Resumen
TP53 is one of the most important tumor suppressor genes, which has been found to be mutated in more than half of human cancers and is considered the ?Guardian of the genome?. However, it is rarely mutated in melanoma (less than 20% of cases). Although several cancer-oriented studies focus on p53 biology, only recently have researchers started to appreciate the importance of shorter p53 isoforms as potential modifiers of p53-dependent responses. In this study, we showed that melanoma-derived cell lines express a wide array of p53 and p73 isoforms, with ?160p53a as the most variable. For the first time, we reported that ?160p53a, and to a lesser extent ?160p53ß, can be recruited on chromatin, and ?160p53? can localize in perinuclear foci; moreover, all ?160p53 isoforms can stimulate proliferation and, potentially, migration. Lastly, we showed an increased expression of the potentially pro-oncogenic ?40p53ß isoform and a decrease in the tumor-suppressive TAp73ß isoform in melanoma cells resistant to vemurafenib (BRAF inhibitor). With this study, we suggest that p53 family isoforms play a significant role in melanoma cells? aggressiveness.