Evidence map›Paper›PMID 27092879›Full record

ArticleOncotarget2016

EZH2-mediated repression of GSK-3β and TP53 promotes Wnt/β-catenin signaling-dependent cell expansion in cervical carcinoma.

Qian Chen, Peng-Sheng Zheng, Wen-Ting Yang

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 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing 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

26 citing papers in PubMed, 75 citations in OpenAlex.

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  9. An SETD1A/Wnt/β-catenin feedback loop promotes NSCLC development.Journal of experimental & clinical cancer research : CR · 2021
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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

3 authors at 2 institutions in 1 country.

Qian ChenDepartment of Reproductive Medicine, The First Affiliated Hospital of The Medical College, Xi'an Jiaotong University, Xi'an, The People's Republic of China.
Peng-Sheng ZhengDepartment of Reproductive Medicine, The First Affiliated Hospital of The Medical College, Xi'an Jiaotong University, Xi'an, The People's Republic of China.
Wen-Ting YangDepartment of Reproductive Medicine, The First Affiliated Hospital of The Medical College, Xi'an Jiaotong University, Xi'an, The People's Republic of China.
First Affiliated Hospital of Xi'an Jiaotong University · CNMinistry of Education of the People's Republic of China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Enhancer of zeste homolog 2 (EZH2), a catalytic core component of the Polycomb repressive complex 2 (PRC2), stimulates the silencing of target genes through histone H3 lysine 27 trimethylation (H3K27me3). Recent findings have indicated EZH2 is involved in the development and progression of various human cancers. However, the exact mechanism of EZH2 in the promotion of cervical cancer is largely unknown. Here, we show that EZH2 expression gradually increases during the progression of cervical cancer. We identified a significant positive correlation between EZH2 expression and cell proliferation in vitro and tumor formation in vivo by the up-regulation or down-regulation of EZH2 using CRISPR-Cas9-mediated gene editing technology and shRNA in HeLa and SiHa cells. Further investigation indicated that EZH2 protein significantly accelerated the cell cycle transition from the G0/G1 to S phase. TOP/FOP-Flash reporter assay revealed that EZH2 significantly activated Wnt/β-catenin signaling and the target genes of Wnt/β-catenin pathway were up-regulated, including β-catenin, cyclin D1, and c-myc. Moreover, dual-luciferase reporter and chromatin immunoprecipitation (ChIP) assays confirmed that EZH2 inhibited the expression of glycogen synthase kinase-3β (GSK-3β) and TP53 through physically interacting with motifs in the promoters of the GSK-3β and TP53 genes. Additionally, blockage of the Wnt/β-catenin pathway resulted in significant inhibition of cell proliferation, and activation of the Wnt/β-catenin pathway resulted in significant enhancement of cell proliferation, as induced by EZH2. Taken together, our data demonstrate that EZH2 promotes cell proliferation and tumor formation in cervical cancer through activating the Wnt/β-catenin pathway by epigenetic silencing via GSK-3β and TP53.

Indexed as

Animalsbeta CateninCell Line, TumorCell ProliferationCRISPR-Cas SystemsEnhancer of Zeste Homolog 2 ProteinFemaleGene Expression Regulation, NeoplasticGlycogen Synthase Kinase 3HeLa CellsHumansMice, Inbred BALB CMice, NudeRNA InterferenceTransplantation, HeterologousTumor Suppressor Protein p53beta CateninEnhancer of Zeste Homolog 2 ProteinEZH2 protein, humanGlycogen Synthase Kinase 3Tumor Suppressor Protein p53cervical cancerEZH2GSK3β and TP53proliferationWnt/β-catenin signaling

Identifiers

PMID27092879
PMCPMC5094987
OpenAlexW2336141895

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.