downhsa-miR-6382.19up         hsa-miR-6634.52up         hsa-miR-9392.32up         hsa-miR-100*3.47down         hsa-miR-12603.09down         hsa-miR-12803.01down         hsa-miR-1414.5down         hsa-miR-21*4down         hsa-miR-2212.72down                   hsa-miR-455-3p 2.16 downAmong the listed profiles of differentially down-regulated miRNA as compared with non-infected control cells, it was found that miR-574-5p was down regulated (>2-fold, p<0.05) in H5N1 infected cells at 3-hour post-infection. [score:4]
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[+] score: 8
Validation of ITGB1 as a direct target of miR-455-3p. [score:4]
Of these 7 genes, miR-455-3p, miR-183-5p and 3 miR-29 family member have been reported [13– 15] and validated to target ITGB1. [score:3]
The result showed that there were 7 common predicted miRNAs, including miR-455-3p, miR-183-5p, miR-29c-3p, miR-29b-3p, miR-29a-3p miR-124-3p, and miR-493-5p. [score:1]
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Potentially, editing of these miRNAs could therefore be a side effect of other regulatory functions performed by ADARs, which might in turn explain why the deeply conserved editing sites of miR-140*, miR-301a and miR-455 all lie outside of the seed sequence and other parts of the miRNA that may influence targeting properties [22]. [score:4]
One of these events, editing of miR-455 at position 17, had been verified by ADARB1 overexpression experiments in human cell lines [13]. [score:3]
Remarkably, we found that miR-301a and miR-455 were edited in bony fishes, implying that both miRNAs have experienced site-specific RNA editing during the past 450 million years [20]. [score:1]
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[+] score: 8
The selection of the miRNAs is based on their potential role in the pathology of the lung (mmu-miR-1, 146b, -203, -21, -223, -29b, -29c) or on their high and significant differential expression in the mo del (mmu-miR-455, -574-5p, -672, -690) or for their high (mmu-let-7b a, mmu-miR-145) or low (mmu-miR-450a-5p) signal intensity in microarray analysis. [score:3]
Among these miRNAs, miR-455 has been reported to be implicated in brown adipocyte differentiation [53], while the functions or targets of the others are not determined yet. [score:3]
Among these data, 40 out of 42 (95%) gave results and trends similar to those obtained by microarray profiling, except for mmu-miR-29c at ST and LT (Figure 2), although the magnitude of the observed regulation was not always identical (mmu-miR-455 at LT and mmu-miR-450a at IT). [score:2]
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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-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-106a, hsa-mir-16-2, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181a-1, hsa-mir-221, hsa-mir-222, hsa-mir-223, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-23b, hsa-mir-27b, hsa-mir-122, hsa-mir-125b-1, hsa-mir-140, hsa-mir-125b-2, hsa-mir-136, hsa-mir-146a, hsa-mir-150, hsa-mir-206, hsa-mir-155, hsa-mir-181b-2, hsa-mir-106b, hsa-mir-302a, hsa-mir-34b, hsa-mir-34c, hsa-mir-302b, hsa-mir-302c, hsa-mir-302d, hsa-mir-367, gga-let-7i, gga-let-7a-3, gga-let-7b, gga-let-7c, gga-mir-125b-2, gga-mir-155, gga-mir-222a, gga-mir-221, gga-mir-92-1, gga-mir-19b, gga-mir-20a, gga-mir-19a, gga-mir-18a, gga-mir-17, gga-mir-16-1, gga-mir-15a, gga-mir-1a-2, gga-mir-206, gga-mir-223, gga-mir-106, gga-mir-302a, gga-