β-榄香烯调控PI3K/Akt/mTOR信号通路对子宫内膜癌Ishikawa细胞增殖、迁移、侵袭及凋亡的影响  

Effects of β-elemene regulating the PI3K/Akt/mTOR signaling pathway on the proliferation,migration,invasion and apoptosis of endometrial cancer Ishikawa cells

作　　者：庄忆君 孙禹琪 杨微[1] ZHUANG Yijun;SUN Yuqi;YANG Wei(Department of Obstetrics and Gynecology,The First Affiliated Hospital of Jiamusi University,Jiamusi 154000,China;Department of Obstetrics and Gynecology,Yichun Central Hospital)

机构地区：[1]佳木斯大学附属第一医院妇产科,佳木斯154000 [2]伊春市中心医院妇产科

出　　处：《实用肿瘤学杂志》2023年第5期395-402,共8页Practical Oncology Journal

摘　　要：目的 探讨β-榄香烯对子宫内膜癌Ishikawa细胞生物学行为的影响及其作用机制。方法 用不同浓度(0、50、100、150、200、250、300μg/mL)β-榄香烯处理Ishikawa细胞,应用CCK-8法检测细胞存活率,计算β-榄香烯的半数抑制浓度IC50,确定低、中、高药物处理浓度,并设置0μg/mL β-榄香烯作为空白对照组,2μg/mL顺铂阳性对照组。使用AnnexinⅤ-FITC/PI双染法检测细胞凋亡率,通过划痕和Transwell实验检测细胞迁移和侵袭能力,通过Western blot检测Ishikawa细胞中PI3K/Akt/mTOR信号通路相关蛋白的表达水平。结果 β-榄香烯呈浓度依赖性抑制Ishikawa细胞的增殖,其对Ishikawa细胞24 h和48 h的IC50分别为168.9μg/mL和157.1μg/mL。β-榄香烯能够诱导Ishikawa细胞的凋亡,在经0、85、170、255μg/mL β-榄香烯处理24 h后,细胞凋亡率分别为(9.41±0.52)%、(16.67±0.25)%、(21.27±0.30)%和(25.55±0.89)%,组间多重比较具有统计学差异(P<0.001)。β-榄香烯还能够抑制Ishikawa细胞的迁移、侵袭能力,并且抑制作用随着浓度的升高而增强(P<0.001)。此外,β-榄香烯可降低Ishikawa细胞PI3K、p-PI3K、mTOR、p-mTOR蛋白表达水平(P<0.05),p-PI3K和p-mTOR蛋白表达水平显示出明显的浓度依赖性,255μg/mL β-榄香烯组与0μg/mL β-榄香烯组相比,PI3K、p-PI3K、Akt、mTOR、p-mTOR蛋白表达水平明显降低(P<0.001)。结论 β-榄香烯能够抑制子宫内膜癌Ishikawa细胞增殖、迁移和侵袭,促进其凋亡,其机制可能与β-榄香烯能够抑制Ishikawa细胞PI3K/Akt/mTOR信号通路的激活有关。Objective The aim of this study was to investigate the effects ofβ-elemene on the biological behavior of endometrial cancer Ishikawa cells and its mechanism of action.Methods Different concentrations(0,50,100,150,200,250,300μg/mL)ofβ-elemene were used to treat Ishikawa cells.The cell viability was measured using the CCK-8 assay to calculate the half-maximal inhibitory concentration(IC 50)ofβ-elemene and to determining low,medium,and high treatment concentrations.A 0μg/mL ofβ-elemene was set up a blank control group and 2μg/mL of cisplatin for a positive control group.The apoptotic rate was detected using Annexin V-FITC/PI double staining.The scratch wound healing assay and Transwell assay were used to detect the abilities of cell migration and invasion.Western blot was performed to evaluate the expression of PI3K/Akt/mTOR signaling pathway related proteins in Ishikawa cells.Resultsβ-Elemene significantly inhibited the proliferation of Ishikawa cells in a dose-dependent manner.The IC 50 values ofβ-elemene at 24 and 48 hours were 168.9μg/mL and 157.1μg/mL,respectively.β-Elemene induced apoptosis in Ishikawa cells and after treatment withβ-elemene at 0,85,170,and 255μg/mL for 24 hours,the apoptotic rates of Ishikawa cells were(9.41±0.52)%,(16.67±0.25)%,(21.27±0.30)%and(25.55±0.89)%,respectively.There was a statistically significant difference in multiple comparisons between groups(P<0.001).β-Elemene inhibited the migration and invasion ability of Ishikawa cells,and the inhibitory effects increased with concentration(P<0.001).In addition,β-elemene reduced the levels of PI3K,p-PI3K,mTOR and p-mTOR proteins in Ishikawa cells(P<0.05),and the expression of p-PI3K and p-mTOR proteins showed a significant concentration dependence,andβ-elemene at the 255μg/mL of group showed a significant reduction in the expression of PI3K,p-PI3K,Akt and p-mTOR when compared to the 0μg/mL ofβ-elemene group(P<0.001).Conclusionβ-Elemene can inhibit the proliferation,migration,and invasion of endometrial cancer Ishika

关 键 词：Β-榄香烯 子宫内膜癌 ISHIKAWA细胞 PI3K/Akt/mTOR信号通路 

分 类 号：R737.3[医药卫生—肿瘤]