Abstract
The primary causes of cervical cancer are human papillomavirus type 16 (HPV16) and/or other high-risk (Hr -) HPV infections. Hr-HPVE5, E6, and E7 have been identified as oncoproteins that play roles in the development of cancer. However, other HPV proteins, especially E1, may also be involved in cancer development. In this study, the role of HPV16E1 in cervical carcinogenesis was examined by siRNA knockdown experiments using SiHa cells as a model. The results showed that HPV16E1 regulated P-FOXO3a and HPV16E7 expression. Various cell functions associated with the hallmarks of cancer, including cell viability, colony formation, invasion, and anchorage-independent cell growth, were altered when HPV16E1 was downregulated. However, no effect on cell migration and apoptosis properties was found. Moreover, HPV16E1 downregulation resulted in an increase in cisplatin susceptibility. In conclusion, this is the first demonstration that HPV16E1 might be regarded as a possible novel oncoprotein involved in several processes related to oncogenesis.