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BK polyomavirus infection promotes growth and aggressiveness in bladder cancer.

ABSTRACT: 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 ?-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 ?-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.

SUBMITTER: Zeng Y

PROVIDER: S-EPMC7488779 | biostudies-literature | 2020 Sep

REPOSITORIES: biostudies-literature

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BK polyomavirus infection promotes growth and aggressiveness in bladder cancer.

Zeng Yigang Y Sun Jiajia J Bao Juan J Zhu Tongyu T

Virology journal 20200914 1

<h4>Background</h4>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.<h4>Methods</h4>We developed a BKPyV-infected bladder cancer cell model and a mice tumor model to discuss the role of BKPyV ...[more]

PMID: 32928222

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Project description:UNLABELLED:BK polyomavirus (BKPyV) reactivation is associated with severe human disease in kidney and bone marrow transplant patients. The interplay between viral and host factors that regulates the productive infection process remains poorly understood. We have previously reported that the cellular DNA damage response (DDR) is activated upon lytic BKPyV infection and that its activation is required for optimal viral replication in primary kidney epithelial cells. In this report, we set out to determine what viral components are responsible for activating the two major phosphatidylinositol 3-kinase-like kinases (PI3KKs) involved in the DDR: ataxia telangiectasia mutated (ATM) kinase and ATM and Rad3-related (ATR) kinase. Using a combination of UV treatment, lentivirus transduction, and mutant virus infection experiments, our results demonstrate that neither the input virus nor the expression of large T antigen (TAg) alone is sufficient to trigger the activation of ATM or ATR in our primary culture model. Instead, our data suggest that the activation of both the ATM- and ATR-mediated DDR pathways is linked to viral DNA replication. Intriguingly, a TAg mutant virus that is unable to activate the DDR causes substantial host DNA damage. Our study provides insight into how DDRs are activated by polyomaviruses in primary cells with intact cell cycle checkpoints and how the activation might be linked to the maintenance of host genome stability. IMPORTANCE:Polyomaviruses are opportunistic pathogens that are associated with several human diseases under immunosuppressed conditions. BK polyomavirus (BKPyV) affects mostly kidney and bone marrow transplant patients. The detailed replication mechanism of these viruses remains to be determined. We have previously reported that BKPyV activates the host DNA damage response (DDR), a response normally used by the host cell to combat genotoxic stress, to aid its own replication. In this study, we identified that the trigger for DDR activation is viral replication. Furthermore, we show that the virus is able to cause host DNA damage in the absence of viral replication and DDR activation. These results suggest an intricate relationship between viral replication, DDR activation, and host genome instability.

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BK polyomavirus infection promotes growth and aggressiveness in bladder cancer.

Publications

BK polyomavirus infection promotes growth and aggressiveness in bladder cancer.

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