Department of Virology, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran; Student Research Committee, Iran University of Medical Sciences, Tehran, Iran.
Department of Virology, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Int Immunopharmacol. 2020 Nov;88:106913. doi: 10.1016/j.intimp.2020.106913. Epub 2020 Sep 1.
The aim of this study was to determine the presence of HPV in patients with Prostate cancer (PCa) and its possible association with cancer progression.
In this case-control study, fresh prostate tissues and blood samples were collected from 90 individuals, including 58 cases samples with PCa and 32 non-malignant prostate tissue samples as a control group. The expression level of viral genes (E2, E6, and E7) and cellular factors including tumor suppressor proteins (Rb and p53), anti-apoptotic mediators (Bcl-2 and survivin), and some mediators involved in inflammation and angiogenesis was evaluated.
The presence of the HPV genome was identified in 19 out of the 58 cases (32.7%) and five out of the 32 controls (15.6%). However, there was not any statistically significant relationship between the presence of the HPV genome and PCa (OR = 2.63, 95% C.I = 0.89-7.91, P-value = 0.078). Moreover, the HPV high-risk genotypes 16 and 18 were detected in 47.4% and 31.6% of HPV-infected PCa tissues, respectively. The expression level of the tumor suppressor proteins (Rb and p53) significantly decreased in the HPV-infected samples compared to the HPV negative specimens (P-value = 0.01, P-value = 0.01, respectively). However, the expression level of the anti-apoptotic mediators and those involved in angiogenesis and inflammation significantly increased in the HPV-infected PCa group compared to the HPV-negative PCa and control groups (P-value < 0.05, respectively).
Our study suggests that although it is not definitely known whether HPV causes PCa, this virus probably modulates PCa cell behavior by affecting inflammation, angiogenesis, and apoptosis mechanisms, which, in turn, promotes tumorigenesis.
本研究旨在确定前列腺癌(PCa)患者中 HPV 的存在及其与癌症进展的可能关联。
在这项病例对照研究中,我们收集了 90 名个体的新鲜前列腺组织和血液样本,包括 58 例 PCa 病例样本和 32 例非恶性前列腺组织样本作为对照组。评估了病毒基因(E2、E6 和 E7)和细胞因子的表达水平,包括肿瘤抑制蛋白(Rb 和 p53)、抗凋亡介质(Bcl-2 和 survivin)以及一些参与炎症和血管生成的介质。
在 58 例病例中,有 19 例(32.7%)和 32 例对照中 5 例(15.6%)检测到 HPV 基因组的存在。然而,HPV 基因组的存在与 PCa 之间没有统计学上的显著关系(OR=2.63,95%CI=0.89-7.91,P 值=0.078)。此外,在 HPV 感染的 PCa 组织中,检测到 HPV 高危基因型 16 和 18 的比例分别为 47.4%和 31.6%。与 HPV 阴性标本相比,HPV 感染样本中肿瘤抑制蛋白(Rb 和 p53)的表达水平显著降低(P 值=0.01,P 值=0.01)。然而,与 HPV 阴性 PCa 组和对照组相比,HPV 感染的 PCa 组中抗凋亡介质以及参与炎症和血管生成的介质的表达水平显著增加(P 值<0.05,分别)。
我们的研究表明,虽然不能确定 HPV 是否导致 PCa,但该病毒可能通过影响炎症、血管生成和凋亡机制来调节 PCa 细胞的行为,从而促进肿瘤发生。