Mechanisms of Human Papillomavirus-Induced Oncogenesis

Biology of Human Papillomavirus Infections in Head and Neck Carcinogenesis

“…The HPV E7 protein can induce cellular proliferation through several pathways by disrupting the activity of cyclin-dependent kinase (CDK) inhibitors p21 and p27, activation of CDKs and destabilization of the Rb tumor suppressor protein [for review see [20][21][22][23][24]. Rb family members (pRb, p107, p130) are instrumental in the control of cell cycle progression largely through regulation of the E2F family of transcription factors [23,25]. Thus, binding of E7 to hypophosphorylated Rb results in the release of E2F factors that are necessary for transcription of genes involved in proliferation and cell cycle progression.…”

Retinoblastoma family proteins as key targets of the small DNA virus oncoproteins

“…At present, more than 150 different HPV genotypes have been isolated and grouped roughly into mucosal (a) or skin (b) genotypes, according to their preferred target tissue (De Villiers et al, 2004;Munger et al, 2004). Productive HPV infection has long been known to cause benign squamous hyperplasias, also known as warts.…”

INPP4B restrains cell proliferation and metastasis via regulation of the PI3K/AKT/SGK pathway

“…Although human papillomavirus (HPV) vaccines are available, cervical cancer still causes a considerable amount of death because of the limited application of the vaccine. Persistent infection with high‐risk HPV is the main aetiological factor in cervical carcinogenesis 2, 3, 4. However, HPV infection alone does not sufficiently explain the occurrence of cervical cancer because HPV oncogenes E6 and E7 can immortalize but do not transform human epithelial cells 5, 6.…”