Evidence map›Paper›PMID 31597912›Full record

ArticleOncogenesis2019

The crosstalk between STAT3 and p53/RAS signaling controls cancer cell metastasis and cisplatin resistance via the Slug/MAPK/PI3K/AKT-mediated regulation of EMT and autophagy.

Fan Liang, Chunxia Ren, Jingshu Wang, Shuoer Wang, Lina Yang, Xianghui Han, Yaping Chen, Guoqing Tong, Gong Yang

Open access · goldAbstract read
In one paragraph

Article in Oncogenesis, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed, 1 pooled it
6.6field-weighted citation impact, top 2% 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

84 citing papers in PubMed, 1 synthesis or guideline pooled it, 145 citations in OpenAlex.

  1. Prognostic significance of autophagy-related genesThe Journal of international medical research · 2020
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24 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

9 authors at 3 institutions in 1 country.

Fan LiangDepartment of Obstetrics and Gynecology, The Fifth People's Hospital of Shanghai, Fudan University, Shanghai, 200240, China.
Chunxia RenCenter for Reproductive Medicine, Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai, 200120, China.
Jingshu WangDepartment of Obstetrics and Gynecology, The Fifth People's Hospital of Shanghai, Fudan University, Shanghai, 200240, China.
Shuoer WangCentral Laboratory, the Fifth People's Hospital of Shanghai, Fudan University, Shanghai, 200240, China.
Lina YangDepartment of Obstetrics and Gynecology, The Fifth People's Hospital of Shanghai, Fudan University, Shanghai, 200240, China.
Xianghui HanInstitute of Chinese Traditional Surgery, Longhua Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai, 200032, China. hanxianghui1106@163.com.
Yaping ChenDepartment of Obstetrics and Gynecology, The Fifth People's Hospital of Shanghai, Fudan University, Shanghai, 200240, China. chenyaping@5thhospital.com.
Guoqing TongCenter for Reproductive Medicine, Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai, 200120, China. drivftongguoqing@hotmail.com.
Gong YangCentral Laboratory, the Fifth People's Hospital of Shanghai, Fudan University, Shanghai, 200240, China. yanggong@fudan.edu.cn.ORCID http://orcid.org/0000-0002-5137-4104
Fudan University · CNShanghai University of Traditional Chinese Medicine · CNShanghai Medical College of Fudan University · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81372797National Natural Science Foundation of China (National Science Foundation of China) 81402153National Natural Science Foundation of China (National Science Foundation of China) 81572553National Natural Science Foundation of China (National Science Foundation of China) 81772789
6 · The paper itself

Abstract

Chemoresistance has been the biggest obstacle in ovarian cancer treatment, and STAT3 may play an important role in chemoresistance of multiple cancers, but the underlying mechanism of STAT3 in ovarian cancer chemoresistance has long been truly illusive, particularly in association with p53 and RAS signaling. In this study, by using wild type, constitutive active, and dominant negative STAT3 constructs, wild-type p53, and RAS-mutant V12, we performed a series of in vitro and in vivo experiments by gene overexpression, drug treatment, and animal assays. We found that phosphorylation of STAT3 Y705 but not S727 promoted cancer cell EMT and metastasis through the Slug-mediated regulation of E-cadherin and Vimentin. The phosphorylation of STAT3 at Y705 also activated the MAPK and PI3K/AKT signaling to inhibit the ERS-mediated autophagy through down-regulation of pPERK, pelf2α, ATF6α, and IRE1α, which led to increased cisplatin resistance. Induction of wild type p53 in STAT3-DN-transfected cells further diminished the chemoresistance and tumor growth through the upregulation of the MAPK- and PI3K/AKT-mediated ERS and autophagy. Introduction of STAT3-DN deprived the RAS

Identifiers

PMID31597912
PMCPMC6785561
OpenAlexW2979888464

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.