In a new article, scientists from the International Agency for Research on Cancer (IARC) and partners describe a novel virus-driven mechanism that converts p53 from a tumour suppressor protein into a pro-proliferative factor. The article was published in the journal PLoS Pathogens.
In the study, the authors dissect a new mechanism driven by cutaneous beta human papillomavirus (HPV) type 38 in altering the function of p53. This may have an important impact in understanding the biology of wild-type p53 in cancer-transformed cells. p53 is a key protein that is altered in all cancer cells. In about half of human cancers, p53 is inactivated through DNA mutation. The other half of cancers harbour a wild-type p53 gene whose tumour suppressor functions are altered by different mechanisms, which are not yet completely understood.
Romero-Medina MC, Venuti A, Melita G, Robitaille A, Ceraolo MG, Pacini L, et al.
Human papillomavirus type 38 alters wild-type p53 activity to promote cell proliferation via the downregulation of integrin alpha 1 expression
PLoS Pathog, Published online 19 August 2020;