Evidence map›Paper›PMID 27472460›Full record

ArticleOncotarget2016

EZH2-mediated Puma gene repression regulates non-small cell lung cancer cell proliferation and cisplatin-induced apoptosis.

Haidan Liu, Wei Li, Xinfang Yu, Feng Gao, Zhi Duan, Xiaolong Ma, Shiming Tan, Yunchang Yuan, Lijun Liu, Jian Wang and 2 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.1field-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

33 citing papers in PubMed, 53 citations in OpenAlex.

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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

12 authors at 4 institutions in 2 countries.

Haidan LiuClinical Center for Gene Diagnosis and Therapy, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China.
Wei LiDepartment of Radiology, The Third Xiangya Hospital of Central South University, Changsha, Hunan, China.
Xinfang YuHunan Cancer Hospital and The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan, China.
Feng GaoDepartment of Ultrasonography, The Third Xiangya Hospital of Central South University, Changsha, Hunan, China.
Zhi DuanAlbert Einstein College of Medicine, Bronx, NY, USA.
Xiaolong MaDepartment of Cardiovascular Surgery, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China.
Shiming TanDepartment of Hemopathology, The Third Xiangya Hospital of Central South University, Changsha, Hunan, China.
Yunchang YuanDepartment of Thoracic Surgery, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China.
Lijun LiuClinical Center for Gene Diagnosis and Therapy, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China.
Jian WangClinical Center for Gene Diagnosis and Therapy, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China.
Xinmin ZhouDepartment of Cardiovascular Surgery, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China.
Yifeng YangClinical Center for Gene Diagnosis and Therapy, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China.
Central South University · CNSecond Xiangya Hospital of Central South University · CNAlbert Einstein College of Medicine · USHunan Cancer Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Polycomb group (PcG) proteins are highly conserved epigenetic effectors that maintain the silenced state of genes. EZH2 is the catalytic core and one of the most important components of the polycomb repressive complex 2 (PRC2). In non-small cell lung cancer (NSCLC) cells and primary lung tumors, we found that PRC2 components, including EZH2, are overexpressed. High levels of EZH2 protein were associated with worse overall survival rate in NSCLC patients. RNA interference mediated attenuation of EZH2 expression blunted the malignant phenotype in this setting, exerting inhibitory effects on cell proliferation, anchorage-independent growth, and tumor development in a xenograft mouse model. Unexpectedly, we discovered that, in the suppression of EZH2, p53 upregulated modulator of apoptosis (PUMA) expression was concomitantly induced. This is achieved through EZH2 directly binds to the Puma promoter thus epigenetic repression of PUMA expression. Furthermore, cisplatin-induced apoptosis of EZH2-knocking down NSCLC cells was elevated as a consequence of increased PUMA expression. Our work reveals a novel epigenetic regulatory mechanism controlling PUMA expression and suggests that EZH2 offers a candidate molecular target for NSCLC therapy and EZH2-regulated PUMA induction would synergistically increase the sensitivity to platinum agents in non-small cell lung cancers.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsAntineoplastic AgentsApoptosisApoptosis Regulatory ProteinsCarcinoma, Non-Small-Cell LungCell Line, TumorCell ProliferationCisplatinDown-RegulationEnhancer of Zeste Homolog 2 ProteinEpigenetic RepressionGene Knockdown TechniquesHEK293 CellsHumansLungAntineoplastic AgentsApoptosis Regulatory ProteinsBBC3 protein, humanCisplatinEnhancer of Zeste Homolog 2 ProteinEZH2 protein, humanProto-Oncogene ProteinsRNA, Small InterferingcisplatinEZH2non-small cell lung cancerpolycomb repressive complex 2PUMA

Identifiers

PMID27472460
PMCPMC5302918
OpenAlexW2481774055

What OpenQuestion holds

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LicenceCC BY
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.