Abstract
Objectives Some DNA viruses, such as BKPyV, are capable of inducing neoplastic transformation in human tissues through still unclear mechanisms. The goal of this study is to investigate the carcinogenic potential of BK polyomavirus (BKPyV) in human embryonic kidney 293 (Hek293) cells, dissecting the molecular mechanism that determines the neoplastic transformation. Materials and Methods BKPyV, isolated from urine samples of infected patients, was used to infect monolayers of Hek293 cells. Subsequently, intracellular redox changes, GSH/GSSH concentration by HPLC, and reactive oxygen/nitrogen species (ROS/RNS) production were monitored. Moreover, to understand the signaling pathway underlying the neoplastic transformation, the redox-sensitive HFS1-Hsp27 molecular axis was examined using the flavonoid quercetin and polishort hairpin RNA technologies. Results The data obtained show that while BKPyV replication is closely linked to the transcription factor p53, the increase in Hek293 cell proliferation is due to the activation of the signaling pathway mediated by HSF1-Hsp27. In fact, its inhibition blocks viral replication and cell growth, respectively. Conclusions The HSF1-Hsp27 signaling pathway is involved in BKPyV infection and cellular replication and its activation, which could be involved in cell transformation.
Highlights
BK polyomavirus (BKPyV) is a nonenveloped virus with an icosahedral structure containing a circular double-stranded DNA genome of ≃5 kb
We previously demonstrated that the increase of the Hsp70 and Hsp27 expression levels, in addition to heat shock factor 1 (HSF1) activation, efficiently buffered the redox events downstream of chemical GSH depletion leading to an antiapoptotic action [26]
BKPyV Infection Relies on p53 in Human human embryonic kidney 293 (Hek293) Cells
Summary
BK polyomavirus (BKPyV) is a nonenveloped virus with an icosahedral structure containing a circular double-stranded DNA genome of ≃5 kb. It belongs to the Polyomaviridae family, genus polyomavirus. The virus is ubiquitous in the human population. BKPyV establishes a lifelong latency within the urogenital tract [2]. Under different circumstances, such as the use of immunosuppressive drugs, BKPyV can be reactivated, and it can be responsible for a series of clinical syndromes: allograft rejection, ureteral stenosis, hemorrhagic cystitis, nephropathy, and cancer [3, 4]
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