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.
Highlights
In cervical cancer, the carcinogenic mechanism of human papillomavirus (HPV) occurs through the integration of viral DNA into the host genome
The ratios of E2/E6 genes in 11 HPV-16 or HPV-18 positive samples were analyzed by quantitative polymerase chain reaction (qPCR) in order to assess the integration status of HPV genomes
E6 gene was detected in the rest of HPV positive samples without E2 gene, which indicated the presence of integrated form of viral DNA in the entire HPV positive samples (Table 1)
Summary
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. Objectives: The objective of this study was to determine the physical status (episomal/ integral) of HPV genome in esophageal squamous cell carcinoma (ESCC). 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. One of the main procedures of HPV which induce carcinogenesis is the integration of its genome into the host DNA.[6,7] the physical status (episomal/integral) of HPV genome is not absolute for the carcinogenesis and confirmation of insertional mutagenesis.[8]
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