本文采用的英格恩产品: CCAA细胞凋亡检测试剂盒(PI)
ATP release mediated by TRPM3 enhances invasion in glioblastoma
Affiliations
- 1 Department of Biological Science, Chungnam National University, Daejeon, Republic of Korea.
- 2 Group of Cognitive Glioscience, Center for Memory and Glioscience, Institute for Basic Science, Daejeon, Republic of Korea.
- 3 Department of Neurosurgery, Brain Tumor Center, Gangnam Severance Hospital, Seoul, Republic of Korea.
- 4 Center for Global Biopharmaceutical Research, Korea Institute of Toxicology, Daejeon, Republic of Korea.
- PMID: 41710303
- PMCID: PMC12912218
- DOI: 10.1080/19768354.2026.2629066
Abstract
Glioblastoma (GBM) is the most aggressive and lethal form of primary brain tumor, characterized by uncontrolled proliferation and invasion into surrounding brain tissue. Mechanical stimulation (MS) in the tumor microenvironment (TME) has been correlated to tumor progression, partly via ATP release. However, the underlying molecular mechanisms remain poorly understood. In this study, we found that transient receptor potential melastatin 3 (TRPM3) channel mediates MS-induced ATP release from GBM cells. Genetic knockdown of TRPM3 significantly attenuated ATP release and suppressed GBM cell invasion, indicating its functional relevance in tumor dissemination. Furthermore, TRPM3 regulated ATP release in a Ca2+-independent manner, suggesting a noncanonical mechanism of mechanosensitive signaling. Consequently, targeting TRPM3 may offer a novel target to reduce the invasion of GBM within the TME.
Keywords: ATP; Glioblastoma; TRPM3; invasion; mechanical stimulation.
