A melanoma cell state distinction influences sensitivity to MAPK pathway inhibitors

David J. Konieczkowski, Cory M. Johannessen, Omar Abudayyeh, Jong Wook Kim, Zachary A. Cooper, Adriano Piris, Dennie T. Frederick, Michal Barzily-Rokni, Ravid Straussman, Rizwan Haq, David E. Fisher, Jill P. Mesirov, William C. Hahn, Keith T. Flaherty, Jennifer A. Wargo, Pablo Tamayo, Levi A. Garraway

Research output: Contribution to journalArticlepeer-review

Abstract

Most melanomas harbor oncogenic BRAFV600 mutations, which constitutively activate the MAPK pathway. Although MAPK pathway inhibitors show clinical benefit in BRAF V600 -mutant melanoma, it remains incompletely understood why 10% to 20% of patients fail to respond. Here, we show that RAF inhibitor-sensitive and inhibitor-resistant BRAFV600 -mutant melanomas display distinct transcriptional profiles. Whereas most drug-sensitive cell lines and patient biopsies showed high expression and activity of the melanocytic lineage transcription factor MITF, intrinsically resistant cell lines and biopsies displayed low MITF expression but higher levels of NF-κB signaling and the receptor tyrosine kinase AXL. In vitro, these MITF-low/NF-κB-high melanomas were resistant to inhibition of RAF and MEK, singly or in combination, and ERK. Moreover, in cell lines, NF-κB activation antagonized MITF expression and induced both resistance marker genes and drug resistance. Thus, distinct cell states characterized by MITF or NF-κB activity may influence intrinsic resistance to MAPK pathway inhibitors in BRAF V600 -mutant melanoma.

Original languageEnglish
Pages (from-to)816-827
Number of pages12
JournalCancer Discovery
Volume4
Issue number7
DOIs
StatePublished - Jul 2014
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Oncology

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