Journal
ONCOTARGET
Volume 8, Issue 66, Pages 110166-110175Publisher
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.22698
Keywords
melanoma; ID3; drug-resistance; targeted therapy; BRAF
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Funding
- German Research Council [RTG2099]
- German Cancer Aid (Max Eder Research Group)
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Adaptive resistance to targeted therapy such as BRAF inhibitors represents in melanoma a major drawback to this otherwise powerful treatment. Some of the underlying molecular mechanisms have recently been described: hyperactivation of the BRAF-MAPK pathway, of the AKT pathway, of the TGF beta/EGFR/PDGFRB pathway, or the low MITF/AXL ratio. Nevertheless, the phenomenon of early resistance is still not clearly understood. In this report, we show that knockdown of neural crest-associated gene ID3 increases the melanoma sensitivity to vemurafenib short-term treatment. In addition, we observe an ID3-mediated regulation of cell migration and of the expression of resistance-associated genes such as SOX10 and MITF. In sum, these data suggest ID3 as a new key actor of melanoma adaptive resistance to vemurafenib and as a potential drug target.
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