%0 Journal Article
%T Reply to: Biological role of miR-204 and miR-211 in melanoma (published in Oncoscience, Vol 5 (7-8), July 2018)
%A Joaquin Teixid¨®
%A Lola Alonso
%A Luc¨ªa Benito-Jard¨®n
%A Marta D¨ªaz-Mart¨ªnez
%J Archive of "Oncoscience".
%D 2018
%R 10.18632/oncoscience.473
%X 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¨CAkt 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
%K mmelanoma
%K resistance
%K microRNA
%U https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6231445/