Abstract
In this study, we determined whether binase, a ribonuclease from Bacillus pumilus, increases interferon sensitivity and apoptosis in SiHa cervical cancer cells infected with high-risk human papilloma virus (HPV) strain 16. Binase treatment increased SiHa cell apoptosis in a time- and concentration-dependent manner, as determined by flow cytometry, WST tests and real time xCelligence cell index analysis. Binase-treated SiHa cells showed reduced expression of E6 and E7 viral oncoproteins and increased expression of their intracellular targets, p53 and pRb. Combined treatment with binase and IFNα2b enhanced the interferon sensitivity of HPV-positive SiHa cells. By contrast, combined treatment with binase and IFNα2b in HPV-negative C33A cervical cancer cells, which do no expess E6 and E7, elicited no changes in interferon sensitivity or p53 and pRb expression. These findings suggest binase enhances interferon sensitivity and apoptosis in HPV-positive SiHa cervical cancer cells by suppressing E6 and E7 viral protein expression.
Highlights
Human papilloma virus (HPV) infection is one of the most common causes of sexually transmitted diseases worldwide
We determined whether binase, a ribonuclease from Bacillus pumilus, increases interferon sensitivity and apoptosis in SiHa cervical cancer cells infected with high-risk human papilloma virus (HPV) strain 16
By contrast, combined treatment with binase and IFNα2b in HPV-negative C33A cervical cancer cells, which do no expess E6 and E7, elicited no changes in interferon sensitivity or p53 and retinoblastoma protein (pRb) expression. These findings suggest binase enhances interferon sensitivity and apoptosis in HPV-positive SiHa cervical cancer cells by suppressing E6 and E7 viral protein expression
Summary
Human papilloma virus (HPV) infection is one of the most common causes of sexually transmitted diseases worldwide. To promote virus replication in HPV infected epithelial cells, the E6 and E7 viral proteins interfere with cellular functions like cell division and stress surveillance. These changes result in uncontrolled divisions of the infected cells coupled to their escape from apoptosis. Unscheduled DNA replication elicits p53 pathway in normal cells, which results in apoptosis. To counteract this response, the viral E6 protein directs ubiquitin-mediated proteasome degradation of p53. IFN therapy could be beneficial for HPV-positive cancers if combined with treatments that abrogate the virus-mediated effects and restore IFN signaling. Treatments that target HPV-mediated effects in cancer cells are currently not available
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