AI Article Synopsis
- Vemurafenib, a drug for BRAF V600E melanoma, has shown effectiveness but is limited by the development of resistance mediated by AKT phosphorylation.
- This study established a vemurafenib-resistant melanoma cell line and tested the effects of vemurafenib and resveratrol on cell growth and protein expression.
- Results indicated that resveratrol can suppress cell proliferation and AKT activity, suggesting it may help overcome resistance to vemurafenib in treatment.
Article Abstract
Background/aim: The serine/threonine-protein kinase B-Raf (BRAF) V600E mutant (BRAF(V600E)) inhibitor vemurafenib, has improved clinical outcomes for patients with BRAF(V600E) melanoma, but acquired cellular resistance mediated by AKT serine/threonine kinase 1 (AKT) phosphorylation limits its efficacy. We examined the effect of resveratrol on vemurafenib-resistant melanoma cells.
Materials And Methods: A vemurafenib-resistant human metastatic melanoma cell line positive for the BRAF V600E mutation was established. The anti-tumorigenic effects of vemurafenib and resveratrol, both alone and in combination, were examined through analysis of cell proliferation and protein expression.
Results: The level of phosphorylated AKT (p-AKT) was increased in the primary melanoma cells after treatment with vemurafenib, and the basal level of p-AKT was increased in vemurafenib-resistant melanoma cells. Notably, resveratrol both alone and in combination with vemurafenib effectively suppressed cell proliferation and AKT phosphorylation in both parental and vemurafenib-resistant melanoma cells.
Conclusion: Vemurafenib resistance can be reversed by addition of resveratrol in patients undergoing treatment with BRAF inhibitors.
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