ArticleAmerican journal of cancer research2024
ITM2A inhibits the progression of bladder cancer by downregulating the phosphorylation of STAT3.
Article in American journal of cancer research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- The emerging roles of ITM2A: At the molecular crossroads of development and pathogenesis.iScience · 2026Review
- ITM2A promotes thyroid cancer differentiation through metabolic reprogramming and enhances PD-L1-dependent T-cell responses.Clinical and experimental medicine · 2026Article
- Wnt5a Regulates Embryonic Müllerian Duct Development Through the Non-Canonical Wnt PCP Pathway.Cells · 2026Article
- Machine Learning-Based Gene Expression Analysis to Identify Prognostic Biomarkers in Upper Tract Urothelial Carcinoma.Cancers · 2025Article
- Integrating traditional omics and AI-driven approaches for discovery and validation of novel MicroRNA biomarkers and therapeutic targets in thyroid cancer.Frontiers in pharmacology · 2025Article
- ITM2A as a potential prognostic marker for triple-negative breast cancer.Journal of Cancer · 2025Article
- Integrating machine learning, bioinformatics and experimental verification to identify a novel prognostic marker associated with tumor immune microenvironment in head and neck squamous carcinoma.Frontiers in immunology · 2024Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bladder cancer stands as one of the prevalent malignancies in urological clinics, highlighting the pressing need to uncover prognostic or therapeutic avenues. ITM2A, a transmembrane protein, has been identified as a suppressor in tumor progression recently. Our study underscored a significant correlation between low ITM2A expression in bladder cancer tissues and high tumor grade, AJCC stage, and poor overall survival time. Additionally, our findings demonstrated that reinstating ITM2A expression impeded cell proliferation, migration, and invasion, while conversely, its suppression enhanced these malignant behaviors. Furthermore, we elucidated that ITM2A could suppress malignant phenotypes of bladder cancer cells via inhibiting activation of the STAT3 induced by IL-6. In conclusion, our research unveiled the mechanistic role of ITM2A in inhibiting tumor progression, shedding light on its potential as a prognostic predictor and therapeutic target in bladder cancer management.
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