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7 publications mentioning mmu-mir-770

Open access articles that are associated with the species Mus musculus and mention the gene name mir-770. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

[+] score: 183
Other miRNAs from this paper: mmu-mir-185, mmu-mir-34a, mmu-mir-214, mmu-mir-421
To identify potential targets of miR-770-5p in miR-770-5p -mediated apoptosis, we analyzed our previous expression array data reflecting changes in global mRNA expression profiles upon IR exposure. [score:7]
Overexpression of miR-770-5p induced apoptosis, and elevation of miR-770-5p sensitized MCF7 breast carcinoma and A549 lung carcinomas to IR through direct targeting of PBK. [score:6]
In contrast, anti-770-5p -transfected cells showed restored expression levels of PBK post irradiation (Figure 5a), suggesting that miR-770-5p is a key factor in the regulation of PBK expression upon IR exposure. [score:6]
From the IR-responsive expression profile and bioinformatics analyses, we finally identified PBK as a strong candidate since it was both highly repressed by IR and shown to contain a target sequence for miR-770-5p in its 3′UTR. [score:5]
Specifically, miR-770-5p was shown to be highly expressed in type 2 diabetes mellitus patients, [24] whereas miR-770-5p was found to be downregulated in a rat mo del of temporal lobe epilepsy compared with the control group. [score:5]
These data indicate that miR-770-5p sensitized tumors to radiotherapy through the suppression of PBK expression. [score:5]
Because of the existence of multiple targets for a single miRNA, [11] we examined whether or not miR-770-5p exerts a proapoptotic effect through targeting of PBK. [score:5]
These data indicate that miR-770-5p suppresses PBK expression, resulting in tumor growth retardation. [score:5]
[22] Zhao et al. [25] reported very recently that miR-770-5p expression served as a prognostic biomarker and overexpression of miR-770-5p reduced survival in cisplatin -treated ovarian cancer cells. [score:5]
35, 36, 37 Consistent with the role of PBK in previous studies, this study suggests that PBK could be a useful therapeutic target for a sensitized IR response and could be achieved through ectopic expression of miR-770-5p. [score:5]
They showed that miR-770-5p inhibits cisplatin chemoresistance by targeting ERCC2 in vivo and in vitro in human ovarian cancer. [score:5]
These data demonstrate that miR-770-5p negatively regulates PBK expression through direct binding to its 3′UTR. [score:5]
PBK is a direct target of miR-770-5p. [score:4]
Despite numerous studies regarding the oncogenic potential of PBK, we report here for the first time that miR-770-5p can directly target PBK in the radiation response. [score:4]
In this study, we identified miR-770-5p as an upregulated miRNA in response to IR. [score:4]
These results indicate that miR-770-5p potentiates cell viability through direct targeting of PBK. [score:4]
Taken together, our data suggest that IR-responsive miR-770-5p plays a role in induction of apoptosis via regulation of PBK expression. [score:4]
To examine the physiological relationship between miR-770-5p and PBK in response to IR, we irradiated anti-miR-Con- and anti-miR-770-5p -transfected MCF7 cells and then examined level changes in PBK expression. [score:3]
Ectopic expression of miR-770-5p per se induces apoptosis. [score:3]
We tracked the extent of PBK expression in tumor tissues injected with miR-770-5p- and miR-Con -transfected cells. [score:3]
We also used miRSVR score [19] to predict potential miR-770-5p targets based on the microRNA. [score:3]
Western blot analysis demonstrated that PBK expression was attenuated in tumor tissues bearing miR-770-5p (Figure 7b). [score:3]
Ectopic expression of miR-770-5p per se induces apoptosisSince we observed profound decreases in relative cell number, and clonogenicity in miR-770-5p -transfected MCF7 and A549 cells, we examined whether or not miR-770-5p could affect cell death. [score:3]