mir-181a-1, gga-mir-181b-1, gga-mir-16-2, gga-mir-15b, gga-mir-140, gga-let-7g, gga-let-7d, gga-let-7f, gga-let-7a-1, gga-mir-146a, gga-mir-181b-2, gga-mir-181a-2, gga-mir-1a-1, gga-mir-1b, gga-let-7a-2, gga-mir-34b, gga-mir-34c, gga-let-7j, gga-let-7k, gga-mir-23b, gga-mir-27b, gga-mir-24, gga-mir-122-1, gga-mir-122-2, hsa-mir-429, hsa-mir-449a, hsa-mir-146b, hsa-mir-507, hsa-mir-92b, hsa-mir-449b, gga-mir-146b, gga-mir-302b, gga-mir-302c, gga-mir-302d, gga-mir-455, gga-mir-367, gga-mir-429, gga-mir-449a, hsa-mir-449c, gga-mir-21, gga-mir-1458, gga-mir-1576, gga-mir-1612, gga-mir-1636, gga-mir-449c, gga-mir-1711, gga-mir-1729, gga-mir-1798, gga-mir-122b, gga-mir-1811, gga-mir-146c, gga-mir-15c, gga-mir-449b, gga-mir-222b, gga-mir-92-2, gga-mir-125b-1, gga-mir-449d, gga-let-7l-1, gga-let-7l-2, gga-mir-122b-1, gga-mir-122b-2
MiR-1a, miR-140 and miR-449 were significantly up-regulated in both tissues, while miR-455, miR-34b and miR-34c were only up-regulated with AIV infection in tracheae. [score:7]
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[+] score: 7
As reflected by the lower overall correlation values (Table 2), the relative expression of the FFPE9a sample indicated that qPCR -based expression was highly divergent in nine of 37 miRNA transcripts with the other expression platforms (let-7a, miR-125a-5p, miR-31, miR-484, miR-16, miR-455-3p, miR-26b, let-7f, and miR-29b; Table S3b). [score:7]
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Conversely, in the advanced fibrosis group they demonstrated an upregulation of miR-1 and miR-10b-5p, and a downregulation of miR-20b-5p and miR-455-3p, implicated in immune response and cellular senescence. [score:7]
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[+] score: 6
Interestingly, miR-455 which is expressed at low levels in white preadipocytes and white mature adipocytes is reported to be upregulated during brown pre-adipocyte differentiation [85]. [score:6]
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40
[+] score: 6
Yoo et al. demonstrated that miR-29b is downregulated in senescent hBM-MSC compared to young hBM-MSCs, but miR-455-3p, unlike in our study, was upregulated [86]. [score:6]
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[+] score: 5
Stem-loop real-time PCR was used to further examine the expression of the 5p arm and 3p arm miRNAs of miR-324 and miR-455 in 10 paired (tumor and adjacent normal) breast cancer tissue samples. [score:3]
In Figure 4, the NGS data showed that the expression ratios of the 5p arm to 3p arm miRNAs of miR-324 and miR-455 were individually increased and decreased in the tumor, respectively, compared with in normal tissue. [score:2]
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[+] score: 5
Several miRNAs are regulated by Sox9 (e. g. miR-140 and miR-455) [13– 15] or regulate Sox9 expression (e. g. miR-675 and miR-145) [16, 17]. [score:5]
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[+] score: 5
It has been reported that miR-195, miR-455-3p and miR-10a* are highly expressed in the induced TMZ-resistant U251R cell line and that miR-195 inhibition enhances TMZ -induced cell death [6]. [score:5]
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[+] score: 5
Chai et al. found that miR-455 inhibited proliferation and invasion of colorectal cancer through inhibiting RAF (rapidly accelerated fibrosarcoma) proto-oncogene serine/threonine-protein kinase [15]. [score:5]
