Evidence map›Paper›PMID 26824182›Full record

ArticleOncotarget2016

MiR-129 triggers autophagic flux by regulating a novel Notch-1/ E2F7/Beclin-1 axis to impair the viability of human malignant glioma cells.

Xiong Chen, Yingying Zhang, Yingying Shi, Haiwei Lian, Huilin Tu, Song Han, Jun Yin, Biwen Peng, Beiyan Zhou, Xiaohua He and 1 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
7.4field-weighted citation impact, top 2% 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

25 citing papers in PubMed, 53 citations in OpenAlex.

  1. Regulation of autophagy by non-coding RNAs in human glioblastoma.Medical oncology (Northwood, London, England) · 2024
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  15. LncRNA MALAT1/miR-129 axis promotes glioma tumorigenesis by targeting SOX2.Journal of cellular and molecular medicine · 2018
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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

11 authors at 3 institutions in 2 countries.

Xiong ChenSchool of Basic Medical Sciences, Wuhan University, Wuhan 430071, China.
Yingying ZhangSchool of Basic Medical Sciences, Wuhan University, Wuhan 430071, China.
Yingying ShiSchool of Basic Medical Sciences, Wuhan University, Wuhan 430071, China.
Haiwei LianDepartment of Neurosurgery, Wuhan University Renmin Hospital, Wuhan 430060, China.
Huilin TuSchool of Basic Medical Sciences, Wuhan University, Wuhan 430071, China.
Song HanSchool of Basic Medical Sciences, Wuhan University, Wuhan 430071, China.
Jun YinSchool of Basic Medical Sciences, Wuhan University, Wuhan 430071, China.
Biwen PengSchool of Basic Medical Sciences, Wuhan University, Wuhan 430071, China.
Beiyan ZhouDepartment of Veterinary Physiology and Pharmacology, College of Veterinary Medicine and Biomedical Sciences, Texas A & M University, Texas 77843, USA.
Xiaohua HeSchool of Basic Medical Sciences, Wuhan University, Wuhan 430071, China.
Wanhong LiuSchool of Basic Medical Sciences, Wuhan University, Wuhan 430071, China.
Wuhan University · CNHubei Provincial Center for Disease Control and Prevention · CNTexas A&M University · US

Funding

MicroRNA Regulated Macrophage Polarization in Adipose Tissue InflammationR01DK098662 · NIDDK · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI ZHOU, BEIYAN · 2013 to 2017
$1.6M
NIDDK NIH HHS R01 DK098662
6 · The paper itself

Abstract

Abnormalities of autophagy have been implicated in an increasing number of human cancers, including glioma. To date, there is a wealth of evidence indicating that microRNAs (miRNAs) contribute significantly to autophagy in a variety of cancers. Previous studies have suggested that miR-129 functioned as an important inhibitor of the cell cycle and could promote the apoptosis of many cancer cell lines in vitro. Here, we reported that miR-129 acted as a potent inducer of autophagy. Forced expression of miR-129 could induce autophagic flux by targetedly suppressing Notch-1 in glioma cells. The autophagy induced by miR-129 could restrain the activity of mammalian target of rapamycin (mTOR) and upregulate Beclin-1. Moreover, we demonstrated that E2F transcription factor 7 (E2F7) could also trigger autophagic flux by upregulating Beclin-1 and mediating miR-129-induced autophagy. Additionally, knockdown of Notch-1 could upregulate the expression of E2F7, whereas downregulation of E2F7 alleviated shNotch-1-induced autophagic flux. In particular, knockdown of endogenous Beclin-1 could effectively reduce autophagic flux stimulated by miR-129 and E2F7. Interestingly, upon attenuation of miR-129- or E2F7-triggered autophagic flux rescued cell viability suppressed by them. More importantly, intratumoral injection of pHAGE-miR-129 lentivirus in a nude mouse xenograft model significantly restrained tumor growth and triggered autophagy. In conclusion, these findings identify a new function for miR-129 as a potent inducer of autophagy through a novel Notch-1/E2F7/Beclin-1 axis in glioma.

Indexed as

AnimalsAutophagyBeclin-1Cell LineE2F7 Transcription FactorGliomaHEK293 CellsHumansMiceMice, NudeMicroRNAsNeoplasm TransplantationReceptor, Notch1RNA InterferenceRNA, Small InterferingTOR Serine-Threonine KinasesBeclin-1BECN1 protein, humanE2F7 protein, humanE2F7 Transcription FactorMicroRNAsMirn129 microRNA, humanMTOR protein, humanNOTCH1 protein, humanReceptor, Notch1RNA, Small InterferingTOR Serine-Threonine KinasesautophagyE2F7gliomamiR-129Notch-1

Identifiers

PMID26824182
PMCPMC4891036
OpenAlexW2274453784

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.