Evidence map›Paper›PMID 26507454›Full record

ArticleScientific reports2015

miR-346 and miR-138 competitively regulate hTERT in GRSF1- and AGO2-dependent manners, respectively.

Ge Song, Renjie Wang, Junfei Guo, Xuyuan Liu, Fang Wang, Ying Qi, Haiying Wan, Min Liu, Xin Li, Hua Tang

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 1 pooled it
4.1field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

44 citing papers in PubMed, 1 synthesis or guideline pooled it, 81 citations in OpenAlex.

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  20. Androgen Receptor-Related Non-coding RNAs in Prostate Cancer.Frontiers in cell and developmental biology · 2021
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 1 institution in 1 country.

Ge SongTianjin Life Science Research Center, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Renjie WangTianjin Life Science Research Center, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Junfei GuoTianjin Life Science Research Center, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Xuyuan LiuTianjin Life Science Research Center, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Fang WangTianjin Life Science Research Center, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Ying QiTianjin Life Science Research Center, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Haiying WanTianjin Life Science Research Center, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Min LiuTianjin Life Science Research Center, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Xin LiTianjin Life Science Research Center, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Hua TangTianjin Life Science Research Center, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Tianjin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

miRNAs typically downregulate the expression of target genes by binding to their 3'UTR, and dysregulation of miRNAs may contribute to tumorigenesis. Here, we found that miR-346 and miR-138 competitively bind to a common region in the 3'UTR of hTERT mRNA and have opposite effects on the expression and function of hTERT in human cervical cancer cells. Furthermore, G-rich RNA sequence binding factor 1 (GRSF1) mediates the miR-346-dependent upregulation of hTERT by binding to the miR-346 middle sequence motif (CCGCAU) which forms a "bulge loop" when miR-346 is bound to the hTERT 3'UTR, facilitating the recruitment of hTERT mRNA to ribosomes to promote translation in an AGO2-independent manner. Conversely, miR-138 suppresses hTERT expression in an AGO2-dependent manner. Interestingly, replacement of the miR-138 middle sequence with that of miR-346 results in an upregulation of hTERT expression in a GRSF1-dependent manner. Moreover, miR-346 depends on GRSF1 to upregulate another target gene, activin A receptor, type IIB (ACVR2B), in which miR-346 "CCGCAU" motif is essential. These findings reveal novel mechanisms of miRNA-mediated upregulation of target gene expression and describe the coordinated action of multiple miRNAs to control the fate of a single target mRNA through binding to its 3'UTR.

Indexed as

3' Untranslated RegionsAnimalsArgonaute ProteinsCell Line, TumorDown-RegulationFemaleGene Expression Regulation, NeoplasticHeLa CellsHumansMice, Inbred BALB CMice, NudeMicroRNAsPoly(A)-Binding ProteinsTelomerase3' Untranslated RegionsAGO2 protein, humanArgonaute ProteinsGRSF1 protein, humanMicroRNAsMIRN138 microRNA, humanMIRN346 microRNA, humanPoly(A)-Binding ProteinsTelomeraseTERT protein, human

Identifiers

PMID26507454
PMCPMC4623477
OpenAlexW2265434753

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LicenceCC BY
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.