When we performed immunoblot analysis, miR-770-5p evidently reduced the level of endogenous PBK, but had no effect on PBK expression from p3 × Flag-PBK-ORF (Figure 6b, bottom). [score:3]
pFluc-PBK-3′UTR-Mut harboring miR-770-5p seed region mutations (GTACTGG to GTAGTGC) was generated from pFluc-PBK-3′UTR-WT as a template with 5′-GCACTTFFAATTGTAGTGCGTTTTCTGTAAAG-3′ and 5′-CTTTACAGAAAACGCACTACAATTCCAAGTGC-3′ using a QuikChange Site-Directed Mutagenesis Kit (Agilent Technologies, Santa Clara, CA, USA). [score:3]
[33] RL reporter control plasmid (pRluc) was co -transfected into 293 T cells with pFluc, pFluc-PBK-3′UTR-Wt, or pFluc-PBK-3′UTR-Mut, together with miR-770-5p -expressing plasmid using FuGENE6 (Promega, Madison, WI, USA). [score:3]
Correlation between miR-770-5p and PBK mRNA levels in tumor tissues was normalized and assessed using the Pearson correlation coefficient, and the R-value indicated a negative correlation between miR-770-5p and PBK expression (R=−0.656). [score:3]
Flag-tagged PBK lacking its 3′UTR containing the target region of miR-770-5p (p3 × Flag-PBK-ORF) was generated and co -transfected with miR-770-5p into MCF7 cells. [score:3]
To confirm that reduction of PBK expression was due to the effects of miR-770-5p transfection in vivo, we analyzed miR-770-5p and PBK mRNA levels using quantitative reverse transcription-PCR (qRT-PCR) in tumor tissues (Figure 7c). [score:3]
Ectopic expression of miR-770-5p in tumor tissue exhibited retarded tumor growth in xenograft mo del mice. [score:3]
Alteration of miR-770-5p expression upon IR can be used not only as a promising method for improving the efficacy of cancer radiotherapy, but also as a biomarker for IR exposure. [score:3]
Collectively, our results suggest that miR-770-5p could be a potential target for the radiotherapy. [score:3]
Since there is no report regarding the cellular function of miR-770-5p, which was evidently induced by IR exposure, we decided to explore the roles of miR-770-5p and its target in the radiation response. [score:3]
Plasmid expressing hsa-miR-770-5p was generated using genomic DNA from A549 cell lines as a template, as well as 5′-atgcctcgagAAAGTGGGGTGCTCAGGAAT-3′ and 5′-atgcgcggccgcGGAGAAGCTTCAGCAGGTGT-3′ as primers. [score:2]
To verify whether or not miR-770-5p regulates PBK expression, we evaluated changes in PBK level after transfection of miR-770-5p. [score:2]
MiR-770-5p -induced cell death was evidently reduced by ectopic expression of p3 × Flag-PBK-ORF (Figure 6b, top). [score:2]
These data demonstrate that miR-770-5p plays a critical role in enhancing radiosensitivity via PBK regulation in tumor cells. [score:2]
Combination treatment group (miR-770-5p+IR) significantly suppressed tumor growth compared to other groups of mice (miR-Con, miR-770-5p, and miR-Con+IR) (Figure 8a). [score:2]
MiR-770-5p retards tumor growth in a xenograft tumor mouse mo del through PBK targeting. [score:2]
MiR-770-5p is an IR-inducible suppressor of cancer cell survival. [score:2]
Plot of the miR-770-5p and PBK mRNA levels from each tumor tissue showed distinct clustering (Figure 7d). [score:1]
However, we showed that miR-770-5p renders radiosensitivity through blockade of the PBK signaling pathway. [score:1]
Trypan Blue exclusion assay showed that ectopic expression of miR-770-5p induced cell death in both MCF7 and A549 cells compared to that in miR-Con -transfected cells (Figure 3a). [score:1]
Reconstitution of PBK rescues tumor cells from miR-770-5p -induced cell death. [score:1]
To explore the biological significance of our in vitro observations, we examined the role of miR-770-5p in a xenograft tumor mouse mo del. [score:1]
In the same way, cells were transfected with either anti-miR-770-5p or anti-miR control. [score:1]
