摘要
目的:探讨重组人白细胞介素24(recombinant human interleukin-24,rhIL-24)诱导人卵巢癌SKOV3细胞株、SKOV3/ddp人卵巢癌耐顺铂细胞株的凋亡相关6个基因表达的变化。方法:体外培养人卵巢癌SKOV3细胞株、人卵巢癌耐顺铂SKOV3/ddp细胞株,用rhIL-24单独及其联合顺铂作用于两种不同的细胞株,提取RNA,经逆转录和聚合酶链反应,应用多基因遗传表达分析系统(GeXP)同时检测6个凋亡基因。结果:rhIL-24诱导上调人卵巢癌SKOV3细胞株Bax、Rb、P53基因,激活Caspase-3,下调Bcl-2、Birc5基因;rhIL-24诱导上调人卵巢癌耐顺铂SKOV3/ddp细胞株Bax、Rb基因,激活Caspase-3,下调Bcl-2基因;rhIL-24联合DDP组其上述基因表达变化更加显著。结论:rhIL-24诱导人卵巢癌细胞凋亡主要通过上调Bax、Rb、P53,激活Caspase3,下调Bcl-2,Birc5等凋亡相关基因。
Objective:To detect the change of apoptosis-associated genes in human ovarian cancer cell lines SKOV3 cells and SKOV3/ddp cells, which were induced by the recombinant human interleukin-24 (rhlL-24). Methods: The human ovarian cancer cell lines SKOV3 cells and SKOV3/ddp cells in vitro culture, both of the cells were induced by rhlL-24, and rhlL-24 combined with eispla- tin (DDP). Extracting RNA, and by revesing transcription and polymerizing chain reaction to detect six genes expression level by GeXP genetic analysis system at the same time. Results: The genes expression level of Caspase-3, Bax, Rb, P53 was obviously unreg- ulated; and Bcl-2, Birc5 was down regulated in SKOV3 cells after induced by rhlL-24. On the SKOV3/ddp cells was unregulated the Caspase-3, Bax, Rb. And down regulate the Bcl-2. All the results were more obviously when all genes mentioned above induced by rhlL-24 combined with DDP. Conclusion: The potential mechanism of rhlL-24 on human ovarian cancer cells in vitro relate to the ap- optosis-associated genes expression level through the up regulation of Caspase-3, Bax, Rb, P53 and down regulation of Bcl-2, Birc5.
出处
《中国免疫学杂志》
CAS
CSCD
北大核心
2013年第12期1312-1316,共5页
Chinese Journal of Immunology
基金
贵州省免疫学研究生教育创新基地重点培育项目(201101)
遵义医学院研究生学术创新课题(CX201321)资助项目