Urothelial carcinoma of an allograft ureter 10 years after deceased donor kidney transplantation

Background 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. Methods We developed a BKPyV-infected bladder cancer cell model and a mice tumor model to discuss the role of BKPyV infections. Results 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. Conclusions 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.

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Section: Introductionmentioning

confidence: 99%

BK polyomavirus infection promotes growth and aggressiveness in bladder cancer

Zeng

Sun

Bao

et al. 2020

Virol J

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“…Bladder cancer is also a prone tumor type for immunocompromised patients. According to research, kidney transplant recipients are three times more likely to have urothelial cancer than the general population [2,3]. BK polyomavirus (BKPyV) is a human polyomavirus prone to reactivation in immunocompromised populations, especially transplant recipients.…”

Section: Introductionmentioning

confidence: 99%

BK polyomavirus infection promotes growth and aggressiveness in bladder cancer

Zeng

Sun²,

Bao

et al. 2020

Preprint

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Background: 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. Methods: We developed a BKPyV-infected bladder cancer cell model and a mice tumor model to discuss the role of BKPyV infections. Results: 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. Conclusions: 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.

show abstract