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[+] score: 5
For the efficient target RBM38, miR-455-3p repressed it only in normal stage, and it had contribution to the ‘3′-UTR -mediated mRNA stabilization’ process only in CIN I stage. [score:3]
Our finding suggests that based on miR-455-3p’s differential regulation on RBM38, the response for DNA double-strand break may be promoted in CIN I stage by carrying out p53 downstream processes, thus may promote HPV integration. [score:2]
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46
[+] score: 4
Quantitative analysis of miR-32-5p, miR-142-5p, miR-455-3p and miR-1249-3p expression was performed with reverse transcription polymerase chain reaction (RT-PCR) using the TaqMan MicroRNA Reverse Transcription kit (Applied Biosystems, Waltham, MA, USA) and 10 ng of total RNA. [score:3]
Thus, we shortlisted four miRNAs—miR-32-5p, miR-142-5p, miR-455-3p and miR-1249-3p. [score:1]
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47
[+] score: 4
In murine macrophages stimulated by 10 [6] cells/mL heat killed C. albicans, miR-146a and miR-155, as well as miR-455 and miR-125a were upregulated (92), indicative of the involvement of these miRNAs in macrophage polarization. [score:4]
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[+] score: 4
22 hsa-miR-224 1.43 hsa-miR-26a −1.26 hsa-miR-29a −1.21 hsa-miR-376c 1.26 hsa-miR-424 −1.35 hsa-miR-455-3p 1.48 hsa-miR-99a † 1.21 Italic: down-regulated in fat cells from obese. [score:4]
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49
[+] score: 4
Ujifuku et al. [15] showed that miR-195, miR-455-3p and miR-10a upregulated in temozolomide (TMZ)-resistant GBM cells, played a critical role in acquired TMZ resistance. [score:4]
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50
[+] score: 3
For example, the lncRNA H19 was targeted by miR-29b-3p [35], miR-138-5p [36], miR-141-3p [37], miR-200b/c [38], miR-455-5p [39], and miR-675-5p [40]. [score:3]
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51
[+] score: 3
In human acute lymphoblastic leukemia (ALL) cell lines, miR-455-3p was shown to be related to P-gp expression level [80]. [score:3]
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52
[+] score: 3
The expression of miR-218, miR-455–3p and miR-7 was increased to a lesser extent and that of miR-30b was decreased. [score:3]
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53
[+] score: 3
We found that our transcript sequence could be a target of three miRNAs: hsa-miR-455-5p, has-miR-640 and has-miR-1909-3p. [score:3]
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54
[+] score: 3
Several recent studies profiling miRNA expression in skeletal muscle of young and old mice have revealed that several miRNAs, including miR-206, miR-698, miR-744-5p, and miR-468, are increased, whereas others, such as miR-29, miR-434, miR-455, miR-382, miR-181a, and miR-221, are reduced in skeletal muscle cells of old animals [82– 84]. [score:3]
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55
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Huang Z. W. Tian L. H. Yang B. Guo R. M. Long noncoding RNA H19 acts as a competing endogenous RNA to mediate CTGF expression by sponging miR-455 in cardiac fibrosisDNA Cell Biol. [score:3]
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56
[+] score: 3
Of the nine miRNAs were specifically expressed in cashmere goat dorsal skin [18], only four of them were examined in the present study: miR-1, miR-374, miR-455-3p and miR-92b. [score:3]
