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Genome wide expression analysis in HPV16 Cervical Cancer: identification of altered metabolic pathways

Carlos Pérez-Plasencia1 email, Guelaguetza Vázquez-Ortiz2 email, Ricardo López-Romero3 email, Patricia Piña-Sanchez2 email, José Moreno3 email and Mauricio Salcedo2 email

1Unidad de Investigación Biomédica en Cáncer, Instituto de Investigaciones Biomédicas, Universidad Nacional Autonóma de Mexico (UNAM), (INCAN), Mexico City, Mexico

2Laboratorio de Oncología Genómica, Unidad de Investigación Médica en Enfermedades Oncológicas, Hospital de Oncología, CMN Siglo XXI-IMSS, Mexico

3Unidad de Investigación Médica en Enfermedades Autoinmunes, Hospital de Especialidades, CMN Siglo XXI-IMSS, Mexico

author email corresponding author email

Infectious Agents and Cancer 2007, 2:16doi:10.1186/1750-9378-2-16

Published: 6 September 2007

Abstract

Background

Cervical carcinoma (CC) is a leading cause of death among women worldwide. Human papilloma virus (HPV) is a major etiological factor in CC and HPV 16 is the more frequent viral type present. Our aim was to characterize metabolic pathways altered in HPV 16 tumor samples by means of transcriptome wide analysis and bioinformatics tools for visualizing expression data in the context of KEGG biological pathways.

Results

We found 2,067 genes significantly up or down-modulated (at least 2-fold) in tumor clinical samples compared to normal tissues, representing ~3.7% of analyzed genes. Cervical carcinoma was associated with an important up-regulation of Wnt signaling pathway, which was validated by in situ hybridization in clinical samples. Other up-regulated pathways were those of calcium signaling and MAPK signaling, as well as cell cycle-related genes. There was down-regulation of focal adhesion, TGF-β signaling, among other metabolic pathways.

Conclusion

This analysis of HPV 16 tumors transcriptome could be useful for the identification of genes and molecular pathways involved in the pathogenesis of cervical carcinoma. Understanding the possible role of these proteins in the pathogenesis of CC deserves further studies.


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