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Inactivated Sendai Virus Induces Apoptosis in Murine Melanoma Cells by IGF-1R Down-regulation 被引量:3
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作者 GAO Hui XU Xiao Shuang +2 位作者 CHEN Ze Dong ZHANG Quan XU Xiang Ming 《Biomedical and Environmental Sciences》 SCIE CAS CSCD 2013年第12期998-1002,共5页
The mortality of cancer patients has considerably improved due to progress in surgery, chemotherapy and radiotherapy. However, some types of cancers, such as melanoma, remain refractory to conventional strategies. Alt... The mortality of cancer patients has considerably improved due to progress in surgery, chemotherapy and radiotherapy. However, some types of cancers, such as melanoma, remain refractory to conventional strategies. Although melanoma accounts for only 4% of all dermatological malignancies, it is responsible for 80% of mortalities from skin tumors[11. The reported survival rate of melanoma over 5 years is not yet encouraging due to its chemo-resistance and rapid metastasis. Therefore, it is necessary to develop new drugs with potent activity and weak side-effect against melanoma. 展开更多
关键词 IGF inactivated sendai virus Induces Apoptosis in Murine Melanoma Cells by IGF-1R Down-regulation
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Inactivated Sendai Virus Induces ROS-dependent Apoptosis and Autophagy in Human Prostate Cancer Cells 被引量:7
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作者 QIAN Miao TAN Hai Ming +2 位作者 YU Ning WANG Tao ZHANG Quan 《Biomedical and Environmental Sciences》 SCIE CAS CSCD 2018年第4期280-289,共10页
Objective The current study aims to investigate the effect of Hemagglutinating virus of Japan envelope(HVJ-E) on induction of apoptosis and autophagy in human prostate cancer PC3 cells, and the underlying mechanisms... Objective The current study aims to investigate the effect of Hemagglutinating virus of Japan envelope(HVJ-E) on induction of apoptosis and autophagy in human prostate cancer PC3 cells, and the underlying mechanisms. Methods PC3 cells were treated with HVJ-E at various multiplicity of infection(MOI), and the generated reactive oxygen species(ROS), cell viability, apoptosis, and autophagy were detected, respectively. Next, the role of ROS played in the regulation of HVJ-E-induced apoptosis and autuphagy in PC3 cells were analysed. In the end, the relationship between HVJ-E-induced apoptosis and autuophagy was investigated by using rapamycin and chloroquine. Results Flow cytometry assay revealed that HVJ-E treatment induced dose-dependent apoptosis and that the JNK and p38 MAPK signaling pathways were involved in HVJ-E-induced apoptosis in PC3 cells. In addition, HVJ-E was able to induce autophagy in PC3 cells via the class III PI3 K/beclin-1 pathway. The data also implyed that HVJ-E-triggered autophagy and apoptosis were ROS dependent. When ROS was blocked with N-acetylcysteine(NAC), HVJ-E-induced LC3-II conversion and apoptosis were reversed. Interestingly, HVJ-E-induced apoptosis was significantly increased by an inducer of autophagy, rapamycin pretreatment, both in vitro and in vivo. Conclusion HVJ-E exerts anticancer effects via autophagic cell death in prostate cancer cells. 展开更多
关键词 inactivated sendai virus(HVJ-E) Reactive oxygen species(ROS) Apoptosis Autophagy
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Induction of Apoptosis in Hormone-resistant Human Prostate Cancer PC3 Cells by Inactivated Sendai Virus
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作者 GAO Hui GONG Xiao Cheng +3 位作者 CHEN Ze Dong XU Xiao Shuang ZHANG Quan XU Xiang Ming 《Biomedical and Environmental Sciences》 SCIE CAS CSCD 2014年第7期506-514,共9页
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... 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-β(IFN-β) production, and the cell viability and apoptosis were detected by ELISA, MTl--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. 展开更多
关键词 inactivated sendai virus (HVJ-E) APOPTOSIS CASPASE Mitogen-activated protein kinase(MAPK)
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Inactivated Sendai Virus Induces Apoptosis Mediated by Reactive Oxygen Species in Murine Melanoma Cells
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作者 GAO Hui LI Ling YU +1 位作者 ZHANG Man ZHANG Quan 《Biomedical and Environmental Sciences》 SCIE CAS CSCD 2016年第12期877-884,共8页
Objective This paper aims to investigate the apoptotic effect of inactivated Sendai virus (hemagglutinating virus of Japan-enveloped, HVJ-E) on routine melanoma cells (B16FlO) and the possible mechanisms involved ... Objective This paper aims to investigate the apoptotic effect of inactivated Sendai virus (hemagglutinating virus of Japan-enveloped, HVJ-E) on routine melanoma cells (B16FlO) and the possible mechanisms involved in the putative apoptotic reactions. Methods B16F10 cells were treated with HVJ-E at various multiplicities of infection (MOI), and the reactive oxygen species (ROS), cell viability, and apoptosis were measured. Next, the roles of ROS in the regulation of Bcl-2/Bax and the activation of mitogen-activated protein kinase (MAPK) pathways in HVJ-E-treated B16F10 cells were analyzed. To further evaluate the cytotoxic effect of HVJ-E-generated ROS on B16FlO cells, HVJ-E was intratumorally injected, both with and without N-acetyI-L-cysteine (NAC), into melanoma tumors on BALB/c mice. Tumor volume was then monitored for 3 weeks, and the tumor proteins were separated for immunoblot assay. Results Treatment of B16F10 cells with HVJ-E resulted in a dose-dependent inhibition of cell-viability and an induction of apoptosis. The latter effect was associated with the generation of ROS. Inhibition of ROS generation by NAC resulted in a significant reduction of HVJ-E-induced Erkl/2, JNK, and p38 MAPK activation. Additionally, ROS inhibition caused a decrease in the Bcl-2/Bax ratio as well as promoting activation of apoptosis both in vitro and in vivo. Conclusion These results suggest that HVJ-E possesses potential anticancer activity in B16F10 cells through ROS-mediated mitochondrial dysfunction involving the MAPK pathway. 展开更多
关键词 inactivated sendai virus (HVJ-E) Reactive oxygen species MAPK APOPTOSIS
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