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BK Polyomavirus Activates HSF1 Stimulating Human Kidney Hek293 Cell Proliferation
Sara Baldelli1,2, Dolores Limongi1,2, Cristiana Coni2
1IRCCS San Raffaele Pisana, Department of Human Sciences and Promotion of the Quality of Life, San Raffaele Roma Open University, Rome, Italy.
Oxidative Medicine and Cellular Longevity
|November 30, 2021
Summary
BK polyomavirus (BKPyV) infection activates the HSF1-Hsp27 pathway, promoting Hek293 cell proliferation and viral replication. This pathway
Area of Science:
- Virology
- Molecular Biology
- Oncology
Background:
- BK polyomavirus (BKPyV) is a DNA virus implicated in neoplastic transformation.
- The precise molecular mechanisms underlying BKPyV-induced cell transformation remain unclear.
Purpose of the Study:
- To investigate the carcinogenic potential of BKPyV in human embryonic kidney 293 (Hek293) cells.
- To elucidate the molecular pathways driving BKPyV-mediated neoplastic transformation.
Main Methods:
- BKPyV infection of Hek293 cells.
- Monitoring of intracellular redox status, glutathione levels (GSH/GSSH), and reactive oxygen/nitrogen species (ROS/RNS).
- Assessment of the HSF1-Hsp27 signaling axis using quercetin and shRNA technology.
Main Results:
- BKPyV replication correlates with the transcription factor p53.
- Increased Hek293 cell proliferation is mediated by the HSF1-Hsp27 signaling pathway.
- Inhibition of HSF1-Hsp27 blocks both viral replication and cell growth.
Conclusions:
- The HSF1-Hsp27 signaling pathway plays a critical role in BKPyV infection and cellular replication.
- Activation of the HSF1-Hsp27 pathway is implicated in BKPyV-induced cell transformation.