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57
[+] score: 2
Six miRNA RNA-immunoprecipitated in GW/P bodies were predicted to regulate KIF3A (kinesin family member 3A) and include miR-29, miR-199, miR-181, miR-455, miR-155 and miR-145. [score:2]
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58
[+] score: 2
Expression of miR-130b and miR-455 was at similar levels in both assays. [score:2]
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59
[+] score: 2
Another experiment found that miRNA-140 and miRNA-455 are involved with cartilage development, and miRNA-9 and miRNA-98 are involved in endochondral ossification in bone matrix gelatin rat mo dels [29]. [score:2]
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60
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Moreover, miR-195, miR-455-3p, and miR-10a* were shown to mediate glioma cell resistance to temozolomide, although the specific underlying mechanism remains unclear [90]. [score:1]
Ujifuku K. Mitsutake N. Takakura S. Matsuse M. Saenko V. Suzuki K. Hayashi K. Matsuo T. Kamada K. Nagata I. miR-195, miR-455-3p and miR-10a (*) are implicated in acquired temozolomide resistance in glioblastoma multiforme cells Cancer Lett. [score:1]
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61
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After applying the inclusion criteria (|FC| <0.2 or> 5 and p adjusted <0.05), as previously mentioned, biological validation was performed by RT-qPCR of the 13 differently regulated miRNAs (hsa-miR-9, hsa-miR-135b*, hsa-miR-194*, hsa-miR-489, hsa-miR-592, hsa-miR-369-5p, hsa-miR-876-5p, hsa-miR-31, hsa-miR-135b, hsa-miR-211, hsa-miR-944, hsa-miR-142-5p, hsa-miR-455-3p), in an independent set of 46 samples corresponding to 19 SA, 8 UA and 19 controls. [score:2]
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62
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In macrophages infected by C. albicans, Monk et al. in 2010 reported that miR-455, miR-125, miR-146 and miR-155 may play significant roles in regulating macrophage function following PRR stimulation [34]. [score:2]
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63
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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-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-671, 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
Levels of eight circulating serum miRNAs (miR-148a, miR-143, miR-324-3p, miR-628-3p, miR-206, miR-140-5p, miR-455-5p, and miR-362-3p) were significantly higher in sera of patients with enteroviral infections (215). [score:1]
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64
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79 ** hsa-mir-365 7.13 *** 77.53 *** hsa-mir-429 54.63 *** 85.25 *** hsa-mir-454 33.25 *** 87.31 - hsa-mir-455-3p 42.76 *** 96.4 - hsa-mir-484 4.83 *** 78.73 - hsa-mir-485-3p 4.75 *** 71.49 *** hsa-mir-501-3p 69.25 *** 91.25 *** hsa-mir-512-5p 21.37 *** 72.89 *** hsa-mir-532-3p 9.5 *** 85.93 *** hsa-mir-541 69.87 *** 97.77 - hsa-mir-600 35.63 *** 93.48 - hsa-mir-625* 28.5 *** 72.89 *** Hits of functional screen Relative percentage of myotubes 1, % of control p value, Mann Whitney test Relative cell count 2, % of control p value, Mann Whitney test hsa-mir-636 2.37 *** 81.98 *** hsa-mir-663 21.38 *** 84.73 *** hsa-mir-664 7.13 *** 82.85 *** hsa-mir-766 45.13 *** 73. [score:1]
