Evidence map›Paper›PMID 28595907›Full record

ArticleBiochemical and biophysical research communications2017

miR-141-3p functions as a tumor suppressor modulating activating transcription factor 5 in glioma.

Mengyuan Wang, Ming Hu, Zhaohua Li, Dongmeng Qian, Bin Wang, David X Liu

Abstract read
In one paragraph

Article in Biochemical and biophysical research communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
–field-weighted citation impact
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

22 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Review
  6. Review
  7. Review
  8. Review
  9. Study on effects of miR-141-3p in proliferation, migration, invasion and apoptosis of colon cancer cells by inhibiting Bcl2.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2021
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Long Non-Coding RNA (lncRNA) CRNDE Regulated Lipopolysaccharides (LPS)-Induced MRC-5 Inflammation Injury Through Targeting MiR-141.Medical science monitor : international medical journal of experimental and clinical research · 2020
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. The miR-200 family: multiple effects on gliomas.Cancer management and research · 2018
    Review
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

6 authors.

Mengyuan WangDepartment of Microbiology, College of Life Sciences, Qingdao University Shandong 266071, PR China.
Ming HuDepartment of Basic Medical Sciences, Qingdao University, Shandong 266071, China.
Zhaohua LiDepartment of Basic Medical Sciences, Qingdao University, Shandong 266071, China.
Dongmeng QianDepartment of Basic Medical Sciences, Qingdao University, Shandong 266071, China. Electronic address: qiandongmeng@sina.com.
Bin WangDepartment of Basic Medical Sciences, Qingdao University, Shandong 266071, China. Electronic address: wangbinmedical@163.com.
David X LiuDepartment of Pharmaceutical Sciences, Washington State University College of Pharmacy, Riverpoint Blvd Spokane, WA 992082, USA.

Funding

Mechanism of ATF5 addition in breast cancerR15CA205375 · NCI · WASHINGTON STATE UNIVERSITY · PI LIU, DAVID X · 2017 to 2017
$453k
NCI NIH HHS R15 CA205375
6 · The paper itself

Abstract

Glioma is the most common malignant primary brain tumor which arises from the central nervous system. Our studies reported that an anti-apoptotic factor, activating transcription factor 5 (ATF5), is highly expressed in malignant glioma specimens and cell lines. Downregulation by dominant-negetive ATF5 could repress glioma cell proliferation and accelerate apoptosis. Here, we further investigate the upstream factor which regulates ATF5 expression. Bioinformatic analysis showed that ATF5 was a potential target of miR-141-3p. Luciferase reporter assay verified that miR-141-3p specifically targeted the ATF5 3'-UTR in glioma cells. Functional studied suggested that miR-141-3p overexpression inhibited proliferation and promoted apoptosis of glioma cells (U87MG and U251). Xenograft experiments proved the inhibition of miR-141-3p on glioma growth in vivo. Moreover, exogenous ATF5 without 3'-UTR restored the cell proliferation inhibition triggered by miR-141-3p. Taken together, we put forward that miR-141-3p is a new upstream target towards ATF5. It can serve as a crucial tumor suppressor in regulating the ATF5-regulated growth of malignant glioma.

Indexed as

Antineoplastic AgentsApoptosisCCAAT-Enhancer-Binding Protein-betaCell Line, TumorCell ProliferationDrug Screening Assays, AntitumorGliomaHumansMicroRNAsStructure-Activity RelationshipAntineoplastic AgentsCCAAT-Enhancer-Binding Protein-betaCEBPB protein, humanMicroRNAsMIRN141 microRNA, humanActivating transcription factor 5ApoptosisCell proliferationGliomamiR-141-3p

Identifiers

PMID28595907
PMCPMC5759330

What OpenQuestion holds

Textmetadata
LicenceTDM
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.