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EBV and HPV Infections in Colorectal Cancer and Their Effect on P53 and P16 Protein Expression
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Arefeh Ebrahimian Shiadeh1    , Vahideh Hamidi Sofiani1 , Saghar Saber Amoli2 , Mahdie Taheri1 , Alijan Tabarraei1 , Hadi Razavi nikoo1 , Farzin Sadeghi3 , Sorayya Khafri4 , Ghodsieh Kamrani5 , Yousef Yahyapour 6, Abdolvahab Moradi1 |
1- Department of Medical Microbiology, Faculty of Medicine, Golestan University of Medical Science, Gorgan, Iran.
2- Department of Medical Microbiology and Biotechnology, School of Medicine, Babol University of Medical Sciences, Babol, Iran.
3- Cellular and Molecular Biology Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, Iran.
4- Social Determinants of Health Research Center, Health research institute, Babol University of Medical Sciences, Babol, Iran.
5- Clinical Research Development Center, Shahid Beheshti Hospital, Babol University of Medical Sciences, Babol, Iran.
6- Infectious Diseases and Tropical Medicine Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, Iran. , uyahyapoor@yahoo.com |
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Abstract: (249 Views) |
| Viral infections contribute to 15-20% of newly diagnosed cancers worldwide. There is evidence of a possible etiological role of Epstein-Barr virus (EBV) and high-risk human papillomaviruses (HR-HPVs) in colorectal carcinoma (CRC). Loss of p53 and p16 function has been found in many cancers and this may occur in many different ways, including gene mutation or interaction with viral oncoproteins. This study aimed to evaluate the presence of EBV and HPV in CRC patients in northern Iran and to assess p53 and p16 protein expression related to these viral infections. Real-time PCR was used to amplify the DNA sequences of these viruses in 55 colorectal tumoral tissues, along with their corresponding non-tumoral adjacent tissues. Additionally, immunohistochemistry (IHC) was utilized to determine p53 and p16 protein expression. EBV DNA was detected in 49.1% of CRC tissues. Furthermore, HPV DNA was present in 7.3% of CRC tissues. Notably, the prevalence of EBV infection in tumoral tissues was significantly higher than in non-tumoral tissues (P=0.001). The EBV DNA polymerase catalytic subunit (BALF5) copy number in tumoral tissues was higher than in non-tumoral tissues and this difference was statistically significant (P=0.008). P53 was positive in 21/26 (80.8%) EBV-positive and in 11/25 (44%) EBV-negative samples and this difference was significant (P=0.007). P16 was positive in 13/26 (50%) EBV-positive and in 14/25 (58.3%) EBV-negative samples (P= 0.668). Our findings suggest that EBV infection can increase the risk of CRC. In addition, EBV seems to stabilize p53 in EBV-positive CRC which needs further research. No significant correlation was detected between EBV infection and p16 expression. Also, we could not find a causal relationship between HPV infection and CRC in the study population. |
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| Keywords: HPV, EBV, p53, p16, colorectal cancer |
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Full-Text [PDF 477 kb]
(77 Downloads)
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Type of Study: Original Article |
Subject:
Infectious disease (Molecular and Cellular aspects)
Received: 2023/12/24 | Accepted: 2024/02/6 | Published: 2024/04/6
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