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65
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In the cerebellum, novel_circRNA_007362 was predicted to combine with 24 miRNAs (tch-let-7e-5p, tch-let-7i-5p, tch-let-7f-5p, tch-miR-125a-5p, tch-miR-1301, tch-miR-135a-5p, tch-miR-135b-5p, tch-miR-15b-5p, tch-miR-195-5p, tch-miR-1-5p, tch-miR-218-5p, tch-miR-22-3p, tch-miR-26a-5p, tch-miR-26b-5p, tch-miR-296-3p, tch-miR-335-5p, tch-miR-34a-5p, tch-miR424-5p,tch-miR-491-5p, tch-miR-455-3p,tch-miR-503, tch-miR-592, tch-miR-9771e, and tch-miR-98-5p). [score:1]
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66
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We focused our analysis on 12 miRNAs (miR-22, miR-29a-3p, miR-34a, miR-126, miR-140-3p, miR-141, miR-181c-5p, miR-202, miR-455-5p, miR-508-3p, miR-517a-3p and miR-576-3p). [score:1]
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67
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99E-02hsa-miR-486-5p632167−1.925.85E-02hsa-miR-16-5p683186−1.882.05E-02hsa-miR-455-3p22061−1.855.70E-02hsa-miR-222-3p389116−1.751.34E-02hsa-miR-195-5p902290−1.645.19E-02hsa-miR-221-3p25282−1.621.13E-02hsa-miR-22-3p302104−1.543.02E-02hsa-miR-331-3p21678−1.479.03E-02hsa-miR-43241409540−1.389.86E-02hsa-miR-30c-5p28221107−1.352.87E-02hsa-miR-378d17169−1.328.68E-02hsa-miR-125a-5p35061488−1.246.63E-02hsa-miR-151a-5p622267−1.225.18E-02hsa-miR-143-3p1732746−1.224.85E-02hsa-miR-151b556253−1.133.69E-02hsa-miR-44541276582−1.133. [score:1]
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68
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Using this approach, we report here a strong increase of miR-146a and a significant decrease of miR-140, miR-199a, and miR-455 which are in good agreement with previous studies in OA chondrocytes [17– 20, 51, 52]. [score:1]
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69
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For example, Hamrick et al., (2010) reported that miR-7, miR-468, miR-542, and miR-698 levels in mouse muscle tissue substantially increased with age, whereas miR-124a, miR-181a, miR-221, miR-382, miR-434, and miR-455 levels substantially decreased with age. [score:1]
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70
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Interestingly, the signature revealed a simultaneous increase of the 5p and 3p forms for miR-122, miR-125b, miR-194, miR-455 and miR-99a, which has been previously observed in the case of miR-455 in HBV-infected children [28]. [score:1]
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71
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Eleven of the miRs (hsa-miR-876-5p, hsa-miR-1255b, hsa-miR573, hsa-miR-29a, hsa-miR-455-3p, hsa-miR374b, hsamiR- 545, hsa-miR-486-3p, hsa-miR-541, hsa-miR-656, and hsa-miR-let-7c) were of poor prognosis. [score:1]
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72
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Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-32, hsa-mir-33a, hsa-mir-99a, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-107, mmu-let-7g, mmu-let-7i, mmu-mir-15b, mmu-mir-99a, mmu-mir-126a, mmu-mir-128-1, mmu-mir-130a, mmu-mir-140, mmu-mir-154, mmu-mir-204, mmu-mir-143, hsa-mir-204, hsa-mir-211, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-222, hsa-mir-223, mmu-mir-301a, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-128-1, hsa-mir-130a, hsa-mir-140