Abstract
Melanoma cells with acquired resistance to dabrafenib display changes in miRNA expression pattern and respond to this drug with an increase of invasiveness, which is abrogated by inhibition of NFB or the PI3K/mTOR signalling pathway Simona Caporali, Ester Alvino, Adriana Amaro, Pedro Miguel Lacal, Lauretta Levati, Maria Grazia Atzori, Gian Carlo Antonini Cappellini, Federica Ruffini, Enzo Bonmassar, Ulrich Pfeffer, Stefania D’Atri
Highlights
The therapeutic success of BRAF inhibitors (BRAFi) is limited by the emergence of drug resistance [1,2]
In vitro ECM invasion by A375R cells treated with the NF-B inhibitor NEMO-binding domain (NBD) peptide (50 μM, 48 hours) or the PI3K/ mTOR inhibitor GSK-2126458 (20 nM, 48 hours), alone or in combination with 100 nM dabrafenib, was evaluated
Eighty-nine miRNAs were up-regulated and 47 miRNAs were downregulated in the A375R cells with respect to A375 cells
Summary
The therapeutic success of BRAF inhibitors (BRAFi) is limited by the emergence of drug resistance [1,2]. Several mechanisms underlying acquired resistance to BRAFi have been identified [1,2], further studies are required to disclose their entire spectrum. Altered expression and/or function of microRNAs (miRNAs) is involved in tumor onset, progression and drug resistance [3]. We determined miRNA expression profiles of melanoma cells sensitive or resistant to the BRAFi dabrafenib, and investigated the effect of this drug on their invasiveness. We evaluated the consequences of inhibiting NF-B or the PI3K/mTOR signalling pathway on the invasive capacity of dabrafenib-resistant cells
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