Transcription factors as critical players in melanoma invasiveness, drug resistance, and opportunities for therapeutic drug development

Karine A. Cohen-Solal, Howard L. Kaufman, Ahmed Lasfar

    Research output: Contribution to journalReview articlepeer-review

    16 Scopus citations

    Abstract

    Resistance to targeted therapy in cancer is often coupled with the acquisition of a pro-invasive phenotype by tumors cells and a highly permissive tumor microenvironment promoting drug resistance. Transcription factors are frequently shown as major points of convergence of multiple dysregulated receptors and signaling pathways in cancer. Several transcription factors are now incriminated as drivers of both drug resistance and invasiveness. We focused this review on critical transcription factors playing a causal role in both the resistance to BRAF V600E-targeted therapy and the pro-invasive behavior of melanoma cells. Simultaneous rewiring of pro-oncogenic signaling pathways, phenotype switching or phenotypic plasticity supporting pro-invasive/pro-metastatic behavior, actin remodeling, and bidirectional interactions between tumor microenvironment and melanoma cells represent major challenges for overcoming resistance to BRAF V600E inhibitors (BRAFi) and will be discussed. Although it represents an underdeveloped area of translational investigation, inhibition of transcription factors may open new avenues to combat resistance to BRAFi.

    Original languageEnglish (US)
    Pages (from-to)241-252
    Number of pages12
    JournalPigment Cell and Melanoma Research
    Volume31
    Issue number2
    DOIs
    StatePublished - Mar 2018

    All Science Journal Classification (ASJC) codes

    • Oncology
    • Biochemistry, Genetics and Molecular Biology(all)
    • Dermatology

    Keywords

    • invasiveness
    • melanoma
    • microenvironment
    • resistance to therapy
    • targeted therapy
    • transcription factors

    Fingerprint

    Dive into the research topics of 'Transcription factors as critical players in melanoma invasiveness, drug resistance, and opportunities for therapeutic drug development'. Together they form a unique fingerprint.

    Cite this