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Silencing of hpv16 e6 and e7 oncogenic activities by small interference rna induces autophagy and apoptosis in human cervical cancer cells

Author(s): Jonathan Salazar-León | Fabiola Reyes-Román | Angélica Meneses-Acosta | Horacio Merchant | Alfredo Lagunas-Martínez | Elizabeth Meda-Monzón | María Luisa Pita-López | Claudia Gómez-Cerón | Victor Hugo Bermúdez-Morales | Vicente Madrid-Marina | Oscar Peralta-Zaragoza

Journal: Journal of Nucleic Acids Investigation
ISSN 2036-7996

Volume: 2;
Issue: 1;
Start page: e10;
Date: 2011;
Original page

Keywords: Cervical cancer | gene therapy | HPV16 E6 and E7 oncogenes | RNAi | siRNA.

Cervical cancer is the second most common form of death by cancer in women worldwide and has special attention for the development of new treatment strategies. Human Papilloma Virus (HPV) persistent infection is the main etiological agent of this neoplasia, and the main cellular transformation mechanism is by disruption of p53 and pRb function by interaction with HPV E6 and E7 oncoproteins. This generates alterations in cellular differentiation and cellular death inhibition. Thus, HPV E6 and E7 oncogenes represent suitable targets for the development of gene therapy strategies against cervical cancer. An attractive technology platform is developing for post-transcriptional selective silencing of gene expression, using small interference RNA. Therefore, in the present study, we used SiHa cells (HPV16+) transiently transfected with specific siRNA expression plasmids for HPV16 E6 and E7 oncogenes. In this model we detected repression of E6 and E7 oncogene and oncoprotein expression, an increase in p53 and hypophosphorylated pRb isoform protein expression, and autophagy and apoptosis morphology features. These findings suggest that selective silencing of HPV16 E6 and E7 oncogenes by siRNAs, has significant biological effects on the survival of human cancer cells and is a potential gene therapy strategy against cervical cancer.
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