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• W2808863372 abstract "Whereas significant anti-tumor responses are observed in most BRAFV600E-mutant melanoma patients exposed to MAPK-targeting agents, resistance almost invariably develops. Here, we show that in therapy-responsive cells BRAF inhibition induces downregulation of the processing of Sterol Regulator Element Binding (SREBP-1) and thereby lipogenesis. Irrespective of the escape mechanism, therapy-resistant cells invariably restore this process to promote lipid saturation and protect melanoma from ROS-induced damage and lipid peroxidation. Importantly, pharmacological SREBP-1 inhibition sensitizes BRAFV600E-mutant therapy-resistant melanoma to BRAFV600E inhibitors both in vitro and in a pre-clinical PDX in vivo model. Together, these data indicate that targeting SREBP-1-induced lipogenesis may offer a new avenue to overcome acquisition of resistance to BRAF-targeted therapy. This work also provides evidence that targeting vulnerabilities downstream of oncogenic signaling offers new possibilities in overcoming resistance to targeted therapies." @default.
• W2808863372 created "2018-06-29" @default.
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• W2808863372 date "2018-06-27" @default.
• W2808863372 modified "2023-10-17" @default.
• W2808863372 title "Sustained SREBP-1-dependent lipogenesis as a key mediator of resistance to BRAF-targeted therapy" @default.
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• W2808863372 doi "https://doi.org/10.1038/s41467-018-04664-0" @default.
• W2808863372 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6021375" @default.
• W2808863372 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/29950559" @default.
• W2808863372 hasPublicationYear "2018" @default.
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