The role of RNA viruses in human cancers

Abstract

Many RNA viruses have been reported to be oncogenic (or carcinogenic) in a variety of animal and human cancers. The increase in the incidence and prevalence of cancer-causing viruses in human populations can be known as a key precursor to the development of various cancers. The retrovirus family and Hepatitis C virus (HCV) are also reported to cause cancer. Viral oncoproteins such as Tax of HTLV 1 interacts with cellular ubiquitination complex such as cyclindromatosis tumor suppressor, ubiquitin-specific proteases 7, 11, 15 and 20, A-20 and signal-transducing adaptor molecule binding protein-like-1 in order to improve the cellular signaling pathways. The viral oncoproteins binding to DUB, leading to proliferation of virus-infected cells and cell transformation. Proto-oncogenes (c-onc genes) are the cellular form of v-onc genes. The activation of c-onc genes leads to cell growth. C-onc genes are transformed into an oncogenic form by viral infection. C-onc genes play some roles such as protein kinases, growth factors, growth factor receptors, and DNA binding proteins. The study of transforming retroviruses and their oncogenes and the multiple mechanisms deployed by other RNA viruses to use the growth-suppressive and proapoptotic function of tumor suppressor genes has been added to our current understanding of cancer biology. Oncogenic RNA viruses are important experimental models to study molecular investigation such as cellular networks, including the discovery of oncogenes and tumor suppressors. Understanding of different strategies of RNA viruses as well as the function of their proteins helps to make more extensive plans regarding the adoption of follow-up, prevention and treatment strategies in cancer patients caused by viral origin.