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[Preprint]. 2023 Nov 14:2023.11.10.564582. [Version 1] doi: 10.1101/2023.11.10.564582

MITF regulates IDH1 and NNT and drives a transcriptional program protecting cutaneous melanoma from reactive oxygen species

Elisabeth Roider, Alexandra IT Lakatos, Alicia M McConnell, Poguang Wang, Alina Mueller, Akinori Kawakami, Jennifer Tsoi, Botond L Szabolcs, Anna A Ascsillán, Yusuke Suita, Vivien Igras, Jennifer A Lo, Jennifer J Hsiao, Rebecca Lapides, Dorottya MP Pál, Anna S Lengyel, Alexander Navarini, Arimichi Okazaki, Othon Iliopoulos, István Németh, Thomas G Graeber, Leonard Zon, Roger W Giese, Lajos V Kemeny, David E Fisher
PMCID: PMC10680652  PMID: 38014031

Abstract

Microphthalmia-associated transcription factor (MITF) plays pivotal roles in melanocyte development, function, and melanoma pathogenesis. MITF amplification occurs in melanoma and has been associated with resistance to targeted therapies. Here, we show that MITF regulates a global antioxidant program that increases survival of melanoma cell lines by protecting the cells from reactive oxygen species (ROS)-induced damage. In addition, this redox program is correlated with MITF expression in human melanoma cell lines and patient-derived melanoma samples. Using a zebrafish melanoma model, we show that MITF decreases ROS-mediated DNA damage in vivo . Some of the MITF target genes involved, such as IDH1 and NNT , are regulated through direct MITF binding to canonical enhancer box (E-BOX) sequences proximal to their promoters. Utilizing functional experiments, we demonstrate the role of MITF and its target genes in reducing cytosolic and mitochondrial ROS. Collectively, our data identify MITF as a significant driver of the cellular antioxidant state.

One Sentence Summary

MITF promote melanoma survival via increasing ROS tolerance.

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