Recent studies have confirmed the integration of the BK polyomavirus (BKPyV) gene into the cellular genome of urothelial carcinomas in transplant recipients, further confirming the correlation between BKPyV and urothelial carcinomas after transplantation. However, the role BKPyV infections play in the biological function of bladder cancer remains unclear. We developed a BKPyV-infected bladder cancer cell model and a mice tumor model to discuss the role of BKPyV infections. Our research proves that BKPyV infections promote the proliferation, invasion and migration of bladder cancer cells, while the activation of β-catenin signaling pathway is one of its mediation mechanisms. We first described BKPyV infection promotes the proliferation, invasion and migration of bladder cancer. We verified the role of β-catenin signaling pathway and Epithelial-Mesenchymal Transition effect in BKPyV-infected bladder cancer. These results provide meaningful information towards the diagnosis and treatment of clinical bladder cancer.

中文翻译：

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BK多瘤病毒感染可促进膀胱癌的生长和侵袭性。

最近的研究已证实将BK多瘤病毒（BKPyV）基因整合到移植受者尿路上皮癌的细胞基因组中，进一步证实了BKPyV与移植后尿路上皮癌之间的相关性。然而，BKPyV感染在膀胱癌的生物学功能中所起的作用仍不清楚。我们开发了BKPyV感染的膀胱癌细胞模型和小鼠肿瘤模型，以讨论BKPyV感染的作用。我们的研究证明BKPyV感染可促进膀胱癌细胞的增殖，侵袭和迁移，而β-catenin信号通路的激活是其介导机制之一。我们首先描述了BKPyV感染可促进膀胱癌的增殖，侵袭和迁移。我们验证了β-catenin信号通路和上皮-间充质转化作用在BKPyV感染的膀胱癌中的作用。这些结果为临床膀胱癌的诊断和治疗提供了有意义的信息。