摘要
目的探讨程序性细胞死亡因子4(programmed cell death protein 4,PDCD4)对卵巢癌细胞生长、凋亡及磷酸化信号转导和转录激活因子3(phosphorylated signal transducer and activator of transcription 3,p-STAT3)、磷酸化p38丝裂原激活蛋白激酶(phosphorylated p38 mitogen activation protein kinase,p-p38MAPK)表达的影响。方法卵巢癌细胞SKO-V3转染PDCD4过表达载体(pDsRes2-N1-PDCD4)和对照载体(pDsRes2-N1),分别记为过表达组和阴性组,同时以不转染的细胞作为对照组。以下列方法对三组细胞进行检测和比较:以实时逆转录聚合酶链反应和蛋白质印迹法检测细胞PDCD4蛋白和mRNA表达水平,以噻唑蓝比色法和细胞克隆实验检测细胞增殖能力,以流式细胞术检测细胞凋亡情况,以蛋白质印迹法检测p-p38MAPK、p-STAT3水平。结果阴性组和对照组细胞中PDCD4 mRNA和蛋白表达水平、光密度(optical density,OD)、细胞克隆形成数目、凋亡率、p-p38MAPK和p-STAT3表达水平比较均无显著差异(P_均> 0.05)。过表达组细胞中PDCD4mRNA和蛋白表达水平及细胞凋亡率均明显高于对照组和阴性组(P_均<0.01),细胞OD和克隆形成数目均明显低于对照组和阴性组(P_均<0.01)。过表达组细胞p-STAT3/STAT3比值明显低于对照组(P <0.01),p-p38MAPK/p38MAPK比值明显高于对照组(P <0.01)。结论 PDCD4抑制卵巢癌细胞生长,促进卵巢癌细胞凋亡,这可能与其抑制STAT3信号通路激活和促进p38MAPK信号通路激活有关。
Objective To investigate the effects of programmed cell death factor 4(PDCD4) on growth, apoptosis and phosphorylation of phosphorylated signal transducer and activator of transcription 3(p-STAT3) and phosphorylated p38 mitogen activation protein kinase(p-p38 MAPK) in ovarian cancer cells. Method Ovarian cancer cell SKO-V3 was transfected with PDCD4 overexpression vector(pDsRes2-N1-PDCD4) and control vector(pDsRes2-N1), named as over expression group and negative group,the non-transfected cells were used as control group, three groups of cells were detected and compared by the following methods: the expression of PDCD4 protein and mRNA was detected by real-time reverse transcriptase PCR and Western blotting, the proliferation of cells was detected by MTT colorimetry and cell cloning assay, and the apoptosis was detected by ?ow cytometry, the levels of p-p38 MAPK and p-STAT3 were detected by Western blotting. Result There were no signi?cant differences in the expression levels of PDCD4 mRNA and protein, optical density(OD), the number of cell clones, apoptosis rate, p-p38 MAPK and p-STAT3 expression levels between negative group and control group(Pall> 0.05). The expression levels of PDCD4 mRNA and protein and apoptosis rate in over expression group were signi?cantly higher than those in control group and negative group(Pall< 0.01), the number of cell OD and clone formation was signi?cantly lower than that of control group and negative group(Pall< 0.01). The ratio of p-STAT3/STAT3 in over expression group were signi?cantly lower than that of control group(P < 0.01), the ratio of p-p38 MAPK/p38 MAPK was signi?cantly higher than that of control group(P < 0.01). Conclusion PDCD4 inhibits the growth of ovarian cancer cells and promotes the apoptosis of ovarian cancer cells, which may be related to the inhibition of STAT3 signaling pathway activation and the promotion of p38 MAPK signaling pathway activation.
作者
熊佳易
陈蕾
魏燕
圣娟娟
钱桂兰
XIONG Jia-yi;CHEN Lei;WEI Yan;SHENG Juan-juan;QIAN Gui-lan(Department of Gynecology,the Six Medical Center of PLA General Hospital,Beijing 100048,China)
出处
《中国医学前沿杂志（电子版）》
2019年第2期144-148,共5页
Chinese Journal of the Frontiers of Medical Science(Electronic Version)
关键词
卵巢癌
程序性细胞死亡因子4
凋亡
生长
Ovarian cancer
Programmed cell death protein 4
Apoptosis
Growth
