New role of ID3 in melanoma adaptive drug-resistance

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 TGFβ/EGFR/PDGFR...

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Published inOncotarget Vol. 8; no. 66; pp. 110166 - 110175
Main Authors Sachindra, Larribère, Lionel, Novak, Daniel, Wu, Huizi, Hüser, Laura, Granados, Karol, Orouji, Elias, Utikal, Jochen
Format Journal Article
LanguageEnglish
Published United States Impact Journals LLC 15.12.2017
Subjects
Research Paper
targeted therapy
ID3
drug-resistance
melanoma
BRAF
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Summary: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 TGFβ/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 increases the melanoma sensitivity to vemurafenib short-term treatment. In addition, we observe an -mediated regulation of cell migration and of the expression of resistance-associated genes such as and . 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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ISSN:1949-2553
1949-2553
DOI:10.18632/oncotarget.22698