Evidence map›Paper›PMID 26233544›Full record

ArticleDigestive diseases and sciences2015

MiR-141 Inhibits Gastric Cancer Proliferation by Interacting with Long Noncoding RNA MEG3 and Down-Regulating E2F3 Expression.

Xiaoying Zhou, Guoping Ji, Xiquan Ke, Huiyuan Gu, Wujuan Jin, Guoxin Zhang

Abstract read
PubMed Publisher
In one paragraph

Article in Digestive diseases and sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
4.5field-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

37 citing papers in PubMed, 1 synthesis or guideline pooled it, 77 citations in OpenAlex.

  1. Perspectives of long non-coding RNAs in cancer.Molecular biology reports · 2017
    Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Long Noncoding RNA-Maternally Expressed Gene 3 Contributes to Hypoxic Pulmonary Hypertension.Molecular therapy : the journal of the American Society of Gene Therapy · 2019
    Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article
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 at 3 institutions in 1 country.

Xiaoying ZhouDepartment of Gastroenterology, First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, China.
Guoping JiDepartment of Gastroenterology, First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, China.
Xiquan KeDepartment of Gastroenterology, First Affiliated Hospital, School of Medicine, Xi'an Jiaotong University, Xi'an, 710061, Shanxi, China.
Huiyuan GuDepartment of Gastroenterology, First Affiliated Hospital of Soochow University, Suzhou, China.
Wujuan JinDepartment of Gastroenterology, First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, China.
Guoxin ZhangDepartment of Gastroenterology, First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, China. 15850668395@163.com.
Nanjing Medical University · CNFirst Affiliated Hospital of Xi'an Jiaotong University · CNSoochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMiR-141 and long noncoding RNA MEG3 have been independently reported to be tumor suppressor genes in various cancers. However, their expression has never been previously associated with gastric cancer (GC).

aimsTo investigate the interaction of miR-141 and MEG3 in GC.

methodsQRT-PCR was used to detect miR-141, MEG3, and E2F3 in gastric tissues and cells. CCK-8 and flow cytometry analysis were used to detect cell functions. Western blot and luciferase activity were used to identify E2F3 as one of the direct targets of miR-141.

resultsWe found that expression of both miR-141 and MEG3 was significantly reduced in GC compared with levels in matched nonmalignant tissues. Positive correlation between miR-141 and MEG3 was found in both tumor tissues and control tissues. Furthermore, the over-expression of either miR-141 or MEG3 in 7901 and MKN45 cells inhibited cell proliferation and cell cycle progression and promoted cell apoptosis. E2F3 was identified as a target of miR-141, and its inhibition significantly reduced MEG3 expression. E2F3 expression was also found to be negatively associated with both MEG3 and miR-141. E2F3 over-expression partly reversed the changes caused by transfection of miR-141 mimic, and inhibition of miR-141 or MEG3 overrides MEG3- or miR-141-induced modulation of cell growth in GC.

conclusionsThese findings together suggested that miR-141 could be interacting with MEG3 and targeting E2F3, and these factors may play important anti-tumor effects in GC pathogenesis and provide therapeutic targets in the clinics.

Indexed as

Cell ProliferationApoptosisCase-Control StudiesCell Cycle CheckpointsCell Line, TumorDown-RegulationE2F3 Transcription FactorFemaleGene Expression Regulation, NeoplasticHEK293 CellsHumansMaleMicroRNAsMiddle AgedRNA, Long NoncodingSignal TransductionE2F3 protein, humanE2F3 Transcription FactorMEG3 non-coding RNA, humanMicroRNAsMIRN141 microRNA, humanRNA, Long NoncodingCell cycleCell growthGastric cancerMEG3MiR-141

Identifiers

PMID26233544
OpenAlexW1899418860

What OpenQuestion holds

Textmetadata
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.