论文部分内容阅读
Objective Inactivated Sendai virus particle[hemagglutinating virus of Japan envelope(HVJ-E)]has a potential oncolytic effect due to its ability to induce apoptosis in tumor cells.However,the molecular mechanism of apoptosis induction in cancer cells mediated by HVJ-E has not been fully elucidated.This paper aims to investigate the underlying mechanism of apoptosis induction by HVJ-E in prostate cancer cells(PC3).Methods PC3 cells were treated with HVJ-E at various MOI,and then interferon-6(IFN-S) production,and the cell viability and apoptosis were detected by ELISA,MTT-based assay and flow cytometry,respectively.Next,the roles of Jak-Stat,MAPK and Akt pathways played in HVJ-E-induced apoptosis in PC3 cells were analyzed by immunoblot assay.To further evaluate the cytotoxic effect of HVJ-E on PC3 cells,HVJ-E was intratumorally injected into prostate cancers on BALB/c-nude mice,and the tumor volume was monitored for 36 days.Results HVJ-E induced IFN-β production and activated Jak-Stat signaling pathway,which resulted in the activation of caspase-8,caspase-3,and PARP in PC3 prostate cancer cells post HVJ-E treatment.Furthermore,we observed for the first time that p38 and Jnk MAPKs in PC3 cells contributed to HVJ-E-induced apoptosis.In addition,intratumoral HVJ-E treatment displayed a direct inhibitory effect in an in vivo BALB/c nude mouse prostate cancer model.Conclusion Our findings have provided novel insights into the underlying mechanisms by which HVJ-E induces apoptosis in tumor cells.
Objective Inactivated Sendai virus particle [hemagglutinating virus of Japan envelope (HVJ-E)] has a potential oncolytic effect due to its ability to induce apoptosis in tumor cells. Host, the molecular mechanism of apoptosis induction in cancer cells mediated by HVJ-E has not been fully elucidated. This paper aims to investigate the underlying mechanism of apoptosis induction by HVJ-E in prostate cancer cells (PC3). Methods PC3 cells were treated with HVJ-E at various MOI, and then interferon-6 respectively .Next, the roles of Jak-Stat, MAPK and Akt pathways played in HVJ-E-induced apoptosis in PC3 cells were analyzed by immunoblot assay. further evaluate the cytotoxic effect of HVJ-E on PC3 cells, HVJ-E was intratumorally injected into prostate cancers on BALB / c-nude mice, and the tumor volume was monitored for 36 days. Results HVJ-E induced IFN-β production and activated Jak-Stat signaling pathway, which resulted in the activation of caspase-8, caspase-3, and PARP in PC3 prostate cancer cells post HVJ-E treatment. Thermoremore, we observed for the first time that p38 and Jnk MAPKs in PC3 cells contributed to HVJ- E-induced apoptosis.In addition, intratumoral HVJ-E treatment displayed a direct inhibitory effect in an in vivo BALB / c nude mouse prostate cancer model. Contact Our findings have provided novel insights into the underlying mechanisms by which HVJ-E induces apoptosis in tumor cells.