, hsa-mir-143, hsa-mir-126, hsa-mir-129-2, hsa-mir-154, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-26a-1, mmu-mir-26b, mmu-mir-29a, mmu-mir-29c, mmu-mir-27a, mmu-mir-129-2, mmu-mir-103-1, mmu-mir-103-2, mmu-mir-340, mmu-mir-107, mmu-mir-32, mmu-mir-218-1, mmu-mir-218-2, mmu-mir-223, mmu-mir-26a-2, mmu-mir-211, mmu-mir-222, mmu-mir-128-2, hsa-mir-128-2, hsa-mir-29c, hsa-mir-101-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-301a, hsa-mir-26a-2, hsa-mir-379, mmu-mir-379, hsa-mir-340, mmu-mir-409, hsa-mir-409, hsa-mir-499a, hsa-mir-670, mmu-mir-1249, mmu-mir-670, mmu-mir-499, mmu-mir-455, bta-mir-26a-2, bta-mir-29a, bta-let-7f-2, bta-mir-101-2, bta-mir-103-1, bta-mir-16b, bta-mir-222, bta-mir-26b, bta-mir-27a, bta-mir-499, bta-mir-99a, bta-mir-126, bta-mir-128-1, bta-mir-34b, bta-mir-107, bta-mir-140, bta-mir-15b, bta-mir-218-2, bta-let-7d, bta-mir-29c, bta-mir-455, bta-let-7g, bta-let-7a-1, bta-let-7f-1, bta-let-7i, bta-mir-34c, bta-let-7a-2, bta-let-7a-3, bta-let-7b, bta-let-7c, bta-let-7e, bta-mir-103-2, bta-mir-204, hsa-mir-1249, hsa-mir-1306, hsa-mir-103b-1, hsa-mir-103b-2, bta-mir-128-2, bta-mir-129-2, bta-mir-130a, bta-mir-143, bta-mir-154a, bta-mir-211, bta-mir-218-1, bta-mir-223, bta-mir-26a-1, bta-mir-301a, bta-mir-32, bta-mir-33a, bta-mir-340, bta-mir-379, bta-mir-409a, bta-mir-670, mmu-mir-1306, bta-mir-1306, bta-mir-1249, bta-mir-2284i, bta-mir-2285a, bta-mir-2284s, bta-mir-2285d, bta-mir-2284l, bta-mir-2284j, bta-mir-2284t, bta-mir-2285b-1, bta-mir-2284d, bta-mir-2284n, bta-mir-2284g, bta-mir-2284p, bta-mir-2284u, bta-mir-2284f, bta-mir-2284a, bta-mir-2284k, bta-mir-2284c, bta-mir-2284v, bta-mir-2285c, bta-mir-2284q, bta-mir-2284m, bta-mir-2284b, bta-mir-2284r, bta-mir-2284h, bta-mir-2284o, bta-mir-2284e, hsa-mir-1260b, bta-mir-2284w, bta-mir-2284x, bta-mir-409b, hsa-mir-499b, bta-mir-1260b, bta-mir-2284y-1, bta-mir-2285e-1, bta-mir-2285e-2, bta-mir-2285f-1, bta-mir-2285f-2, bta-mir-2285g-1, bta-mir-2285h, bta-mir-2285i, bta-mir-2285j-1, bta-mir-2285j-2, bta-mir-2285k-1, bta-mir-2285l, bta-mir-6119, mmu-let-7j, bta-mir-2285o-1, bta-mir-2285o-2, bta-mir-2285n-1, bta-mir-2285n-2, bta-mir-2285p, bta-mir-2285m-1, bta-mir-2285m-2, bta-mir-2284y-2, bta-mir-2285n-3, bta-mir-2285n-4, bta-mir-2284y-3, bta-mir-154c, bta-mir-154b, bta-mir-2285o-3, bta-mir-2285o-4, bta-mir-2285m-3, bta-mir-2284y-4, bta-mir-2284y-5, bta-mir-2284y-6, bta-mir-2285m-4, bta-mir-2285o-5, bta-mir-2285m-5, bta-mir-2285n-5, bta-mir-2285n-6, bta-mir-2284y-7, bta-mir-2285n-7, bta-mir-2284z-1, bta-mir-2284aa-1, bta-mir-2285k-2, bta-mir-2284z-3, bta-mir-2284aa-2, bta-mir-2284aa-3, bta-mir-2285k-3, bta-mir-2285k-4, bta-mir-2284z-4, bta-mir-2285k-5, bta-mir-2284z-5, bta-mir-2284z-6, bta-mir-2284z-7, bta-mir-2284aa-4, bta-mir-2285q, bta-mir-2285r, bta-mir-2285s, bta-mir-2285t, bta-mir-2285b-2, bta-mir-2285v, bta-mir-2284z-2, mmu-let-7k, mmu-mir-126b, bta-mir-2285g-2, bta-mir-2285g-3, bta-mir-2285af-1, bta-mir-2285af-2, bta-mir-2285y, bta-mir-2285w, bta-mir-2285x, bta-mir-2285z, bta-mir-2285u, bta-mir-2285aa, bta-mir-2285ab, bta-mir-2284ab, bta-mir-2285ac, bta-mir-2285ad, bta-mir-2284ac, bta-mir-2285ae, chi-let-7a, chi-let-7b, chi-let-7c, chi-let-7d, chi-let-7e, chi-let-7f, chi-let-7g, chi-let-7i, chi-mir-103, chi-mir-107, chi-mir-1249, chi-mir-126, chi-mir-1306, chi-mir-130a, chi-mir-140, chi-mir-143, chi-mir-154a, chi-mir-154b, chi-mir-15b, chi-mir-16b, chi-mir-204, chi-mir-211, chi-mir-222, chi-mir-223, chi-mir-2284a, chi-mir