A German study has identified the mechanism behind papilloma virus (HPV) skin cancer. The key lies in a particular molecular pathway, which makes people with more vomiting (EV) more vulnerable epidermodysplasia.
The beta-beta or beta-HPV virus papilloma is also able to infect skin cells. It therefore increases the risk not only of uterine cancer, but also of skin cancer. To date, the virus's action was not understood. Previous research had suggested a role of the protein called E6, present in the virus. However, the molecular mechanism behind the action of E6 was unclear.
Saarland University researchers focused on HPV on patients with verdure-like epidermodysplasia, a rare genetic disorder. The risk is much more present in these subjects. They have analyzed samples of some skin lesions of patients. Some were positive to beta-papillomas.
Positive HPV lesions showed much lower levels than the average of microRNA-203. The latter regulates the growth of skin cells and their differentiation. The lesions also had higher levels of p63, a protein regulated by the microRNA-203 and associated with the development of tumors.
Laboratory experiments revealed a molecular bond between microRNA-203 and the effects of papilloma virus. The beta-HPV protein E6 suppresses the expression of C / EBP, key protein against skin cancers. The C / EBP rules microRNA-203. Patients with verrucal epidermodysplasia affected by the virus showed very low levels of C / EBP as well as microRNA-203.
Discovery suggests that papilloma interferes with the mechanisms that block the development of skin cancers. Mechanisms that are already weak in subjects with genetic disease.