Evidence map›Paper›PMID 41298804›Full record

ArticleCommunications biology2025

A positive feedback loop between TNS1 and ZEB1 promotes TGFβ-induced epithelial-to-mesenchymal transition in lung cancer.

Tingting Zhang, Zhang Li, Yue Ming, Jiao Li, Zixia Ye, Dongdong Luo, Rui Wang, Yang Yang, Xiaojuan Yang, Yong Peng

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Communications biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. CTHRC1Frontiers in immunology · 2026
    Article
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

10 authors.

Tingting Zhang *Center for Molecular Oncology, Frontiers Science Center for Disease-related Molecular Network, State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University, Chengdu, China.
Zhang Li *Center for Molecular Oncology, Frontiers Science Center for Disease-related Molecular Network, State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University, Chengdu, China.
Yue MingCenter for Molecular Oncology, Frontiers Science Center for Disease-related Molecular Network, State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University, Chengdu, China.
Jiao LiCenter for Molecular Oncology, Frontiers Science Center for Disease-related Molecular Network, State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University, Chengdu, China.
Zixia YeCenter for Molecular Oncology, Frontiers Science Center for Disease-related Molecular Network, State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University, Chengdu, China.
Dongdong LuoCenter for Molecular Oncology, Frontiers Science Center for Disease-related Molecular Network, State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University, Chengdu, China.
Rui WangAdvanced Mass Spectrometry Center, Research Core Facility, Frontiers Science Center for Disease-Related Molecular Network, West China Hospital, Sichuan University, Chengdu, China.
Yang YangCenter for Molecular Oncology, Frontiers Science Center for Disease-related Molecular Network, State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University, Chengdu, China.
Xiaojuan YangCenter for Molecular Oncology, Frontiers Science Center for Disease-related Molecular Network, State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University, Chengdu, China. yangxiaojuan@wchscu.edu.cn.ORCID http://orcid.org/0009-0008-6441-6298
Yong PengCenter for Molecular Oncology, Frontiers Science Center for Disease-related Molecular Network, State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University, Chengdu, China. yongpeng@scu.edu.cn.ORCID http://orcid.org/0000-0002-1181-3467

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epithelial-mesenchymal transition (EMT) plays a pivotal role in tumor metastasis initiation. Although emerging evidence suggests that Tensin-1 (TNS1) contributes to tumor metastasis, its precise function in EMT during lung cancer progression and the underlying mechanisms remain unclear. Here, we identify that TNS1 is upregulated in a TGFβ-induced EMT cell model. Functional studies demonstrate that TNS1 knockdown significantly attenuates both TGFβ- and hypoxia-induced EMT, highlighting its critical role in this process. Furthermore, TNS1 overexpression promotes EMT and enhances the metastatic potential of lung cancer cells in vitro and in vivo, while knockdown of TNS1 exhibits opposite effects. Mechanistically, TNS1 upregulation during TGFβ- mediated EMT is found to be transcriptionally regulated by ZEB1 and SMAD3. Notably, elevated TNS1 levels stabilizes ZEB1 through their interaction, thereby suppressing its ubiquitin-proteasomal degradation. Collectively, these findings uncover a positive feedback loop between TNS1 and ZEB1 that amplifies TGFβ-induced EMT and promotes lung cancer metastasis.

Indexed as

Epithelial-Mesenchymal TransitionLung NeoplasmsTensinsTransforming Growth Factor betaZinc Finger E-box-Binding Homeobox 1A549 CellsAnimalsCell Line, TumorFeedback, PhysiologicalGene Expression Regulation, NeoplasticHumansMiceTensinsTNS1 protein, humanTransforming Growth Factor betaZEB1 protein, humanZinc Finger E-box-Binding Homeobox 1

Identifiers

PMID41298804
PMCPMC12657872

What OpenQuestion holds

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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.