The effect of the E7 oncoprotein and PKM2 on the growth of HPV-induced cervical cancer

Abstract

Human papillomavirus (HPV) is a sexually transmitted infection (STI) that affects a huge proportion of the global population. High-risk HPVs lead to cervical cancer, which proves fatal for many patients. One of the major proteins related to the increased cell growth of high-risk strains is E7. Furthermore, the high-risk type HPV16 has been found to interact with the key metabolic enzyme pyruvate kinase M2 (PKM2), which is thought to contribute to increased cancerous growth. This project examines the influence of HPV16 E7 on the activation of three transcription factors known to be relevant in the growth of other forms of cancer: phospho-YAP, phospho-STAT3, and B-catenin. Beta-catenin was not found at increased levels when E7 was present, while phospho-YAP was found in larger proportions as a result of E7 influence. STAT3 had inconclusive results for its interaction with E7 but did show a decrease in transcription factor activation when PKM2 was knocked out in the cell line. YAP similarly showed decreased activation in the PKM2 knockout samples.