Evidence map›Paper›PMID 26858085›Full record

ArticleTechnology in cancer research & treatment2017

Enhancement of Proliferation and Invasion of Gastric Cancer Cell by KDM5C Via Decrease in p53 Expression.

Liming Xu, Wei Wu, Guilian Cheng, Mingjie Qian, Kewei Hu, Guojian Yin, Shaofeng Wang

RetractedOpen access · hybridAbstract readRetracted Publication
In one paragraph

Article in Technology in cancer research & treatment, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 17% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Targeting epigenetic regulators to overcome drug resistance in cancers.Signal transduction and targeted therapy · 2023
    Review
  8. Article
  9. The Chromatin-Oxygen Sensor GeneInternational journal of molecular sciences · 2022
    Article
  10. Review
  11. Article
  12. Article
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  15. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Liming Xu1 Department of gastroenterology, the Second Affiliated Hospital of Soochow University, Soochow, China.
Wei Wu1 Department of gastroenterology, the Second Affiliated Hospital of Soochow University, Soochow, China.
Guilian Cheng1 Department of gastroenterology, the Second Affiliated Hospital of Soochow University, Soochow, China.
Mingjie Qian1 Department of gastroenterology, the Second Affiliated Hospital of Soochow University, Soochow, China.
Kewei Hu1 Department of gastroenterology, the Second Affiliated Hospital of Soochow University, Soochow, China.
Guojian Yin1 Department of gastroenterology, the Second Affiliated Hospital of Soochow University, Soochow, China.
Shaofeng Wang1 Department of gastroenterology, the Second Affiliated Hospital of Soochow University, Soochow, China.
Soochow University · CNSecond Affiliated Hospital of Soochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gastric cancer is a malignancy with high incidence and the second leading cause of cancer death worldwide. Development of efficient therapies against gastric cancer is urgent. Until now, the mechanisms of gastric cancer genesis remain elusive. The KDM5C is a histone demethylase that promotes cancer cell growth and is enriched in drug-resistant cancer cells. But the pathogenic breadth and mechanistic aspects of this effect relative to gastric cancer have not been defined. In present study, we found that KDM5C was overexpressed in gastric cancer cell lines and gastric cancer tissues but not in normal gastric tissues. The proliferation and invasive potential of gastric cancer cells was significantly increased by ectopic expression of KDM5C. Contrarily, RNA interference targeting KDM5C in gastric cancer cells significantly decreased the proliferation and invasive potential of cells. Moreover, we also found that the expression of p53 was modulated by KDM5C. Cells with overexpression of KDM5C exhibited greatly decreased p53 expression, whereas silencing of KDM5C expression dramatically increased p53 expression at both the messenger RNA and protein levels. Inhibition of p53 by small-interfering RNA reversed the shKDM5C-induced proliferation and invasion. Our results collectively suggested that KDM5C played a role in gastric cancer cells proliferation and invasion, which may be partly associated with the p53 expression.

Indexed as

Gene Expression Regulation, NeoplasticBiomarkersCell Line, TumorCell MovementCell ProliferationHistone DemethylasesHumansNeoplasm InvasivenessNeoplasm MetastasisStomach NeoplasmsTumor Suppressor Protein p53BiomarkersHistone DemethylasesKDM5C protein, humanTumor Suppressor Protein p53gastric cancerinvasionKDM5Cp53proliferation

Identifiers

PMID26858085
PMCPMC5616025
OpenAlexW2287534161

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.