Saikosaponin D inhibits proliferation and promotes apoptosis in breast cancer cells through down-regulating JAK2/STAT3 pathway

FENG Jiexin; WU Xiong; CHEN Jianhui; LIN Qinghai; YE Zelin

doi:10.16016/j.1000-5404.202010217

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Saikosaponin D inhibits proliferation and promotes apoptosis in breast cancer cells through down-regulating JAK2/STAT3 pathway

更新时间：2021-08-02

- Saikosaponin D inhibits proliferation and promotes apoptosis in breast cancer cells through down-regulating JAK2/STAT3 pathway
- Journal of Army Medical University Vol. 43, Issue 9, Pages: 852-857(2021)
- 作者机构：
  
  福建医科大学附属漳州市医院乳腺外科
- 作者简介：
- 基金信息：
- DOI：10.16016/j.1000-5404.202010217
  CLC： R737.9;R285.5;R730.53
- Published：2021，
  
  Published Online：15 May 2021，
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[1]冯杰鑫,吴雄,陈建辉,等.柴胡皂苷D通过下调JAK2/STAT3通路抑制乳腺癌细胞的增殖并促进其凋亡[J].陆军军医大学学报(原第三军医大学学报),2021,43(09):852-857.FENG Jiexin,WU Xiong,CHEN Jianhui,et al.Saikosaponin D inhibits proliferation and promotes apoptosis in breast cancer cells through down-regulating JAK2/STAT3 pathway[J].J Amry Med Univ (J Third Mil Med Univ),2021,43(09):852-857.

FENG Jiexin, WU Xiong, CHEN Jianhui, et al. Saikosaponin D inhibits proliferation and promotes apoptosis in breast cancer cells through down-regulating JAK2/STAT3 pathway. [J]. Journal of Army Medical University 43(9):852-857(2021)
[1]冯杰鑫,吴雄,陈建辉,等.柴胡皂苷D通过下调JAK2/STAT3通路抑制乳腺癌细胞的增殖并促进其凋亡[J].陆军军医大学学报(原第三军医大学学报),2021,43(09):852-857.FENG Jiexin,WU Xiong,CHEN Jianhui,et al.Saikosaponin D inhibits proliferation and promotes apoptosis in breast cancer cells through down-regulating JAK2/STAT3 pathway[J].J Amry Med Univ (J Third Mil Med Univ),2021,43(09):852-857. DOI： 10.16016/j.1000-5404.202010217.

FENG Jiexin, WU Xiong, CHEN Jianhui, et al. Saikosaponin D inhibits proliferation and promotes apoptosis in breast cancer cells through down-regulating JAK2/STAT3 pathway. [J]. Journal of Army Medical University 43(9):852-857(2021) DOI： 10.16016/j.1000-5404.202010217.

摘要

目的探讨柴胡皂苷D通过JAK2/STAT3通路对乳腺癌MCF-7细胞增殖和凋亡的影响。方法将乳腺癌MCF-7细胞分为对照组（0 μmol/L），低（5 μmol/L）、中（10 μmol/L）和高（20 μmol/L）剂量柴胡皂苷D组，采用四甲基偶氮唑盐（tetramethylazolium salt，MTT）比色法测定各组MCF-7细胞活力；用流式细胞术检测各组细胞凋亡情况；用免疫组化检测柴胡皂苷D对MCF-7细胞JAK2和STAT3表达情况；同时用免疫蛋白印迹法检测各组细胞JAK2、STAT3和Ki-67蛋白的表达。结果对照组、低剂量组、中剂量组和高剂量组MCF-7细胞活力差异有统计学意义（F=5.099、38.908、159.680、234.885、344.866、386.914，P<0.05)。与对照组相比较，在12、24、36、48、60、72 h后，低剂量组、中剂量组和高剂量组MCF-7细胞活力均有显著降低（P<0.05），且低剂量组细胞活力在24、36 h均高于中剂量组和高剂量组（P<0.05），中剂量组细胞活力在24、36 h均高于高剂量组（P<0.05）。对照组、低剂量组、中剂量组和高剂量组MCF-7细胞凋亡率比较差异具有统计学意义（χ2=21.609，P<0.05)；与对照组比较，低剂量组、中剂量组和高剂量组的细胞凋亡率均升高（P<0.05)，低剂量组细胞凋亡率低于中剂量组和高剂量组（P<0.05），中剂量组细胞凋亡率低于高剂量组（P<0.05）。免疫组化结果显示，对照组、低剂量组、中剂量组和高剂量组MCF-7细胞JAK2、STAT3蛋白相对表达量比较差异具有统计学意义（F=44.343、46.389，P<0.05）；与对照组比较，低剂量组、中剂量组和高剂量组MCF-7细胞JAK2、STAT3表达均降低（P<0.05），且低剂量组细胞JAK2、STAT3表达均高于中剂量组和高剂量组（P<0.05），中剂量组细胞JAK2、STAT3表达均高于高剂量组（P<0.05）。Western blot检测结果显示，对照组、低剂量组、中剂量组和高剂量组MCF-7细胞JAK2、STAT3和Ki-67蛋白相对表达量比较差异具有统计学意义（F=25.241、18.102、14.997，P<0.05)；与对照组比较，低剂量组、中剂量组和高剂量组的细胞JAK2、STAT3和Ki-67相对表达量均降低（P<0.05)，低剂量组细胞JAK2、STAT3相对表达量均高于中剂量组和高剂量组（P<0.05），中剂量组细胞JAK2、STAT3相对表达量均高于高剂量组（P<0.05）。结论柴胡皂苷D能够抑制乳腺癌MCF-7细胞增殖，促进MCF-7细胞凋亡，其作用机制可能与JAK2/STAT3通路有关。

