Evidence map›Paper›PMID 27938379›Full record

ArticleMolecular cancer2016

STAT3 signaling drives EZH2 transcriptional activation and mediates poor prognosis in gastric cancer.

Yuan-Ming Pan, Cheng-Gang Wang, Min Zhu, Rui Xing, Jian-Tao Cui, Wen-Mei Li, De-Dong Yu, Shu-Bin Wang, Wei Zhu, Ying-Jiang Ye and 3 more

Open access · goldAbstract read
In one paragraph

Article in Molecular cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
106citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 10% 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

106 citing papers in PubMed, 1 synthesis or guideline pooled it, 201 citations in OpenAlex.

  1. Pooled it
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  14. Targeting p16Leukemia · 2025
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  20. Mechanisms and Therapeutic Implications of EZH2 in Nasal Diseases.Clinical reviews in allergy & immunology · 2025
    Review

46 more citing papers are in PubMed but not listed here.

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

13 authors at 5 institutions in 1 country.

Yuan-Ming PanKey Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Laboratory of Molecular Oncology, Peking University Cancer Hospital & Institute , 52 Fucheng Road, Haidian District, Beijing, 100142, China.
Cheng-Gang WangDepartment of Gastroenterology Surgery, Surgical Oncology Laboratory, People's Hospital, Peking University, Beijing, 100044, China.
Min ZhuKey Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Laboratory of Molecular Oncology, Peking University Cancer Hospital & Institute , 52 Fucheng Road, Haidian District, Beijing, 100142, China.
Rui XingKey Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Laboratory of Molecular Oncology, Peking University Cancer Hospital & Institute , 52 Fucheng Road, Haidian District, Beijing, 100142, China.
Jian-Tao CuiKey Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Laboratory of Molecular Oncology, Peking University Cancer Hospital & Institute , 52 Fucheng Road, Haidian District, Beijing, 100142, China.
Wen-Mei LiKey Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Laboratory of Molecular Oncology, Peking University Cancer Hospital & Institute , 52 Fucheng Road, Haidian District, Beijing, 100142, China.
De-Dong YuDepartment of Oncology/Institute for Cancer Research, Baotou Central Hospital, Inner Mongolia, 014040, China.
Shu-Bin WangDepartment of Oncology/Institute for Cancer Research, Baotou Central Hospital, Inner Mongolia, 014040, China.
Wei ZhuDepartment of Oncology/Institute for Cancer Research, Baotou Central Hospital, Inner Mongolia, 014040, China.
Ying-Jiang YeDepartment of Gastroenterology Surgery, Surgical Oncology Laboratory, People's Hospital, Peking University, Beijing, 100044, China.
Yun WuDepartment of Oncology/Institute for Cancer Research, Baotou Central Hospital, Inner Mongolia, 014040, China. yunwu_baotou@sina.com.
Shan WangDepartment of Gastroenterology Surgery, Surgical Oncology Laboratory, People's Hospital, Peking University, Beijing, 100044, China. shanwang11@gmail.com.
You-Yong LuKey Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Laboratory of Molecular Oncology, Peking University Cancer Hospital & Institute , 52 Fucheng Road, Haidian District, Beijing, 100142, China. youyonglu@hsc.pku.edu.cn.
Peking University · CNBaotou Central Hospital · CNBeijing Anzhen Hospital · CNPeking University Cancer Hospital · CNPeking University People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSTAT3 signaling plays the pivotal role in tumorigenesis through EZH2 epigenetic modification, which enhanced STAT3 activity by increased tyrosine phosphorylation of STAT3. Here, another possible feedback mechanism and clinical significance of EZH2 and STAT3 were investigated in gastric cancer (GC).

methodsSTAT3, p-STAT3 (Tyr 705) and EZH2 expression were examined in 63 GC specimens with matched normal tissues by IHC staining. EZH2 and STAT3 were also identified in five GC cell lines using RT-PCR and western blot analyses. p-STAT3 protein was detected by western blotting. In order to investigate whether EZH2 expression was directly regulated by STAT3, EZH2 expression was further detected using siRNA for STAT3 or IL-6 stimulation, with dual luciferase reporter analyses, electrophoretic mobility shift assay (EMSA) and chromatin immunoprecipitation (ChIP) assays. The clinical significance of STAT3, p-STAT3 and EZH2 expression was evaluated by multi-factor COX regression and Kaplan-Meier analyses.

resultsHyper-activation of STAT3, p-STAT3 and EZH2 expression were observed in GC cells and tissues. STAT3 signaling was correlated with EZH2 expression in GC (R = 0.373, P = 0.003), which was consistent with our data showing that STAT3 as the transcriptional factor enhanced EZH2 transcriptional activity by binding the relative promoter region (-214 ~ -206). STAT3 was an independent signature for poor survival (P = 0.002). Patients with STAT3

conclusionsOur results indicate that STAT3 status mediated EZH2 upregulation, associated with advanced TNM stage and poor prognosis, suggesting that combination with knockdown of STAT3 and EZH2 inhibitor might be a novel therapy in GC treatment. Collectively, STAT3, p-STAT3 and EZH2 expression were provided for the precision medicine in GC patients.

Indexed as

Signal TransductionTranscriptional ActivationAdultAgedApoptosisCell Cycle CheckpointsCell Line, TumorEnhancer of Zeste Homolog 2 ProteinFemaleGene Expression Regulation, NeoplasticHumansImmunohistochemistryMaleMiddle AgedNeoplasm GradingNeoplasm MetastasisEnhancer of Zeste Homolog 2 ProteinSTAT3 Transcription Factor3-deazaneplanocin AEZH2Gastric cancerPrognosisp-STAT3STAT3

Identifiers

PMID27938379
PMCPMC5148878
OpenAlexW2559891252

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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.