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Reshmi, G and Pillai, MR (2012) Interplay Between HPV Oncoproteins and MicroRNAs in Cervical Cancer. From Bench to Bedside – Research Aspects.

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For close to a century, researchers have known that Papillomavirus infections in humans cause a variety of benign proliferations including warts, epithelial cysts, intraepithelial neoplasias, oral laryngeal, pharyngeal papillomas and other types of hyperkeratosis. However the molecular mechanisms involved are far from understood. HPV has been detected in more than 90% of cervical cancers and therefore implicated as the main etiological agents in cervical cancer. The pathogenesis of cervical cancer is well-known to involve a multi-step process that includes the transformation of normal cervical epithelium to pre-neoplastic cervical intraepithelial neoplasia that is subsequently transformed to invasive cervical cancer. Although the causal relationship between high-risk human papillomavirus (HPV) infection and cervical cancer has been well-documented in epidemiologic and functional studies, HPV infection alone is not sufficient to induce the malignant transformation of HPV-infected cells. Hence, other unidentified genetic alterations, such as microRNAs the master switches, are required. A class of molecules discovered quite recently, microRNAs (miRNAs), appear to play a significant role in cell proliferation and differentiation, and aberrant miRNAs are associated with several cancers. An new era focusing on micro RNAs, and the studies on HPV and host miRNA interactions will continue shedding more light on understanding of the HPV life cycle and the mechanistic underpinnings of HPV-induced oncogenesis. These small non-coding RNAs can contribute to the repertoire of host pathogen interactions during viral infection. This interplay has important consequences, both for the virus and the host. There has been reported evidence of host-cellular miRNAs modulating expression of various viral genes, thereby playing a pivotal role in the host–pathogen interaction network. In the hide-and-seek game between the pathogens and the infected host, viruses have evolved highly sophisticated gene-silencing mechanisms to evade host-immune response. Recent reports indicate that virus also encode miRNAs that protect them against cellular antiviral response. Furthermore, they may exploit the cellular miRNA pathway to their own advantage. This chapter aims to summarize our current knowledge about miRNA profiles in cervical cancer cell lines and tissues as well as recapitulate recent updates on miRNAinduced gene-silencing mechanism; modulating host–virus interactions of HPV integrated Cervical Carcinomas.

Item Type: Article
Subjects: Cancer Research
Depositing User: Rgcb Library
Date Deposited: 29 Jun 2018 08:06
Last Modified: 29 Jun 2018 08:07
URI: http://rgcb.sciencecentral.in/id/eprint/630

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