Affiliation:
1. Department of Microbiology, The Chinese University of Hong Kong, Prince of Wales Hospital, Hong Kong SAR
2. International Centre for Genetic Engineering and Biotechnology, Trieste, Italy
Abstract
Epidemiological studies have revealed that a wild-type variant of HPV58 carrying an E7 variation, T20I/G63S (V1), is associated with a higher risk of cervical cancer. We previously reported that this increased oncogenicity could be the result of the virus’s greater ability to degrade pRB, thereby leading to an increased ability to grow in an anchorage-independent manner. In addition to this, this report further showed that this HPV variant induced activation of the AKT and K-Ras/ERK signaling pathways, thereby explaining its genuine oncogenicity in promoting cell proliferation, migration, invasion, and formation of tumors, all to a greater extent than the prototype HPV58 and other common variants.
Funder
Research Grants Council, University Grants Committee
Publisher
American Society for Microbiology
Subject
Virology,Insect Science,Immunology,Microbiology
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