BK polyomavirus infection promotes growth and aggressiveness in bladder cancer
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RESEARCH
Open Access
BK polyomavirus infection promotes growth and aggressiveness in bladder cancer Yigang Zeng1†, Jiajia Sun1,2†, Juan Bao1 and Tongyu Zhu1,2*
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 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 BKPyVinfected bladder cancer. These results provide meaningful information towards the diagnosis and treatment of clinical bladder cancer. Keywords: BK polyomavirus, Bladder cancer, Cell growth, Cell aggressiveness
Introduction Urothelial carcinoma is one of the most common and highly malignant tumors in the urinary system. According to 2018 statistics from the American Cancer Society, bladder cancer is the sixth most common malignancy in males after lung, prostate, colorectal, stomach and liver [1]. 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, * Correspondence: [email protected] † Yigang Zeng and Jiajia Sun contributed equally to this work. 1 Department of Urology, Shanghai Public Health Clinical Center, Fudan University, Shanghai 201508, China 2 Shanghai Key Laboratory of Organ Transplantation, Shanghai, China
especially transplant recipients. BKPyV reactivation after renal transplantation causes symptoms such as viremia, viruria, ureteral stricture and BKPyV-related nephropathy, as well as hemorrhagic cystitis after hematopoietic stem cell transplantation [4]. In 2012, at the International Agency for Research on Cancer (IARC) meeting, BKPyV and JCPyV were classified as “possibly” carcinogenic to human (group 2B) because of the “sufficient evidence” in experimental animals and the “inadequate evidence” in humans for their carcinogenicity [5]. So far, whether BKPyV has a causal role in the development of cancer was controversial. Early studies detected the presence of BKPyV large T antigens in prostate-, bladder- and kidney tumors [6–8], but several researchers thought BKPyV was unlikely to be involved in the etiology of most renal and bladder tumors because t
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