What are the therapeutic implications of increased collagen expression in melanoma cells treated with vemurafenib?

In a recent article published in Matrix Biology, M Jenkins, W Croteau, D Mullins and I described the effect of the mutant BRAFV600E inhibitor, vemurafenib/PLX4032, on collagen synthesis in melanoma cells [1]. We found that this small molecule inhibitor, which blocks the sequential MAPK, RAS, RAF, MEK, ERK signaling pathway [2–4], substantially increased the synthesis of type I collagen in several human and murine melanoma cell lines. Importantly, we also found that the MEK inhibitor, U0126, which targets the wild-type MAPK pathway [2–4], also increased collagen production, indicating that this effect is not limited to cells harboring mutant BRAF.

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