Evidence map›Paper›PMID 29751820›Full record

ArticleJournal of experimental & clinical cancer research : CR2018

Physical interaction of STAT1 isoforms with TGF-β receptors leads to functional crosstalk between two signaling pathways in epithelial ovarian cancer.

Xiaoling Tian, Wencai Guan, Lingyun Zhang, Wenwen Sun, Daibing Zhou, Qunbo Lin, Weimin Ren, Lubna Nadeem, Guoxiong Xu

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

37 citing papers in PubMed, 59 citations in OpenAlex.

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  13. STAT1 suppresses the transcriptional activity of TRIM21 in gastric cancer.Journal of cancer research and clinical oncology · 2023
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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.

Xiaoling TianCenter Laboratory, Jinshan Hospital, Fudan University, 1508 Longhang Road, Shanghai, 201508, People's Republic of China.
Wencai GuanCenter Laboratory, Jinshan Hospital, Fudan University, 1508 Longhang Road, Shanghai, 201508, People's Republic of China.
Lingyun ZhangCenter Laboratory, Jinshan Hospital, Fudan University, 1508 Longhang Road, Shanghai, 201508, People's Republic of China.
Wenwen SunCenter Laboratory, Jinshan Hospital, Fudan University, 1508 Longhang Road, Shanghai, 201508, People's Republic of China.
Daibing ZhouCenter Laboratory, Jinshan Hospital, Fudan University, 1508 Longhang Road, Shanghai, 201508, People's Republic of China.
Qunbo LinCenter Laboratory, Jinshan Hospital, Fudan University, 1508 Longhang Road, Shanghai, 201508, People's Republic of China.
Weimin RenCenter Laboratory, Jinshan Hospital, Fudan University, 1508 Longhang Road, Shanghai, 201508, People's Republic of China.
Lubna NadeemLunenfeld Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, ON, M5G 1X5, Canada.
Guoxiong XuCenter Laboratory, Jinshan Hospital, Fudan University, 1508 Longhang Road, Shanghai, 201508, People's Republic of China. guoxiong.xu@fudan.edu.cn.
Jinshan Hospital of Fudan University · CNShanghai Medical College of Fudan University · CNLunenfeld-Tanenbaum Research Institute · CA

Funding

Committee of Science and Technology of Jinshan District JSKJ-KTMS-2015-01National Natural Science Foundation of China 81272880Natural Science Foundation of Shanghai 17ZR1404100Science and Technology Commission of Shanghai Municipality 124119b1300Shanghai Municipal Commission of Health and Family Planning 201640287
6 · The paper itself

Abstract

backgroundThe signal transducer and activator of transcription (STAT) and transforming growth factor-β (TGF-β) signaling pathways play important roles in epithelial ovarian cancer (EOC). However, the mechanism of crosstalk between two pathways is not completely understood.

methodsThe expression of STAT1 protein was detected by tissue microarray and immunoblotting (IB). The interaction of STAT1 isoforms with TGF-β receptors was confirmed by immunoprecipitation and IB. The effect of TGF-β signaling on STAT1 activation was examined in EOC and non-tumorous HOSEpiC cells treated with TGF-β1 in the presence or absence of the inhibitor of TGF-β type I receptor. The gain-of-function and loss-of-function approaches were applied for detecting the role of STAT1 on EOC cell behaviours.

resultsThe high level of STAT1 was observed in patients with high-grade serous EOC. STAT1 expression was higher in ovarian cancer cells than noncancerous cells. TGF-β1 activated the STAT1 pathway by inducing the phosphorylation of STAT1α on S727 residue. The full-length STAT1α and the truncated STAT1β directly interacted with TGF-β receptors (ALK1/ALK5 and TβRII), which was mediated by TGF-β1. STAT1α and STAT1β blocked the activation of the TGF-β1 signaling pathway in EOC cells by reducing Smad2 phosphorylation. STAT1 overexpression induced EOC cell proliferation, migration, and invasion; whereas its inhibition enhanced TGF-β1-induced phospho-Smad2 and suppressed EOC cell proliferation, migration, and invasion.

conclusionsOur data unveil a novel insight into the molecular mechanism of crosstalk between the STAT1 and TGF-β signaling pathways, which affected the cancer cell behavior. Suppression of STAT1 may be a potential therapeutic strategy for targeting ovarian cancer.

Indexed as

Signal TransductionBiomarkersCarcinoma, Ovarian EpithelialCell Line, TumorCell MovementCell ProliferationCell Transformation, NeoplasticFemaleGene Expression Regulation, NeoplasticHumansNeoplasm GradingNeoplasm StagingProtein BindingProtein IsoformsReceptors, Transforming Growth Factor betaRNA, Small InterferingBiomarkersProtein IsoformsReceptors, Transforming Growth Factor betaRNA, Small InterferingSTAT1 Transcription FactorActivin receptor-like kinaseCell proliferationCrosstalkCytokineGrowth factorReceptorSignal transductionSmadTumorigenesisTβRII

Identifiers

PMID29751820
PMCPMC5948853
OpenAlexW2801123931

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.