Evidence map›Paper›PMID 24473398›Full record

ArticleBritish journal of cancer2014

Jumonji domain-containing protein 2B silencing induces DNA damage response via STAT3 pathway in colorectal cancer.

L Chen, L Fu, X Kong, J Xu, Z Wang, X Ma, Y Akiyama, Y Chen, J Fang

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2014. 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
2.0field-weighted citation impact, top 14% 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, 41 citations in OpenAlex.

  1. Review
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  8. LncRNAInternational journal of molecular sciences · 2021
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  12. EnterotoxigenicGut microbes · 2020
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  13. Histone H3K9 Demethylase JMJD2B Plays a Role in LXRα-Dependent Lipogenesis.International journal of molecular sciences · 2020
    Article
  14. Review
  15. Review
  16. Article
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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

9 authors at 3 institutions in 2 countries.

L ChenDivision of Gastroenterology and Hepatology, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University; Shanghai Institute of Digestive Disease; Key Laboratory of Gastroenterology and Hepatology, Ministry of Health, Shanghai Jiao Tong University, 145 Middle Shandong Road, Shanghai 200001, PR China.
L FuDivision of Gastroenterology and Hepatology, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University; Shanghai Institute of Digestive Disease; Key Laboratory of Gastroenterology and Hepatology, Ministry of Health, Shanghai Jiao Tong University, 145 Middle Shandong Road, Shanghai 200001, PR China.
X KongDivision of Gastroenterology and Hepatology, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University; Shanghai Institute of Digestive Disease; Key Laboratory of Gastroenterology and Hepatology, Ministry of Health, Shanghai Jiao Tong University, 145 Middle Shandong Road, Shanghai 200001, PR China.
J XuDivision of Gastroenterology and Hepatology, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University; Shanghai Institute of Digestive Disease; Key Laboratory of Gastroenterology and Hepatology, Ministry of Health, Shanghai Jiao Tong University, 145 Middle Shandong Road, Shanghai 200001, PR China.
Z WangDivision of Gastroenterology and Hepatology, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University; Shanghai Institute of Digestive Disease; Key Laboratory of Gastroenterology and Hepatology, Ministry of Health, Shanghai Jiao Tong University, 145 Middle Shandong Road, Shanghai 200001, PR China.
X MaDivision of Gastroenterology and Hepatology, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University; Shanghai Institute of Digestive Disease; Key Laboratory of Gastroenterology and Hepatology, Ministry of Health, Shanghai Jiao Tong University, 145 Middle Shandong Road, Shanghai 200001, PR China.
Y AkiyamaDepartment of Molecular Oncology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo 113-0034, Japan.
Y ChenDivision of Gastroenterology and Hepatology, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University; Shanghai Institute of Digestive Disease; Key Laboratory of Gastroenterology and Hepatology, Ministry of Health, Shanghai Jiao Tong University, 145 Middle Shandong Road, Shanghai 200001, PR China.
J FangDivision of Gastroenterology and Hepatology, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University; Shanghai Institute of Digestive Disease; Key Laboratory of Gastroenterology and Hepatology, Ministry of Health, Shanghai Jiao Tong University, 145 Middle Shandong Road, Shanghai 200001, PR China.
Shanghai Institute of Hematology · CNShanghai Jiao Tong University · CNTokyo Medical and Dental University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundJumonji domain-containing protein 2B (JMJD2B), directly targeted by hypoxia-inducible factor 1α, maintains the histone methylation balance important for the transcriptional activation of many oncogenes. Jumonji domain-containing protein 2B has been implicated in colorectal cancer (CRC) progression; however, the mechanism remains unclear.

methodsImmunofluorescence and western blotting detected phosphorylated histone H2AX, characteristic of double-strand breaks, and comet assay was used to investigate DNA damage, in CRC cells after JMJD2B small interfering RNA (siRNA) transfection. We assessed the resulting in vitro responses, that is, cell cycle progression, apoptosis, and senescence coupled with JMJD2B silencing-induced DNA damage, studying the regulatory role of signal transducers and activators of transcription 3 (STAT3). The JMJD2B silencing anti-cancer effect was determined using an in vivo CRC xenograft model.

resultsJumonji domain-containing protein 2B knockdown induced DNA damage via ataxia telangiectasia-mutated (ATM) and ATM and Rad3-related pathway activation, resulting in cell cycle arrest, apoptosis, and senescence in both normoxia and hypoxia. Signal transducers and activators of transcription 3 suppression by JMJD2B silencing enhanced DNA damage. Intratumoural injection of JMJD2B siRNA suppressed tumour growth in vivo and activated the DNA damage response (DDR).

conclusionsJumonji domain-containing protein 2B has an essential role in cancer cell survival and tumour growth via DDR mediation, which STAT3 partially regulates, suggesting that JMJD2B is a potential anti-cancer target.

Indexed as

AnimalsApoptosisAtaxia Telangiectasia Mutated ProteinsCell Cycle CheckpointsCell HypoxiaCell Line, TumorCell ProliferationCell SurvivalCellular SenescenceColorectal NeoplasmsDisease ProgressionDNA DamageDNA RepairGene Expression Regulation, NeoplasticHCT116 CellsHistonesAtaxia Telangiectasia Mutated ProteinsATM protein, humanH2AX protein, humanHIF1A protein, humanHistonesHypoxia-Inducible Factor 1, alpha SubunitJumonji Domain-Containing Histone DemethylasesKDM4B protein, humanRNA, Small InterferingSTAT3 protein, humanSTAT3 Transcription Factor

Identifiers

PMID24473398
PMCPMC3929886
OpenAlexW2010934271

What OpenQuestion holds

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LicenceCC BY-NC-SA
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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.