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A Comprehensive Review on Cross-talk of Human Papilloma Virus Oncoproteins and Developmental/Self-Renewal Pathways During the Pathogenesis of Uterine Cervical Cancer

Author(s):

Afza Ahmad and Irfan Ahmad Ansari*   Pages 1 - 15 ( 15 )

Abstract:


Cervical cancer, a cancer arising from the uterine cervix has been regarded as the fourth most frequent gynecological malignancy among females worldwide. Epidemiological reports have shown that uterine cervical cancer is a global health issue among womens of specially developing countries and consequently creates an economic and medical burden in the society. The main causative agent of cervical carcinoma is high risk human papilloma virus (HPV 16 and HPV 18). Molecular studies have revealed the expression two viral genes E6 and E7 after HPV infection in the epithelial cells of cervix. These gene products are known to inactivate the major tumor suppressors, p53 and retinoblastoma protein (pRB), respectively. Moreover, the role of self-renewal pathways such as Hedgehog, Notch and Wnt has also been linked with drug resistance in cancer cells and epithelial mesenchymal transition during metastasis in pathogenesis of cervical cancer. Although, the mechanism of interaction of HPV E6 and E7 with each and every component of above described developmental pathways is not elucidated yet, but preliminary reports of their crosstalk have begun to emerge. Understanding the interplay between these oncoproteins and developmental/self-renewal pathways is highly important in terms of designing new and targeted therapeutic approach against cervical cancer. Hence, this review cynosure the carcinogenesis of HPV with the brief description of its virology and also establishes the crosstalk between oncoproteins E6 & E7 and Hedgehog, Notch and Wnt signaling pathway.

Keywords:

Cervical cancer, Human Papilloma Virus (HPV), Oncoproteins, Hedgehog, Wnt, Notch

Affiliation:

Department of Biosciences, Integral University, Lucknow, 226026, Department of Biosciences, Integral University, Lucknow, 226026



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