Abstract
BackgroundThis study aimed to evaluate the possible role of human papillomavirus (HPV) and Epstein–Barr virus (EBV) coinfection as an etiological factor for prostate cancer (PCa) development.MethodsThis case-control study was conducted on 67 patients with PCa and 40 control subjects. The expression levels of cellular and viral factors involved in inflammation, tumor progression, and metastasis were quantified, using the enzyme-linked immunosorbent assay (ELISA) and quantitative real-time polymerase chain reaction (qRT-PCR) assay.ResultsThe EBV/HPV coinfection was reported in 14.9% of patients in the case group and 7.5% of the control subjects. The high-risk types of HPV, that is, HPV 16 and HPV 18, were responsible for 50 and 30% of HPV/EBV-coinfected PCa cases (n = 10), respectively. No significant relationship was observed between PCa and HPV/EBV coinfection (OR = 2.9, 95% CI: 0.18–45.2, P = 0.31). However, the highest percentage of HPV genome integration was found in the HPV/EBV-coinfected PCa group (8/10; 80%). Also, the mean expression levels of inflammatory factors (IL-17, IL-6, TNF-α, NF-κB, VEGF, ROS, and RNS), anti-apoptotic mediators (Bcl-2 and survivin), and anti-anoikis factors (Twist and N-cadherin) were significantly higher in the HPV/EBV-coinfected PCa group, compared to the non-coinfected PCa cases. Nevertheless, the tumor-suppressor proteins (p53 and pRb) and E-cadherin (inhibitor of anoikis resistance) showed significant downregulations in the HPV/EBV-coinfected PCa group, compared to the non-coinfected PCa cases.ConclusionThe HPV/EBV coinfection may be an etiological factor for PCa through modulation of cellular behaviors.
Highlights
This study aimed to evaluate the possible role of human papillomavirus (HPV) and Epstein–Barr virus (EBV) coinfection as an etiological factor for prostate cancer (PCa) development
The results showed that all inflammatory factors had an increase in the mean expression level in the HPV/EBV co-infected PCa group when comparing with the mono HPV infected PCa group, but this increase was not significant
Comparison of the expression pattern of apoptosisrelated, tumor suppressor, Anoikis-related factors and CD44 among the study groups Following the identification of differences in the expression levels of inflammatory-related mediators between studies groups, we examined the association between the concentrations of antiapoptotic factors, tumor suppressor factors (p53 and Rb), anoikisrelated mediators (SLUG, Protein Phosphatase Non-Receptor Type 13 (PTPN13), N-cadherin, Ecadherin and TWIST) and CD44 in the samples infected with HPV, the samples infected with EBV, the samples coinfected with HPV/EBV, and control groups
Summary
This study aimed to evaluate the possible role of human papillomavirus (HPV) and Epstein–Barr virus (EBV) coinfection as an etiological factor for prostate cancer (PCa) development. Chronic inflammation and infection may be associated with the development of cancer in various organs, including the thyroid, breast, stomach, liver, cervix, and colon. Inflammation is very common in the adult prostate [3,4,5,6,7]. Factors, such as dietary factors, hormonal changes, cell damage, and infection (especially sexually transmitted infections), are some of the etiological factors that contribute to the initiation of prostatic inflammation. Epithelial cellular injury due to chronic inflammation may lead to the loss of tolerance in normal prostate-associated antigens and trigger a sustained autoimmune reaction [3, 8]
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