Effect of stress-induced polyploidy on melanoma reprogramming and therapy resistance

Melanomas and their precursors, the melanocytes, are frequently exposed to UV due to their anatomic location, leading to DNA damage and reactive oxygen stress related harm. Such damage can result in multinucleation or polyploidy, in particularly in presence of mitotic or cell division failure. As a consequence, the cell encounters either of two fates: mitotic catastrophe, resulting in cell death, or survival and recovery, the latter occurring less frequently. However, when cells manage to recover in an polyploid state, they have often acquired new features, which allow them to tolerate and adapt to oncogene- or therapy induced stress. This review focuses on polyploidy inducers in melanoma and their effects on transcriptional reprogramming and phenotypic adaptation as well as the relevance of polyploid melanoma cells for therapy resistance.

Automated summary

Melanomas and melanocytes are frequently exposed to UV, resulting in DNA damage and reactive oxygen stress related harm. This can lead to multinucleation or polyploidy, with the cells either experiencing mitotic catastrophe and death or surviving and acquiring new features to adapt to stress. This review focuses on polyploidy inducers in melanoma, their effects on transcriptional reprogramming and phenotypic adaptation, and the significance of polyploid melanoma cells in therapy resistance.