ArticleNaunyn-Schmiedeberg's archives of pharmacology2025
LncRNA TRPM2-AS promotes cell proliferation, migration, and invasion by regulating the miR-195-5p/COP1 axis in bladder cancer.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Pathophysiological significance of the TRPM2 ion channel as a potential target in cancer, neurological disorders, and ischemia/reperfusion injury.Pharmacological research · 2026Review
- Roles of lactate and lactylation in tumor immune suppression and drug resistance.Frontiers in immunology · 2026Review
- LncRNAFrontiers in oncology · 2025Article
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Authors and funding
6 authors.
Funding
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Abstract
Bladder cancer (BLCA) is one of the most frequent malignant tumors worldwide, with markedly poor prognosis when distant metastasis occurs. Long noncoding RNA (lncRNA) TRPM2-AS has been reported to play an oncogenic role in several cancers. Although TRPM2-AS was previously revealed to suppress BLCA cell growth, its role in BLCA cell metastasis remains largely unknown. In our study, TRPM2-AS, miR-195-5p, and COP1 relative expression in BLCA cells was estimated by RT-qPCR. Through MTT, EdU, colony formation, wound-healing, Transwell, and western blotting assays, the biological effects of TRPM2-AS and COP1 on BLCA cell proliferation, migration, invasion, and EMT were evaluated. Target association between miR-195-5p and TRPM2-AS (or COP1) was confirmed by RNA pull-down, RIP, and luciferase activity assays. The nucleocytoplasmic localization of TRPM2-AS in BLCA cells was measured by FISH assay. Xenograft mouse models of BLCA were used to validate the role of TRPM2-AS on tumor growth and EMT in vivo. Our results showed that TRPM2-AS and COP1 expression was increased, while miR-195-5p expression was decreased in BLCA cells and tissues. TRPM2-AS silencing repressed BLCA cell growth, migration, invasion, and EMT. TRPM2-AS acted as a competing endogenous RNA (ceRNA) to spongemiR-195-5p, thereby positively regulating COP1 expression and activating the PI3K/AKT signaling. Overexpressing COP1 antagonized the influence of TRPM2-AS knockdown on BLCA cell growth, migration, invasion, and EMT. Additionally, TRPM2-AS knockdown inhibited tumor growth, EMT, and the PI3K/AKT signaling, attenuated COP1 expression, and enhanced miR-195-5p expression in xenograftmouse models. Collectively, TRPM2-AS functions as an oncogene in BLCA development via the miR-195-5p/COP1 axis.
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Registered trials
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