TRMU Confers Resistance of Melanoma Cells to Vemurafenib through Modulating Mitochondrial Activities.

ABSTRACT: Approximately 50% of melanoma patients carry a mutation in the BRAF gene, and over 90% of these mutations lead to the substitution of valine 600 with glutamic acid (V600E). Vemurafenib is an FDA-approved kinase inhibitor for BRAF^V600E; while the drug elicits effective remission of metastatic melanoma, relapse typically occurs within several months after therapy. Recent studies documented critical roles of reversible modifications in RNA in modulating resistance to cancer therapy. Herein we explored the contributions of epitranscriptomic alterations to vemurafenib resistance by assessing the differential expression of epitranscriptomic reader, writer and eraser (RWE) proteins in IGR37 metastatic melanoma cells and the isogenic vemurafenib-resistant cells (IGR37xp). Our res

SUBMITTER: Guo S 

PROVIDER: S-EPMC12673917 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature