To identify the function of TRPV1 in the progression of melanoma and investigate the underlying mechanism. Immunofluorescence, qRT-PCR and Western Blot were performed to detect the expression of TRPV1 in tissue samples of melanocytic nevus, primary melanoma, metastatic melanoma as well as in melanoma cell lines. In addition, using CCK8 assay, Edu and flow cytometry, we identified the effect of TRPV1-specific agonist, capsaicin, on the proliferation and apoptosis of melanoma cells. To identify the molecular mechanism by which TRPV1 regulates the progression of melanoma, we performed western blot assay to detect the expression of p53, PARP, Bcl2, Bax in TRPV-1 activated melanoma cells exposed to Calcinerin blocker FK506. TRPV1 expression was decreased in melanoma cell lines compared with normal melanocytes (P <0.01). Tissue TRPV1 level was drastically reduced in primary and metastatic melanoma compared with melanocytic nevus (P <0.01). Furthermore, TRPV1-specific agonist capsaicin suppressed the proliferation by inhibiting ERK signaling (P <0.05). Notably, TRPV1 activation induced the apoptosis of melanoma cells by activation of Ca 2+ /calcineurin-NFAT-ATF3 pathway, and resulting the elevated expression of p53 (P <0.01). TRPV1 was significantly down-regulated in melanoma, activated TRPV1 suppressed the progression of melanoma via ERK pathway and promote the apoptosis by activating calcineurin. Taken together, TRPV1 acts as a crucial repressor in melanoma progression and can be a promising target in melanoma treatment.
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