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GOLPH3通过PI3K/Akt信号通路调控上皮性卵巢癌细胞增殖与凋亡的研究 被引量:9

The study of GOLPH3 regulates proliferation and apoptosis through PI3K/Akt signaling pathway in epithelial ovarian cancer cell
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摘要 目的:探讨GOLPH3基因对上皮性卵巢癌细胞增殖及凋亡的影响及作用机制。方法:siRNA干扰技术沉默SKOV3细胞株中GOLPH3基因表达,MTT法检测细胞增殖情况,流式细胞术检测细胞凋亡情况,Western blot法检测PI3K/Akt信号通路相关基因Akt、p-Akt 473、p-Akt 308及Bcl-2表达。PI3K/Akt信号通路抑制剂LY294002处理卵巢癌SKOV3细胞后,检测SKOV3细胞的增殖能力及凋亡情况。结果:siRNA干扰SKOV3细胞株中GOLPH3基因,GOLPH3表达下调,细胞增殖减少,凋亡增多;PI3K/Akt信号通路相关基因p-Akt 473、p-Akt 308、抗凋亡基因Bcl-2蛋白表达水平均下降,Akt蛋白水平表达无显著变化。LY294002处理SKOV3细胞后,细胞增殖率降低,凋亡率升高。结论:GOLPH3基因可能通过激活PI3K/Akt信号通路促进卵巢癌细胞增殖,并抑制其凋亡的作用。 Objective:To explore GOLPH3 gene effects on proliferation and apoptosis of epithelial ovarian cancer cell and its mechanism.M ethods:The expression of GOLPH3 gene of SKOV3 cells was silenced by siRNA interference.Cell proliferation was detected by MTT,and cell apoptosis was detected by flow cytometry.The expression of PI3K/A kt signaling pathway related genes(Akt、p-Akt473、p-Akt 308 and B cl-2)was detected by Western blot.The PI3K/Akt signaling blocker LY294002 were used to treat ovarian cancer SKOV3 cells respectively and the proliferation and apoptosis of SKOV3 cells were detected.Results:After GOLPH3 gene expression was down-regulated by siRNA interference,SKOV3 cells proliferation decreased,apoptosis increased,and PI3K/Akt signaling pathway related genes-Akt、p-Akt 473、p-Akt 308 and B cl-2 expression decreased.The cell proliferation decreased and the apoptosis rate increased after LY294002 treatment.Conclusion:GOLPH3 gene may promote the proliferation of ovarian cancer cells and inhibit the apoptosis by activating the PI3K/Akt pathway
作者 王莉 孙云燕 李冬冬 梁延平 钟洁 Wang Li;Sun Yunyan;Li Dongdong(Shanghai General Hospital,Shanghai 200025;Gynecology of Shidong Hospital of Yangpu District,Shanghai 200438)
出处 《现代妇产科进展》 CSCD 北大核心 2018年第9期648-651,共4页 Progress in Obstetrics and Gynecology
基金 上海市自然科学基金项目(No:12ZR1424300)。
关键词 上皮性卵巢癌 GOLPH3基因 PI3K/AKT信号通路 增殖 凋亡 Epithelial ovarian cancer GOLPH3 gene PI3K/Akt signaling pathway Proliferation Apoptosis
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