Solar UV irradiation of the skin causes DNA damage, which if not repaired correctly, can result in mutations. Consistently, cutaneous melanoma frequently has a high mutational burden, making it more aggressive and difficult to treat. However, it is not known whether these cells have specific pro-survival mechanisms or enhanced DNA repair capacity. The transcription factor BRN2 is a known driver of invasiveness and regulator of proliferation in melanoma. In this article published in Genes and Development, Katie Herbert and colleagues from Colin Goding’s lab show that BRN2 associates with sites of DNA damage and promotes a more error-prone DNA repair mechanism. Furthermore, BRN2 also reduces cell death of damaged cells. This work has implications for the treatment of melanoma using DNA-damaging agents in cancers expressing BRN2.
26 February 2019
BRN2 reprogrammes DNA repair and promotes survival in melanoma