Dataset Information

Vemurafenib Drives Epithelial-to-Mesenchymal Transition Gene Expression in BRAF Inhibitor‒Resistant BRAF^V600E/NRAS^Q61K Melanoma Enhancing Tumor Growth and Metastasis in a Bioluminescent Murine Model.

ABSTRACT: BRAF inhibitor (BRAFi) resistance compromises long-term survivorship of patients with malignant melanoma, and mutant NRAS is a major mediator of BRAFi resistance. In this study, employing phenotypic and transcriptomic analysis of isogenic melanoma cells that differ only by NRAS mutational status (BRAFi-sensitive A375-BRAF^V600E/NRAS^Q61 vs. BRAFi-resistant A375-BRAF^V600E/NRAS^Q61K), we show that BRAFi (vemurafenib) treatment selectively targets BRAF^V600E/NRAS^Q61K cells upregulating epithelial-to-mesenchymal transition (EMT) gene expression, paradoxically promoting invasiveness and metastasis in vitro and in vivo. First, NanoString nCounter transcriptomic analysis identified the upregulation of specific gene expression networks

SUBMITTER: Jandova J

PROVIDER: S-EPMC9021323 | biostudies-literature | 2022 May

REPOSITORIES: biostudies-literature

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Dataset Information

Vemurafenib Drives Epithelial-to-Mesenchymal Transition Gene Expression in BRAF Inhibitor‒Resistant BRAF^V600E/NRAS^Q61K Melanoma Enhancing Tumor Growth and Metastasis in a Bioluminescent Murine Model.

OmicsDI is part of the ELIXIR infrastructure

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Dataset Information

Vemurafenib Drives Epithelial-to-Mesenchymal Transition Gene Expression in BRAF Inhibitor‒Resistant BRAFV600E/NRASQ61K Melanoma Enhancing Tumor Growth and Metastasis in a Bioluminescent Murine Model.

OmicsDI is part of the ELIXIR infrastructure

Tweets

Vemurafenib Drives Epithelial-to-Mesenchymal Transition Gene Expression in BRAF Inhibitor‒Resistant BRAF^V600E/NRAS^Q61K Melanoma Enhancing Tumor Growth and Metastasis in a Bioluminescent Murine Model.