Abstract

ObjectiveTo investigate the effect of saikosaponin D on the proliferation and apoptosis of breast cancer MCF-7 cells by JAK2/STAT3 pathway. MethodsThe breast cancer MCF-7 cells were divided into control group

low-dose group

middle-dose

and high-dose groups (treated with 0

10 and 20 μmol/L saikosaponin D for 12

60 or 72 h). Tetramethylazolium salt (MTT) colorimetric assay was used to detect the cell viability in MCF-7 cells of each group. Flow cytometry was adopted to detect cell apoptosis in each group. Immunohistochemical assay was employed to detect the expression of JAK2 and STAT3 in MCF-7 cells. At the same time

Western blotting was used to detect the protein levels of JAK2

STAT3 and Ki-67 in each group of cells. ResultsThere was statistical differences in MCF-7 cell viability among the control

and low-

middle- and high-dose groups (F=5.099

38.908

159.680

234.885

344.866

386.914

P<0.05). Compared with the control group

the cell viability of MCF-7 cells in the low-dose

middle-dose and high-dose groups were significantly reduced after treatment for 12

60 and 72 h (P<0.05)

and the cell viability of the cells in the low-dose group for 24 and 36 h was higher than that of the middle-dose group and the high-dose group (P<0.05)

and the cell viability of the middle-dose group was higher than that of the high-dose group at 24 and 36 h (P<0.05). The apoptotic rate of MCF-7 cells differed significantly among the control group

and low-

middle- and high-dose groups (Chi-square=21.609

P<0.05). The rate was higher in the 3 treatment groups than the control group (P<0.05)

that of the low-dose group was lower than those of the middle-dose group and the high-dose group (P<0.05)

so was that of the middle-dose group lower than that in the high-dose group (P<0.05). The relative expression levels of JAK2 and STAT3 proteins in MCF-7 cells were significantly different among the 4 groups (F=44.343

46.389

P<0.05)

they were obviously lower in the 3 treatment groups than the control group (P<0.05)

and those in the low-dose group were higher than those of the middle-dose group and the high-dose group (P<0.05)

so were in the medium dose group than those in the high dose group (P<0.05). Western blotting indicated that the relative expression levels of JAK2

STAT3 and Ki-67 proteins significantly differed from each other of the 4 groups (F=25.241

18.102

14.997

P<0.05). The levels of the 3 proteins were all decreased in the 3 treatment groups than the control group (P<0.05)

and the levels of JAK2 and STAT3 were higher in the low-dose group were than the medium-dose group and the high-dose group (P<0.05)

and also was higher in the medium-dose group than the high-dose group (P<0.05). ConclusionSaikosaponin D can inhibit the proliferation and promote the apoptosis in breast cancer MCF-7 cells

which may be closely related to the JAK2/STAT3 pathway.

关键词

柴胡皂苷DJAK2/STAT3通路乳腺癌MCF-7增殖凋亡

Keywords

saikosaponin DJAK2/STAT3 pathwaybreast cancerMCF-7 cellsproliferationapoptosis

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