Thus, further increasing the miR-770-5p level in IR-exposed cells can likewise increase the radiosensitivity of tumor cells to IR. [score:1]
Next, MCF7 cells were transfected with either miR-770-5p or anti-miR-770-5p, followed by IR exposure at the indicated doses, as shown in Figures 5b and c. Whereas miR-770-5p further reduced clonogenic ability, anti-miR-770-5p increased clonogenic ability post irradiation (Figures 5b and c). [score:1]
Levels of PBK mRNA and protein were evidently decreased and PARP cleavage was observed in miR-770-5p -transfected HCT116 cells (Supplementary Figure S2). [score:1]
Increased levels of miR-770-5p were confirmed with qRT-PCR at 3 days after transfection in MCF7 and A549 cells (Figure 2b). [score:1]
For xenograft mice mo del experiment to examine effect of miR-770-5p on tumor growth, HCT116 cells (5 × 10 [6]) transfected with 100 nM of miR-Con or miR-770-5p were injected subcutaneously into the lateral hind leg of 6-week-old immunodeficient BALB/c female nude mice (nu/nu; Orient Bio Inc. [score:1]
We also examined PBK level and PARP cleavage in miR-770-5p -transfected HCT116 human colon carcinoma cells (Supplementary Figure S2). [score:1]
We detected an increase in PARP cleavage, a general marker of apoptosis, in a dose -dependent manner of miR-770-5p in both MCF7 and A549 cells at 72 h after transfection (Figure 3b). [score:1]
Since we observed profound decreases in relative cell number, and clonogenicity in miR-770-5p -transfected MCF7 and A549 cells, we examined whether or not miR-770-5p could affect cell death. [score:1]
After confirmation of increased miR-770-5p levels, we examined PBK mRNA and protein levels in miR-770-5p -transfected cells (Figures 4b and c). [score:1]
And then, we injected 10 nM of miR-770-5p to the whole tumor mass and locally exposed 2 Gy of IR to xenograft tumor 1 day after injection. [score:1]
As based on small RNA-seq from ENCODE Database, we identified strong negative correlation between miR-770-5p and PBK (correlation coefficient (r) value was −0.67). [score:1]
Next, since we wanted to know whether miR-770-5p could sensitize tumors to IR in vivo, we developed a xenograft tumor mouse mo del and allowed to form tumor. [score:1]
We searched deep sequencing online data to demonstrate correlation between miR-770-5p and PBK in human tissues (miRGator. [score:1]
MiR-770-5p levels were increased in dose -dependent manner in miR-770-5p -transfected MCF7 and A549 cells (Figure 3c). [score:1]
First, we transfected miR-770-5p mimic into MCF7 cells, and examined relative cell number and clonogenicity. [score:1]
Our findings suggest that IR -induced miR-770-5p potentiates IR sensitivity by promoting apoptotic cell death. [score:1]
PBK harbors a miR-770-5p seed-matched sequence in its 3′UTR, as illustrated in Figure 4d. [score:1]
Effects of miR-770-5p and anti-miR-770-5p transfection on intracellular miR-770-5p levels were validated in non-irradiated and irradiated MCF7 cells (Figures 5a–c). [score:1]
Among them, miR-770-5p, miR-1287, and miR-371-5p exhibited evident induction at every time point post irradiation (2, 8, and 24 h) (Figure 1a). [score:1]
We suggest that miR-770-5p is a promising agent to improve the efficacy of cancer radiotherapy. [score:1]
Cells were transfected with miR-770-5p mimic or mimic control (GenoExplorer) using Lipofectamine RNAiMAX (Invitrogen, Karlsruhe, Germany). [score:1]
When the tumor reached an average volume of ~200 mm [3], 10 nM of miR-Con or miR-770-5p with AteloGenes Local Use (KOKEN, Tokyo, Japan) was injected to wrap up the whole tumor mass. [score:1]
Correlation between PBK mRNA and miR-770-5p levels in tumors was assessed using Pearson's correlation coefficient analysis. [score:1]
Since we applied low concentration of miR-770-5p (10 nM) and low dose of IR (2 Gy) once to evaluate the combination effect of mIR-770-5p and IR, no marked change of either miR-770-5p or PBK expression was observed in either IR- or miR-770-5p -treated groups (Figures 8b and c). [score:1]
