Evidence map›Paper›PMID 24896240›Full record

ArticlePloS one2014

Histone deacetylase HDAC4 promotes gastric cancer SGC-7901 cells progression via p21 repression.

Zhen-Hua Kang, Chun-Yan Wang, Wen-Liang Zhang, Jian-Tao Zhang, Chun-Hua Yuan, Ping-Wei Zhao, Yu-Yang Lin, Sen Hong, Chen-Yao Li, Lei Wang

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

42 citing papers in PubMed, 82 citations in OpenAlex.

  1. Article
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  3. Mechanisms of HDACs in cancer development.Frontiers in immunology · 2025
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  15. Review
  16. Article
  17. Autophagy · 2020
    Article
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  19. Article
  20. Long Noncoding RNAOncoTargets and therapy · 2020
    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

10 authors at 3 institutions in 1 country.

Zhen-Hua KangDepartment of Colorectal and Anus Surgery, First Hospital, Jilin University, Changchun, P. R. China.
Chun-Yan WangThe Tumor Research Institute of JiLin Province, Changchun, P. R. China.
Wen-Liang ZhangDepartment of Colorectal and Anus Surgery, First Hospital, Jilin University, Changchun, P. R. China.
Jian-Tao ZhangDepartment of Colorectal and Anus Surgery, First Hospital, Jilin University, Changchun, P. R. China.
Chun-Hua YuanDepartment of Colorectal and Anus Surgery, First Hospital, Jilin University, Changchun, P. R. China.
Ping-Wei ZhaoDepartment of Colorectal and Anus Surgery, First Hospital, Jilin University, Changchun, P. R. China.
Yu-Yang LinDepartment of Colorectal and Anus Surgery, First Hospital, Jilin University, Changchun, P. R. China.
Sen HongDepartment of Colorectal and Anus Surgery, First Hospital, Jilin University, Changchun, P. R. China.
Chen-Yao LiDepartment of Colorectal and Anus Surgery, First Hospital, Jilin University, Changchun, P. R. China.
Lei WangDepartment of Colorectal and Anus Surgery, First Hospital, Jilin University, Changchun, P. R. China.
First Hospital of Jilin University · CNJilin University · CNJilin Province Tumor Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gastric cancer (GC) is one of the leading causes of cancer death in the world. The role of histone deacetylase 4 (HDAC4) in specific cell and tissue types has been identified. However, its biological roles in the development of gastric cancer remain largely unexplored. Quantitative real time PCR (qRT-PCR) and western blot were used to analyze the expression of HDAC4 in the clinical samples. siRNA and overexpression of HDAC4 and siRNA p21 were used to study functional effects in a proliferation, a colony formation, a adenosine 5'-triphosphate (ATP) assay and reactive oxygen species(ROS) generation, cell cycle, cell apoptosis rates, and autophagy assays. HDAC4 was up-regulated in gastric cancer tissues and several gastric cancer cell lines. The proliferation, colony formation ability and ATP level were enhanced in HDAC4 overexpression SGC-7901 cells, but inhibited in HDAC4 knockdown SGC-7901 cells. HDAC4 knockdown led to G0/G1 phase cell arrest and caused apoptosis and ROS increase. Moreover, HDAC4 was found to inhibit p21 expression in gastric cancer SGC-7901 cells. p21 knockdown dramatically attenuated cell proliferation inhibition, cell cycle arrest, cell apoptosis promotion and autophagy up-regulation in HDAC4-siRNA SGC-7901 cells. We demonstrated that HDAC4 promotes gastric cancer cell progression mediated through the repression of p21. Our results provide an experimental basis for understanding the pro-tumor mechanism of HDAC4 as treatment for gastric cancer.

Indexed as

Gene Expression Regulation, NeoplasticAdenosine TriphosphateAgedApoptosisCase-Control StudiesCell Cycle CheckpointsCell Line, TumorCell ProliferationCyclin-Dependent Kinase Inhibitor p21Histone DeacetylasesHumansMiddle AgedReactive Oxygen SpeciesRepressor ProteinsStomach NeoplasmsTumor Stem Cell AssayAdenosine TriphosphateCyclin-Dependent Kinase Inhibitor p21HDAC4 protein, humanHistone DeacetylasesReactive Oxygen SpeciesRepressor Proteins

Identifiers

PMID24896240
PMCPMC4045860
OpenAlexW2074636474

What OpenQuestion holds

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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.