677 Sestrin2 contributes to vemurafenib resistance in braf mutant metastatic melanoma cells by detoxifying intracellular reactive oxygen species
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چکیده
منابع مشابه
BRAF Fusion as a Novel Mechanism of Acquired Resistance to Vemurafenib in BRAFV600E Mutant Melanoma.
Purpose: Many patients with BRAFV600E mutant melanoma treated with BRAF inhibitors experience a rapid response, but ultimately develop resistance. Insight into the mechanism of resistance is critical for development of more effective treatment strategies.Experimental Design: Comprehensive genomic profiling of serial biopsies was performed in a patient with a BRAFV600E mutant metastatic melanoma...
متن کاملRole of Caspases and Reactive Oxygen Species in Rose Bengal-Induced Toxicity in Melanoma Cells
Objective We have previously shown that Rose Bengal (RB) alone, not as a photosensitiser, could induce apoptotic- and non-apoptotic cell death in different melanoma cell lines. To clarify RB-induced toxicity mechanisms, role of caspases and reactive oxygen specious (ROS) were studied in melanoma cells. Material and Methods Human melanoma cell lines, Me 4405 and Sk-Mel-28 were cultured in DM...
متن کاملOvercoming resistance to BRAF inhibition in BRAF-mutated metastatic melanoma
Almost 50% of metastatic melanoma patients harbor a BRAF(V600) mutation and the introduction of BRAF inhibitors has improved their treatment options. BRAF inhibitors vemurafenib and dabrafenib achieved improved overall survival over chemotherapy and have been approved for the treatment of BRAF-mutated metastatic melanoma. However, most patients develop mechanisms of acquired resistance and abou...
متن کاملDevelopment of potent autophagy inhibitors that sensitize oncogenic BRAF V600E mutant melanoma tumor cells to vemurafenib
Autophagy is a dynamic cell survival mechanism by which a double-membrane vesicle, or autophagosome, sequesters portions of the cytosol for delivery to the lysosome for recycling. This process can be inhibited using the antimalarial agent chloroquine (CQ), which impairs lysosomal function and prevents autophagosome turnover. Despite its activity, CQ is a relatively inadequate inhibitor that req...
متن کاملResveratrol Overcomes Cellular Resistance to Vemurafenib Through Dephosphorylation of AKT in BRAF-mutated Melanoma Cells.
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...
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ژورنال
عنوان ژورنال: Journal of Investigative Dermatology
سال: 2020
ISSN: 0022-202X
DOI: 10.1016/j.jid.2020.03.689