We next generated reporters containing the firefly luciferase gene followed by either wild-type or mutated PBK-3′UTR in the putative miR-770-5p -binding site (PBK-3′UTR-Wt or PBK-3′UTR-Mut) (Figure 4d). [score:1]
We also demonstrated an inverse correlation between miR-770-5p and PBK both in vitro and in vivo. [score:1]
In analysis from TCGA-breast invasive carcinoma Database, r-value between miR-770-5p and PBK was −0.31. [score:1]
For xenograft mice mo del experiment to examine combination effect of miR-770-5p and IR on tumor growth, HCT116 cells (5 × 10 [6]) were injected subcutaneously into the lateral hind leg of 6-week-old immunodeficient BALB/c female nude mice (nu/nu; Orient Bio Inc. ) [score:1]
Negative correlation between miR-770-5p and PBK (R=−0.356) was appeared as shown in Figure 8d. [score:1]
We assessed level changes of miR-770-5p, miR-1287, and miR-371-5p at 2, 8, and 24 h post irradiation by qRT-PCR in MCF7 cells (Figure 1c). [score:1]
[14] Until now, three papers regarding miR-770-5p have been reported. [score:1]
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[+] score: 71
As this miRNA is mainly expressed in the brain and spinal cord (Figure S1B), we hypothesized that the virus could have evolved to suppress these target sequences, thus avoiding the restriction imposed by miR-770-3p on viral replication in the central nervous system. [score:7]
Generation of L929 Cells Overexpressing miR-770-3p and Construction of a miR-142-3p Expressing Vector. [score:5]
The most under-represented miRNA target sequence in the TMEV genome (miR-770-3p) was absent from the viral genome and occurred at a mean frequency of 1.39 in randomly generated sequences coding the same protein, the probability to find 0 miR-770-3p target sequence in random sequences being 0.24. [score:5]
Expression of miR-770-3p was not detected in L929 cells and was upregulated > 271 ± 68 times in the cell populations transduced with ADC48 as compared to background. [score:5]
RT-qPCR was used to assess the expression of miR-770-3p in transduced and mock-transduced L929 cells, using Taqman [®] MiRNA Reverse Transcription Kit and Taqman [®] Gene Expression Master Mix (Applied Biosystems-Thermofisher, Erembodegem, Belgium). [score:5]
In addition, overexpression of a shRNA corresponding to miR-770-3p in L929 cells did not significantly affect replication of TMEV mutants where predicted miR-770-3p target sequences were introduced. [score:5]
As shown in Figure 1C, the presence of miR-770-3p target sequences in the viral genome did not restrict viral replication in cells expressing this miRNA (Figure 1C). [score:5]
The target site sequences thus introduced in the viral genome were those predicted for one of the randomly generated virus sequence (see below) that contained 3 miR-770-3p target sites (5′-CCGGCAGUGUCGUCCACG-3′, 5′-UUGCGCCGAACAGUCGCCCAUG-3′, 5′-CCGUGUCACGGCACGCUUACG-3′). [score:5]
com/1999-4915/8/3/75/s1, Figure S1: Distribution of the number of predicted miR-770-3p targets in viral genomes and expression of miR-770-3p and miR-709 in mouse tissues. [score:5]
A KJ6 derivative (ADC43) was constructed in which 3 miR-770-3p target sequences were introduced by site-directed mutagenesis. [score:4]
To investigate this hypothesis, we generated L929 cells that over-express miR-770-3p and constructed a TMEV mutant virus, ADC43, where 3 predicted miR-770-3p target sites were introduced by site-directed mutagenesis. [score:4]
Control plasmids pADC62 and pADC64 were obtained similarly by cloning 4 tandem miR-770-3p or mirR-142-3p target sequences that carry point mutations preventing their recognition by their cognate miRNA (Table 2). [score:4]
Expression of miR-770-3p was quantified by RT-qPCR in different tissues of C57BL/6 mice, using 10 ng of total RNA prepared previously [32]. [score:3]
The miR-770-3p target sequence was the most under-represented in TMEV genome (no occurrence in TMEV and a mean of 1.39 occurrences in the 100 randomly generated sequences) (Figure S1A). [score:3]
1, which drives the expression of a sequence corresponding to miR770-3p from a RNA polymerase III promoter [39]. [score:3]
In the 3′ UTR region of the Renilla luciferase gene, we subcloned a BsiWI/ XbaI fragment carrying 4 tandem target sequences for miR-770-3p and miR-142-3p, yielding plasmids pADC30 and pADC39, respectively. [score:3]
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[+] score: 15
If these genes are bona fide targets, loss of miR-770 that occurs in the associated pUPD syndromes could contribute to the observed phenotypes by increasing the levels of its targeted genes, many of which are implicated in placental, bone, and muscle biology. [score:5]
Meg3/Gtl2: Imprinting, Expression, and miR-770 Figure 4A shows that Meg3/Gtl2 is maternally expressed using an identified Alw26I restriction site polymorphism between CzechII/Ei and 129S1 mice. [score:5]
Meg3/Gtl2: Imprinting, Expression, and miR-770. [score:3]
In addition, Meg3/Gtl2 contains in its last intron (Relative to Accession number Y13832) the evolutionarily conserved microRNA miR-770 (see Figure 2 and Table 2). [score:1]
org/microrna/) Meg3mmu-miR-770 # Bmp1, Bmp15, Capn3, Casq2, Fosb, Lmna, Mb, Obscn, Peg10, Ppp1ca, Sspn, Tmod1, Trp53 Unidentified mmu-miR-673 Camk2a, Camk2b, Camk2d, Camk2g, Dnmt1, Mtpn, Myh6, Ndn, Pax3, Rbl1, Sln, Tnnt1, Wnt1 Unidentifiedmmu-miR-493 # Cacng5, Camk2g, Cdkn1c, Ctcf, Dag1, Fhl1, Fos, Hras1, Jun, Mib2, Mtap, Peg10, Shh, Tmod1 Unidentifiedmmu-miR-337 # Capza2, Des, Dmd, Dnmt3a, Myh8, Mypn, Nfatc1, Plagl2, Pvalb, Sgcb, Snta1, Tpm3, Trp53 Unidentified mmu-miR-540 Akt3, Bmp2, Bmp7, Capzb, Emd, Itga7, Itgb1, Msc, Myog, Nkx2-5, Pten, Rhoa, Sln, Tlx1, Vim Unidentifiedmmu-miR-665 # Casq2, Igf2, Junb, Ldb3, Peg10, Magel2, Nnat, Pax3, Ryr1, Sntb2, Tln1, Tpm2, Trp53, TtnAnti-Peg11 $ mmu-miR-431 # d Camk2b, Casq1, Dtna, E2f1, Fgf4, Gata3, Igf1, Kit, Max, Peg10, Plagl2, Ppp3r1, Sgcd, Tcf21Anti-Peg11 $ mmu-miR-433 # Bmpr1b, Capza1, Creb1, Ctcf, E2f3, Gata6, Isl1, Jak2, Myh9, Peg10, Plagl2, Ppp3r1, Sntg1Anti-Peg11 $ mmu-miR-127 # d e Auts2, Bcl6, Camk2d, Cdc42, Creb5, E2f3, Igf2, Myo1c, Otx1, Plagl2, Pitx2. [score:1]
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[+] score: 11
Among those miRNAs showing increased expression in the HF fed offspring, histone 4 H4 is a common target for 5 different miRNAs (miR-503*, miR-770-3p, miR-369-3p, miR-197 and miR-667, Fig. 1). [score:5]
However, among those showing increased expression measured with microarray, miR-667, miR-207, miR-197, miR-770-3p and miR-369-3p were very poorly expressed (data not shown). [score:3]
Histone 4 H4 are predicted targets for 5 miRNAs (miR-503*, miR-770-3p, miR-369-3p, miR-197 and miR-667) showing increased levels in maternal HF fed offspring. [score:3]
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[+] score: 3
Nrf2 (+/+) Saline—Nrf2(–/–) Saline miR-128, miR-7a, miR-669c, miR-298, miR-543, miR-770-5p, miR-669b* and miR-544-5p S1 Changes in miRNA expression profile after exposure to paraquat. [score:3]
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[+] score: 1
When a uniform signal was visible across the entire section, the pattern was defined 'ubiquitous' (ubi) (e. g. miR-127 in P0 head and miR-770-3p in P60 eye; Figure 2). [score:1]
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[+] score: 1
According to the microRNA microarray analysis, the first nine highly expressed miRNAs (miR-883b-5p, miR-666-3p, miR-770-5p, miR-804, miR-540-3p, miR-882, miR-125b-5p, miR-450b-3p, and miR-151-3p) were selected out for further investigation. [score:1]
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