Molecular mechanisms of hyperplasia induction by human papillomavirus E7

Oncogene
T UenoH Sakai

Abstract

Infections of human papillomavirus (HPV) induce a variety of benign tumors, such as warts and condylomas. During the process of aberrant cell proliferation, genetic mutations are accumulated in the cells, from which malignant tumor cells arise. The viral oncoproteins E6 and E7 are known to help disrupt the cell cycle checkpoint machinery and accelerate chromosomal instability, events which are critical in malignant conversion. However, the mechanisms involved in the hyperplasia caused by HPV infection have remained unknown. We analysed the effects of regulatory genes of HPV18, a typical high-risk-type HPV, on the formation of the epithelial organ by using an organotypic culture system, and found that E7 had potent activity to induce hyperplasia, to which the disruption of the pRb pathway was well correlated. However, analysis with the E7 variants indicated that other pocket proteins are also involved in the activity.

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Citations

Apr 23, 2011·Journal of Cell Science·Simon S McDadeDennis J McCance
Apr 21, 2009·Uirusu·Ayano Satsuka, Hiroyuki Sakai
Jun 27, 2008·Pathobiology : Journal of Immunopathology, Molecular and Cellular Biology·Shuichi FujitaKan Toriyama
Nov 11, 2009·Science·Vincent Lavallo, Robert H Grubbs
Jan 15, 2009·Journal of Oral Pathology & Medicine : Official Publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology·Alinda Dalma VarnaiRalf Hildenbrand
Feb 20, 2015·Journal of Virology·Halena R VanDeusen, Robert F Kalejta
Jul 18, 2008·Cancer Research·Mako Narisawa-SaitoTohru Kiyono
Jul 14, 2021·JCI Insight·Fiona J RuizJulie K Schwarz

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