TRPV3 (Transient Receptor Potential Cation Channel Subfamily V Member 3)

Using AV3-1, this study demonstrates TRPV3 expression in bladder cancer cells. TRPV3 activation in these cells triggers ATP release, a signal potentially promoting cancer progression.

Skin equivalents generated from PVLP-treated keratinocytes exhibited complete transduction, and PVLP-shRNA treatment significantly reduced hyperkeratosis in skin equivalents from mice bearing the Olmsted syndrome mutation. These findings highlight PVLP as a promising tool for ex vivo skin gene therapy.

Genetic analysis identified a novel heterozygous p.Val306Met missense mutation in the exon 8 of TRPV3. Our findings expand the phenotypic spectrum of TRPV3-related OS and underscore the need for vigilant long-term monitoring of these patients.

Moreover, Erlotinib (EGFR inhibitor) and LY294002 (PI3K inhibitor) diminished Carvacrol induced cell migration and proliferation, promoted cell apoptosis, and increased [Ca2+]i in Carvacrol group. Our results collectively suggest that TRPV3 siRNA inhibits migration and proliferation, and promoted apoptosis in breast cancer cells by EGFR/AKT pathway. These findings indicate that TRPV3 may represent a novel therapeutic strategy for breast cancer.

Taken together, our findings demonstrate the causative role of overactive TRPV3 channel function in the development of UVB-induced skin injury. Therefore, topical inhibition of TRPV3 may hold potential therapy or prevention of UVB radiation-induced skin injury.

Current treatment options, such as isotretinoin, are symptomatic and not very effective. The recent advances in the disease’s genetics have lead to a better understanding of its etiology, made possible the use of diagnostic genetic testing and brought advances in targeted therapies - such as Erlotinib, which could be an effective treatment for patients with TRPV3 mutations. It’s important to report these cases to educate more doctors and help more patients