ArticleInternational journal of medical sciences2023
TRPM2 facilitates tumor progression of clear cell renal cell carcinoma by relieving Endoplasmic Reticulum Stress.
Article in International journal of medical sciences, 2023. 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, 7 citations in OpenAlex.
- CLCN5 inhibits tumorigenesis and fatty acid accumulation in clear cell renal cell carcinoma by regulating Enoyl CoA hydratase and 3-Hydroxyacyl CoA dehydrogenase.International journal of medical sciences · 2025Article
- TRPM channels in human cancers: regulatory mechanism and therapeutic prospects.Biomarker research · 2024Review
- Prognostic Value and Immunological Role of POP7 in Clear Cell Renal Cell Carcinoma.Pharmacogenomics and personalized medicine · 2024Article
- Downregulation of RNA binding protein 47 predicts low survival in patients and promotes the development of renal cell malignancies through RNA stability modification.Molecular biomedicine · 2023Article
- Identification of TRPM2 as a Potential Therapeutic Target Associated with Immune Infiltration: A Comprehensive Pan-Cancer Analysis and Experimental Verification in Ovarian Cancer.International journal of molecular sciences · 2023Article
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
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Abstract
Clear cell renal cell carcinoma (ccRCC) has the highest incidence rate among all pathological types of kidney cancers. Although the role of transient receptor potential (TRP) ion channel TRPM2 has been studied in many cancers, its function in ccRCC is still unexplored. In this study, using the KIRC module of TCGA, we found that TRPM2 was upregulated in ccRCC tissues and was related to poor prognosis. Gene set enrichment analysis (GSEA) showed that TRPM2 was related to epithelial-to-mesenchymal transition (EMT), TCA cycle, fatty acid metabolism, and immune system-related functions. Functional experimental results indicated that TRPM2 could promote ccRCC progression. Furthermore, mechanism analysis showed that knocking out TRPM2 can reverse these phenotypes by increasing endoplasmic reticulum stress and decreasing EMT. We also investigated the potential role of TRPM2 in immune cell infiltration in the tumor microenvironment. Our study indicated that TRPM2 promotes ccRCC progression and may be a novel target for ccRCC therapy.
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