NSD2 and miRNAs as Key Regulators of Melanoma Response to Romidepsin and Interferon-α2b Treatment
De Santis A, De Santis L, Rossi F, Gasparini S, Licursi V, Amico VA, Capone I, Fragale A, D'Atri S, Gabriele L, Presutti C
My role: First author. Ran the full bioinformatics workflow end-to-end: bulk RNA-seq processing, TCGA cohort re-analysis, miRNA-target integration, and differential expression linking NSD2 down-regulation to the de-differentiated, therapy-resistant melanoma phenotype.
In plain language: Combination therapy (Romidepsin + Interferon-α2b) pushes melanoma cells into a de-differentiated state that mirrors clinically resistant tumors. By cross-referencing patient transcriptomes (TCGA) with in-house RNA-seq, we pinpointed NSD2 — an epigenetic regulator — and a small set of miRNAs as the molecular switch behind this transition. Useful for teams searching for resistance biomarkers or rational combination targets in melanoma.