-2284b, chi-mir-2284c, chi-mir-2284d, chi-mir-2284e, chi-mir-26a, chi-mir-26b, chi-mir-27a, chi-mir-29a, chi-mir-29c, chi-mir-301a, chi-mir-33a, chi-mir-340, chi-mir-34b, chi-mir-34c, chi-mir-379, chi-mir-409, chi-mir-455, chi-mir-499, chi-mir-99a, bta-mir-2285ag, bta-mir-2285ah, bta-mir-2285ai, bta-mir-2285aj, bta-mir-2285ak, bta-mir-2285al, bta-mir-2285am, bta-mir-2285ar, bta-mir-2285as-1, bta-mir-2285as-2, bta-mir-2285as-3, bta-mir-2285at-1, bta-mir-2285at-2, bta-mir-2285at-3, bta-mir-2285at-4, bta-mir-2285au, bta-mir-2285av, bta-mir-2285aw, bta-mir-2285ax-1, bta-mir-2285ax-2, bta-mir-2285ax-3, bta-mir-2285ay, bta-mir-2285az, bta-mir-2285an, bta-mir-2285ao-1, bta-mir-2285ao-2, bta-mir-2285ap, bta-mir-2285ao-3, bta-mir-2285aq-1, bta-mir-2285aq-2, bta-mir-2285ba-1, bta-mir-2285ba-2, bta-mir-2285bb, bta-mir-2285bc, bta-mir-2285bd, bta-mir-2285be, bta-mir-2285bf-1, bta-mir-2285bf-2, bta-mir-2285bf-3, bta-mir-2285bg, bta-mir-2285bh, bta-mir-2285bi-1, bta-mir-2285bi-2, bta-mir-2285bj-1, bta-mir-2285bj-2, bta-mir-2285bk, bta-mir-2285bl, bta-mir-2285bm, bta-mir-2285bn, bta-mir-2285bo, bta-mir-2285bp, bta-mir-2285bq, bta-mir-2285br, bta-mir-2285bs, bta-mir-2285bt, bta-mir-2285bu-1, bta-mir-2285bu-2, bta-mir-2285bv, bta-mir-2285bw, bta-mir-2285bx, bta-mir-2285by, bta-mir-2285bz, bta-mir-2285ca, bta-mir-2285cb, bta-mir-2285cc, bta-mir-2285cd, bta-mir-2285ce, bta-mir-2285cf, bta-mir-2285cg, bta-mir-2285ch, bta-mir-2285ci, bta-mir-2285cj, bta-mir-2285ck, bta-mir-2285cl, bta-mir-2285cm, bta-mir-2285cn, bta-mir-2285co, bta-mir-2285cp, bta-mir-2285cq, bta-mir-2285cr-1, bta-mir-2285cr-2, bta-mir-2285cs, bta-mir-2285ct, bta-mir-2285cu, bta-mir-2285cv-1, bta-mir-2285cv-2, bta-mir-2285cw-1, bta-mir-2285cw-2, bta-mir-2285cx, bta-mir-2285cy, bta-mir-2285cz, bta-mir-2285da, bta-mir-2285db, bta-mir-2285dc, bta-mir-2285dd, bta-mir-2285de, bta-mir-2285df, bta-mir-2285dg, bta-mir-2285dh, bta-mir-2285di, bta-mir-2285dj, bta-mir-2285dk, bta-mir-2285dl-1, bta-mir-2285dl-2, bta-mir-2285dm
Among these, 16 precursors were found amongst the 43 conserved between human, mouse, cow and goat in our analysis (let-7 g, mir-101-2, mir-103, mir-107, mir-128-1, mir-1306, mir-140, mir-15b, mir-16b, mir-211, mir-218-1, mir-26a-1, mir-32, mir-33a, mir-455, let-7-2), so the location of these precursors appears to be highly conserved in all vertebrates. [score:1]
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Other miRNAs from this paper: hsa-mir-10a, hsa-mir-195
J Neurooncol 14 Ujifuku K Mitsutake N Takakura S Matsuse M Saenko V 2010 miR-195, miR-455-3p and miR-10a(*) are implicated in acquired temozolomide resistance in glioblastoma multiforme cells. [score:1]
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MiR-9*, 1280, 9, 720 and 1308 were all decreased in RISC with a log2 fold change below −3 and miR-455-3p, 155 and 923 were decreased between −2 and −3 fold (Figure 2A). [score:1]
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75
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38547hsa-miR-210.0132.37583hsa-miR-310.02472.34642hsa-miR-70.0002042.32079hsa-miR-29b0.012.31852hsa-miR-5220.001522.29752hsa-miR-516a-5p0.01012.29596hsa-miR-33a0.02552.28197hsa-miR-1830.0009392.25637hsa-miR-340*2.43E-052.2503hsa-miR-449a0.002762.1729hsa-miR-200b0.01432.13023hsa-miR-455-3p0.003312.10618hsa-miR-4250.008892.05804hsa-miR-181a0.006882.05351hsa-miR-34a0.001552.0393hsa-miR-1000.005092. [score:1]
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