Submitted: 17 Oct 2016
Revised: 01 Dec 2016
Accepted: 04 Dec 2016
First published online: 18 Dec 2016
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Int J Enteric Pathog. 2017;5(1):1-4.
doi: 10.15171/ijep.2017.01
  Abstract View: 813
  PDF Download: 500
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Research Article

Determination of the Physical Status (Episomal/Integral) of HPV by qPCR in Esophageal Squamous Cell Carcinoma

Fariborz Soheili 1,2 * , Bahram Nikkho 1, Mazaher Khodabandehloo 2

1 Cellular and Molecular Research Center, Kurdistan University of Medical Sciences, Sanandaj, Iran
2 Department of Marine Biology, Faculty of Marine Sciences, Chabahar Maritime University, Chabahar, Iran
Corresponding author :Fariborz Soheili Daneshgah street, Departments of Marine Biology, Faculty of Marine Sciences, Chabahar Maritime University, Chabahar, Iran Tel/fax: +98 54 31272342 Email: fariborz.soheili@gmail.com

Abstract

Background: In cervical cancer, the carcinogenic mechanism of human papillomavirus (HPV) occurs through the integration of viral DNA into the host genome. This process initiates with a disruption in the E2 open reading frame (ORF) of the viral genome. Disruption of E2 ORF results in an increased expression of the viral oncoproteins, E6 and E7, by removal of E2 suppression effect on their promoters. E6 and E7 interfere with the normal cell cycle by degrading the p53 and pRb tumor suppressor proteins, respectively.
Objectives: The objective of this study was to determine the physical status (episomal/integral) of HPV genome in esophageal squamous cell carcinoma (ESCC).
Materials and Methods: The rate of copy numbers of E2 and E6 genes in HPV-18 and HPV-16 positive samples were analyzed by quantitative polymerase chain reaction (qPCR) in order to assess the physical status (episomal/integral) of HPV. DNA extracts from HeLa cell line were used as the positive control.
Results: The E2 gene was detected in 1 sample, co-infected with HPV-16 and HPV-18. While, E6 gene was detected in all 11 HPV positive samples. The qPCR analysis showed the presence of integrated form of viral DNA in all HPV positive samples and only 1 mixed episomal-integrated form was detected.
Conclusion: The presence of integrated forms of high risk HPV-16 and HPV-18 genomes might reflect a crucial process towards malignant transformation of ESCC.
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