ArticleTranslational cancer research2020
MEST promotes bladder cancer cell proliferation, migration and invasion via STAT3/Twist-1-mediated EMT.
Article in Translational cancer research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 11 citations in OpenAlex.
- Leveraging the germ layer development patterns to predict prognosis and identify MEST as a novel therapeutic target in glioma.Cancer cell international · 2026Article
- Article
- Role of FHOD1 in tumor cells and tumor immune microenvironment.Frontiers in immunology · 2025Review
- Identification of inflammation related gene signatures for bladder cancer prognosis prediction.Scientific reports · 2024Article
- Hispolon Methyl Ether, a Hispolon Analog, Suppresses the SRC/STAT3/Survivin Signaling Axis to Induce Cytotoxicity in Human Urinary Bladder Transitional Carcinoma Cell Lines.International journal of molecular sciences · 2022Article
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7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMesoderm-specific transcript (MEST) has been demonstrated to be a proto-oncogene or anti-oncogene in various carcinomas. However, the role and mechanism of MEST in bladder cancer (BC) are still unknown. Here we aimed to explore the effect of MEST on malignant biological behaviour in BC and its potential mechanism.
methodsThe expression of MEST in BC tissues and cells was detected by qRT-PCR methods. MEST depletion and overexpression cell lines were established in T24 and 5637 respectively. Then the effects of MEST on cell proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) were investigated. Finally, the STAT3/Twist-1 signaling was verified.
resultsMEST was elevated in BC tissues and cells lines, and its high expression was highly relevant to the clinicopathologic features of patients with BC and to poor prognosis in these patients. MEST depletion impeded cell proliferation, migration and invasion as well as epithelial-mesenchymal transition (EMT), while MEST overexpression promoted malignant biological behaviour in BC. Mechanistically, MEST upregulated p-STAT3 and Twist-1 expression, while treatment with a STAT3 inhibitor clearly attenuated the STAT3 activation and Twist-1 upregulation induced by MEST. Subsequently, rescue assays confirmed that inhibition of STAT3 signalling could remarkably relieve the oncogenic effects of MEST on malignant biological behaviour in BC.
conclusionsOur data confirmed that MEST exerts oncogenic functions in bladder cancer via STAT3/Twist-1 signalling and that MEST may represent a promising target in BC treatment.
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