Reply to: Biological role of miR-204 and miR-211 in melanoma (published in Oncoscience, Vol 5 (7-8), July 2018)

Melanoma treatment with the BRAF V600E inhibitor vemurafenib provides therapeutic benefits, but the frequent emergence of drug resistance remains an important clinical challenge. Although reactivation of the MAPK and PI3K–Akt pathways is a common resistance response in melanoma patients treated with vemurafenib, a significant portion of tumors displays unknown resistance mechanisms that cannot be accounted for genetic alterations. In a recent study we addressed the potential role of microRNAs in resistance to vemurafenib in melanoma, and we showed that rapid upregulation of miR-204-5p and miR-211-5p following vemurafenib treatment enables the emergence of early resistance. These conclusions were experimentally supported by ectopic expression of these miRNAs in drug-na？ve human melanoma cells, which was sufficient to confer vemurafenib resistance and more robust tumor growth in vitro and in vivo. Conversely, silencing the expression of these miRNAs in vemurafenib-resistant cells impaired cell growth in the presence of the inhibitor. In a recent short report by Vitiello and colleagues published in Oncoscience, authors claimed that conclusions of our work were not supported by the published data. In the present answer, we provide a reasoned explanation that confirms and supports our results