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Differentially expressed genes between high-risk human papillomavirus types in human cervical cancer cells
  1. G. Vazquez-Ortiz*,
  2. J. A. García,
  3. C. J. Ciudad,
  4. V. Noé,
  5. S. Peñuelas,
  6. R. LÓPEZ-ROMERO*,
  7. P. Mendoza-Lorenzo*,
  8. P. Piña-Sánchez* and
  9. M. Salcedo*
  1. * Laboratory of Oncogenomics, Oncology Research Unit, Oncology Hospital, National Medical Center SXXI-IMSS, México, DF, Mexico
  2. Keck Graduate Institute of Applied Life Sciences, Claremont, California
  3. Department of Biochemistry and Molecular Biology, School of Pharmacy, University of Barcelona, Barcelona, Spain
  1. Address correspondence and reprint requests to: Mauricio Salcedo, PhD, Laboratorio de Oncología Genómica, Unidad de Investigación Médica en Enfermedades Oncológicas, Hospital de Oncología, Centro Médico Nacional SXXI-IMSS, Av. Cuauhtemoc 330, Col. Doctores, México DF 07780, Mexico. Email: maosal89{at}yahoo.com

Abstract

Cervical carcinoma (CC) is one of the most common cancers among women worldwide and the first cause of death among the Mexican female population. Human papillomavirus (HPV) infection is the most important etiologic factor for CC. Of the oncogenic types, HPV16 and HPV18 are found in 60–70% of invasive CCs worldwide. HPV18 appears to be associated with a more aggressive form of cervical neoplasia than HPV16 infection. At present, there are no studies on differentially expressed cellular genes between transformed cells harboring HPV16 and HPV18 sequences. Based on previous complementaryDNA microarray data from our group, 13 genes were found to be differentially overexpressed between HPV16- and HPV18-transformed cells. These genes were as follows: E6BP, UBE4A, C20orf14, ATF7, ABCC8, SLC6A12, WASF3, SUV39H1, SPAG8, CCNC, E2FFE, BIRC5, and DEDD. Differential expression of six selected genes was confirmed by real-time reverse transcription–polymerase chain reaction (RT-PCR). All real-time RT-PCRs confirmed differential expression between HPV18 and HPV samples. The present work identifies genes from signaling pathways triggered by HPV transformation that could be differentially deregulated between HPV16+ and HPV18+ samples.

  • cervical cancer
  • differential expression
  • HPV

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