SKIN CANCER AND HUMAN PAPILLOMAVIRUS

Abstract

Skin cancer (SC) is the one of the widespread kind of cancers worldwide. Among other risk factors, Human Papillomavirus (HPV) is the potential causative agents for skin tumorigenesis. In previously scientific published research, the underlying role of HPV remained controversial about which kind of HPVs are involved on the onset initiation and progression of non-melanoma skin cancer (NMSC) such as squamous cell carcinoma (SCC), basal cell carcinoma (BCC) and malignant melanoma (MM). Apha and beta HPV have been found with the course and development of keratinocytes mutation and skin tumor malignancies. The pathogenicity of HPV lies in its oncogenic proteins such as E6 and E7 belong to Beta HPV kind along with various other transcriptional factors. E6 and E7 are found to deregulation in the tumor suppressor genes p53 and pRb to disturb normal activity of cell cycle and to help metastasize skin cancer. There are also increasing evidences of weakened immune system in melanoma and non-melanoma skin cancer patients associated with human papillomavirus. The combined influence of ultraviolet radiations (UVA and UVB) has detected with human papillomavirus to trigger and promote melanoma and non-melanoma skin cancer development. These results in altered chromosome structure, uncontrolled S-phase, and inhibit apoptosis to advance skin carcinoma. This review article summarizes not only previous arguments for the involvement of oncogenicity of HPVs strains with skin cancer types but also demonstrates an extensive review of the significant previously published data that were not covered yet.