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Review Article

E6 and E7 Oncoproteins: Potential Targets of Cervical Cancer

[ Vol. 28 , Issue. 39 ]


Ramarao Malla* and Mohammad Amjad Kamal   Pages 8163 - 8181 ( 19 )


Cervical cancer (CC) is the fourth leading cancer in women in the age group of 15-44 years 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 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.


Cervical cancer, early oncogenes, human papilloma virus, phytotherapy, precision testing, HPC genome.


Cancer biology Lab, Department of Biochemistry and Bioinformatics, GIS, (GITAM) Deemed to be University), Visakhapatnam-530045, Andhra Pradesh, King Fahd Medical Research Center, King Abdulaziz University, P. O. Box 80216, Jeddah 21589

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