Editor's Summary

Death to Melanoma

Melanoma is a particularly aggressive form of skin cancer. Although the identification of a specific mutation in the kinase-encoding gene BRAF has facilitated the development of clinical therapies, many melanoma patients with the BRAF^V600E mutation fail to exhibit long-term responsiveness to inhibition of this kinase. Biechele et al. found that some melanoma cell lines exhibited an enhanced apoptotic response when BRAF^V600E was inhibited simultaneously with activation of the Wnt/β-catenin pathway. The susceptibility to this cell death response correlated with the ability of the combination treatment to reduce the abundance of AXIN1, a negative regulator of the Wnt/β-catenin pathway, and knockdown of AXIN1 abundance caused apoptosis-resistant melanoma cell lines to become susceptible to apoptosis in response to the combined treatment. Thus, exploiting this functional crosstalk between BRAF and Wnt/β-catenin signaling may yield more effective therapies for treating melanoma.

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