Evidence map›Paper›PMID 39612152›Full record

ArticleCellular oncology (Dordrecht, Netherlands)2025

TRPV4 drives the progression of leiomyosarcoma by promoting ECM1 generation and co-activating the FAK/PI3K/AKT/GSK3β pathway.

Qiwen Zhou, Yang You, Yingying Zhao, Shuxiu Xiao, Zhengqing Song, Chuxin Huang, Jiali Qian, Weiqi Lu, Hanxing Tong, Yong Zhang and 9 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cellular oncology (Dordrecht, Netherlands), 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. Review
  2. Article
  3. Review
  4. 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

19 authors.

Qiwen Zhou *Department of Oncology, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Yang You *Department of Oncology, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Yingying Zhao *Liver Cancer Institute, Zhongshan Hospital, Fudan University and Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Shanghai, 200032, China.
Shuxiu XiaoClinical Centre for Biotherapy, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Zhengqing SongDepartment of Oncology, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Chuxin HuangDepartment of Endocrinology, Huashan Hospital, Fudan University, Shanghai, 200040, China.
Jiali QianDepartment of Endocrinology, Huashan Hospital, Fudan University, Shanghai, 200040, China.
Weiqi LuDepartment of General Surgery, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Hanxing TongDepartment of General Surgery, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Yong ZhangDepartment of General Surgery, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Zhiming WangDepartment of Oncology, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Wei LiDepartment of Oncology, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Chenlu ZhangDepartment of Oncology, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Xi GuoDepartment of Oncology, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Rongkui LuoDepartment of Pathology, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Yingyong HouDepartment of Pathology, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Jiefeng CuiLiver Cancer Institute, Zhongshan Hospital, Fudan University and Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Shanghai, 200032, China.
Lili LuClinical Centre for Biotherapy, Zhongshan Hospital, Fudan University, Shanghai, 200032, China. lu.lili@zs-hospital.sh.cn.
Yuhong ZhouDepartment of Oncology, Zhongshan Hospital, Fudan University, Shanghai, 200032, China. zhou.yuhong@zs-hospital.sh.cn.

Funding

Wu Jieping Medical Foundation H2021-153
6 · The paper itself

Abstract

purposeLeiomyosarcoma (LMS) is an aggressive mesenchymal malignant tumor with poor therapeutic options, but the molecular mechanisms underlying LMS remain largely unknown. Increasing evidence indicates that transient receptor potential vanilloid 4 (TRPV4) levels are closely related to the advancement of various malignant tumors through diverse molecular mechanisms. However, the roles and regulatory mechanisms of TRPV4 in LMS progression remain unclear.

methodsImmunohistochemistry, Western blot, and immunofluorescence were used to investigate the relationship between TRPV4 expression and LMS. Survival analysis was conducted to evaluate the association between TRPV4 levels and prognosis in LMS patients. Intracellular Ca

resultsTRPV4 was upregulated in LMS tissues and cells and served as a novel prognostic factor. Moreover, TRPV4 overexpression enhanced cell proliferation, cell migration and invasion of LMS cells in vitro, as well as promoted tumor metastasis in vivo, which could be blocked by HC067047 intervention or TRPV4 knockdown. Combined RNA-seq and proteomics analysis of KEGG pathway indicated that ECM receptor interaction was obviously activated. Extracellular matrix protein 1 (ECM1) was identified as downstream gene of TRPV4. Mechanistically, TRPV4 overexpression increased ECM1 level and activated the FAK/PI3K/AKT/GSK3β pathway, which could be reversed by TRPV4 knockdown or LY294002 treatment. Moreover, ECM1 overexpression enhanced the activation of FAK/PI3K/AKT/GSK3β pathway. And simultaneous overexpression of TRPV4 and ECM1 synergistically activated this pathway.

conclusionOur findings provide a novel mechanism by which TRPV4 directly activates Ca

Indexed as

Disease ProgressionExtracellular Matrix ProteinsFocal Adhesion Kinase 1Glycogen Synthase Kinase 3 betaLeiomyosarcomaPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTRPV Cation ChannelsAnimalsCell Line, TumorCell MovementCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansMaleExtracellular Matrix ProteinsFocal Adhesion Kinase 1Glycogen Synthase Kinase 3 betaPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTRPV4 protein, humanTRPV Cation ChannelsECM1FAK pathwayLeiomyosarcomaMetastasisTRPV4

Identifiers

PMID39612152
PMCPMC11996984

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.