摘要
目的:探讨射干苷对卵巢癌SK-OV-3细胞增殖、迁移和侵袭的影响及其作用机制。方法:采用CCK-8法检测0、5、10、50、100μg/L射干苷对SK-OV-3细胞增殖能力的影响,采用细胞划痕实验和Transwell实验检测细胞的迁移和侵袭能力,采用Western blot检测不同浓度射干苷对磷脂酰肌醇-3激酶(PI3K)/丝苏氨酸蛋白激酶(AKT)信号通路蛋白表达的影响。结果:5、10、50、100μg/L射干苷组细胞的吸光度(A)值分别为0.725±0.036、0.611±0.032、0.410±0.027和0.321±0.023,与0μg/L射干苷组(0.857±0.043)比较,差异均有统计学意义(均P<0.05)。5、10、50、100μg/L射干苷组细胞的相对迁移距离分别为0.896±0.092、0.644±0.075、0.432±0.056和0.215±0.043,与0μg/L射干苷组(1.000±0.083)比较,差异均有统计学意义(均P<0.05)。5、10、50、100μg/L射干苷组细胞的侵袭数分别为(93.241±10.251)个、(74.258±7.963)个、(40.236±5.210)个和(32.147±3.458)个,与0μg/L射干苷组[(106.258±11.785)个]比较,差异均有统计学意义(均P<0.05)。5、10、50、100μg/L射干苷组细胞中磷酸化PI3K(p-PI3K)蛋白的表达水平分别为0.875±0.089、0.727±0.075、0.452±0.053和0.365±0.052,与0μg/L射干苷组(1.000±0.079)比较,差异均有统计学意义(均P<0.05)。5、10、50、100μg/L射干苷组细胞中磷酸化AKT(p-AKT)蛋白的表达水平分别为0.816±0.072、0.635±0.079、0.463±0.065和0.305±0.047,与0μg/L射干苷组(1.000±0.070)比较,差异均有统计学意义(均P<0.05)。LY294002组和对照组细胞的A值分别为0.494±0.0381和0.873±0.08,差异有统计学意义(P<0.05)。LY294002组和对照组细胞的相对迁移距离分别为0.523±0.051和1.000±0.081,差异有统计学意义(P<0.05)。LY294002组和对照组细胞的侵袭数分别为(61.243±9.251)个和(106.228±11.783)个,差异有统计学意义(P<0.05)。LY294002组和对照组细胞中p-PI3K蛋白的表达水平分别为0.521±0.046和1.000±0.075,差异有统计学意义(P<0.05)。LY294002组和对照组细胞中p-AKT蛋白水平分别为0.465±0.051和1.000±0.070,差异有统计学意义(P<0.05)。结论:射干苷可通过调控PI3K/AKT信号通路抑制SK-OV-3细胞的增殖、迁移和侵袭能力。
Objective To study the effects of Tectoridin on the proliferation,migration and invasion of ovarian cancer SK-OV-3 cells and its mechanism.Methods SK-OV-3 cells were treated with 0,5,10,50 and 100μg/L Tectoridin for 24 hours.The proliferation of SK-OV-3 cells treated with different concentrations of Tectoridin was detected by cell counting kit-8(CCK-8).The migration was analyzed by wound healing test and the invasion was observed by Transwell.The effects of different concentrations of Tectoridin on the protein levels of phosphoinositide 3-kinase(PI3K)/serine-threonine kinase(AKT)signaling pathway were detected by western blot assay.Results The A values of 0,5,10,50,100μg/L Tectoridin groups were 0.857±0.043,0.725±0.036,0.611±0.032,0.410±0.027,and 0.321±0.023,respectively.The relative migration distances of the cells were 1.000±0.083,0.896±0.092,0.644±0.075,0.432±0.056,and 0.215±0.043,respectively.The numbers of cell invasion were(106.258±11.785),(93.241±10.251),(74.258±7.963),(40.236±5.210),and(32.147±3.458),respectively.The phosphorylated PI3K(p-PI3K)protein levels were 1.000±0.079,0.875±.089,0.727±0.075,0.452±0.053,0.365±0.052,respectively.The phosphorylated AKT(p-AKT)protein levels were 1.000±0.070,0.816±0.072,0.635±0.079,0.463±0.065,0.305±0.047,respectively.Compared with the 0μg/L Tectoridin group,the differences of 5,10,50,100μg/L Tectoridin group were statistically significant(all P<0.05).The A values of the control group and the LY294002 group were 0.873±0.081 and 0.494±0.038,respectively.The relative cell migration distances were 1.000±0.081 and 0.523±0.051,respectively.The numbers of cell invasion were(106.228±11.783)and(61.243±9.251),respectively.The protein levels of p-PI3K were 1.000±0.075,0.521±0.046,respectively.The protein levels of p-AKT were 1.000±0.070,0.465±0.051,respectively.Compared with the control group,the difference in the LY294002 group was statistically significant(P<0.05).Conclusion Tectoridin may inhibit proliferation,migration and invasion of SK-OV-3 cells by regulating PI3K/AKT signaling pathway.
作者
王丽娟
史惠蓉
Wang Lijuan;Shi Huirong(Department of Gynecology,Zhumadian Central Hospital,Zhumadian 463000,China;Department of Gynecology,The First Affiliated Hospital of Zhengzhou University,Zhengzhou 450000,China)
出处
《中华肿瘤杂志》
CAS
CSCD
北大核心
2020年第7期570-574,共5页
Chinese Journal of Oncology
