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Cervical cancer (CC) is the fourth leading cancer in women in the age group 15-44 globally. Experimental as well
as epidemiological studies identified that type16 and 18 HPV cause 70% of precancerous cervical lesions as well as cervical
cancer worldwide by bringing about genetic as well as epigenetic changes in the host genome. The insertion of the HPV genome triggers various defense mechanisms including the silencing of tumor suppressor genes as well as activation of oncogenes associated with cancer metastatic pathway. E6 and E7 are small oncoproteins consisting of 150 and 100 amino acids
respectively. These oncoproteins affect the regulation of the host cell cycle by interfering with p53 and pRb. Further these
oncoproteins adversely affect the normal functions of the host cell by binding to their signaling proteins. Recent studies
demonstrated that E6 and E7 oncoproteins are potential targets for CC. Therefore, this review discusses the role of E6 and
E7 oncoproteins in metastasis and drug resistance as well as their regulation, early oncogene mediated signaling pathways.
This review also uncovers the recent updates on molecular mechanisms of E6 and E7 mediated phytotherapy, gene therapy,
immune therapy, and vaccine strategies as well as diagnosis through precision testing. Therefore, understanding the potential role of E6/E7 in metastasis and drug resistance along with targeted treatment, vaccine, and precision diagnostic strategies could be useful for the prevention and treatment of cervical cancer.
Molecular Characterization of HPV16 E6 and E7 Variants among Women with Cervical Cancer in Morocco
