Evidence map›Paper›PMID 41920409›Full record

ArticleCellular oncology (Dordrecht, Netherlands)2026

Transcriptional repression of TGFB2-AS1 by GATA6 drives triple-negative breast cancer metastasis.

Chang Liu, Qianru Yu, Difei Wang, Zheng Duan, Xin Zhang, Jiao Wang, Xiaoyu Qi, Jiayin Ye, Qian Zhao, Jianrong He and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cellular oncology (Dordrecht, Netherlands), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Review
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

11 authors.

Chang Liu *Institute for Translational Medicine on Cell Fate and Disease, Shanghai Ninth People's Hospital, Key Laboratory of Cell Differentiation and Apoptosis of National Ministry of Education, Department of Pathophysiology, Shanghai Jiao Tong University School of Medicine, 201318, Shanghai, China.
Qianru Yu *Institute for Translational Medicine on Cell Fate and Disease, Shanghai Ninth People's Hospital, Key Laboratory of Cell Differentiation and Apoptosis of National Ministry of Education, Department of Pathophysiology, Shanghai Jiao Tong University School of Medicine, 201318, Shanghai, China.
Difei WangShanghai-MOST Key Laboratory of Health and Disease Genomics, NHC Key Lab of Reproduction Regulation, Shanghai Engineering Research Center of Reproductive Health Drug and Devices, Shanghai Institute for Biomedical and Pharmaceutical Technologies, Pharmacy School, Fudan University, 200032, Shanghai, China.
Zheng DuanInstitute for Translational Medicine on Cell Fate and Disease, Shanghai Ninth People's Hospital, Key Laboratory of Cell Differentiation and Apoptosis of National Ministry of Education, Department of Pathophysiology, Shanghai Jiao Tong University School of Medicine, 201318, Shanghai, China.
Xin ZhangInstitute for Translational Medicine on Cell Fate and Disease, Shanghai Ninth People's Hospital, Key Laboratory of Cell Differentiation and Apoptosis of National Ministry of Education, Department of Pathophysiology, Shanghai Jiao Tong University School of Medicine, 201318, Shanghai, China.
Jiao WangInstitute for Translational Medicine on Cell Fate and Disease, Shanghai Ninth People's Hospital, Key Laboratory of Cell Differentiation and Apoptosis of National Ministry of Education, Department of Pathophysiology, Shanghai Jiao Tong University School of Medicine, 201318, Shanghai, China.
Xiaoyu QiInstitute for Translational Medicine on Cell Fate and Disease, Shanghai Ninth People's Hospital, Key Laboratory of Cell Differentiation and Apoptosis of National Ministry of Education, Department of Pathophysiology, Shanghai Jiao Tong University School of Medicine, 201318, Shanghai, China.
Jiayin YeInstitute for Translational Medicine on Cell Fate and Disease, Shanghai Ninth People's Hospital, Key Laboratory of Cell Differentiation and Apoptosis of National Ministry of Education, Department of Pathophysiology, Shanghai Jiao Tong University School of Medicine, 201318, Shanghai, China.
Qian ZhaoInstitute for Translational Medicine on Cell Fate and Disease, Shanghai Ninth People's Hospital, Key Laboratory of Cell Differentiation and Apoptosis of National Ministry of Education, Department of Pathophysiology, Shanghai Jiao Tong University School of Medicine, 201318, Shanghai, China.
Jianrong HeDepartment of General Surgery, Comprehensive Breast Health Center, Ruijin Hospital, SJTU-SM, 200025, Shanghai, China. hejrong6636@163.com.
Cixiang ZhouInstitute for Translational Medicine on Cell Fate and Disease, Shanghai Ninth People's Hospital, Key Laboratory of Cell Differentiation and Apoptosis of National Ministry of Education, Department of Pathophysiology, Shanghai Jiao Tong University School of Medicine, 201318, Shanghai, China. zhoucx@shsmu.edu.cn.

Funding

Ministry of Science and Technology of the People's Republic of China 2020YFA0803403National Natural Science Foundation of China 81772831Natural Science Foundation of Shanghai Municipality 24ZR1442100
6 · The paper itself

Abstract

purposeHigh recurrence rates, significant metastatic potential, and limited overall survival make triple-negative breast cancer (TNBC) the most challenging subtype among breast cancers. Previous studies have indicated that the downregulation of TGFB2-AS1 can enhance the stem-like properties of tumor cells, thereby promoting TNBC progression. Bioinformatics analysis has revealed the regulatory role of GATA6 in TGFB2-AS1 transcription, providing insights into the transcriptional regulation of TGFB2-AS1 by GATA6 and offering potential prognostic biomarkers and therapeutic strategies for TNBC.

methodsBioinformatics analysis, Western blot, and qPCR were employed to assess the expression of GATA6 and TGFB2-AS1. Immunohistochemistry (IHC) and RNA in situ hybridization (ISH) were performed on clinical samples to evaluate GATA6 and TGFB2-AS1 expression, respectively, with survival analysis based on follow-up data. Fluorescence in situ hybridization (FISH), chromatin immunoprecipitation (ChIP), and dual-luciferase reporter assays were used to elucidate the regulatory mechanisms of GATA6 on TGFB2-AS1. Functional experiments, Western blotting, qPCR, and tail vein metastasis assays, were conducted to investigate the role of GATA6-regulated TGFB2-AS1 in TNBC.

resultsGATA6 binds to the TGFB2-AS1 promoter and represses its transcription, and patients with tumors exhibiting high GATA6 and low TGFB2-AS1 expression are associated with poor prognosis. Both in vivo and in vitro functional experiments confirmed that TGFB2-AS1 critically mediates the tumor-promoting effects of GATA6 in TNBC progression.

conclusionsOur findings reveal that GATA6 drives the progression of TNBC by repressing TGFB2-AS1 transcription.

Indexed as

GATA6 Transcription FactorGene Expression Regulation, NeoplasticTranscription, GeneticTransforming Growth Factor beta2Triple Negative Breast NeoplasmsAnimalsCell Line, TumorFemaleHumansNeoplasm MetastasisPromoter Regions, GeneticGATA6 protein, humanGATA6 Transcription FactorTGFB2 protein, humanTransforming Growth Factor beta2Diagnosis and treatment strategiesGATA6MetastasisTGFB2-AS1Triple-negative breast cancer

Identifiers

PMID41920409
PMCPMC13043960

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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.