Shenbai Jiedu Prescription Inhibits Proliferation of Colorectal Cancer Cells by Regulating PTEN/PI3K/Akt Signaling Pathway

Jianrong LIU; Min HUANG; Minmin FAN; Haibo CHENG; Weixing SHEN; Jun XIAO; Changliang XU; Jiani TAN; Yueyang LAI; Chengtao YU; Dongdong SUN; Liu LI

doi:10.13422/j.cnki.syfjx.20220721

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Shenbai Jiedu Prescription Inhibits Proliferation of Colorectal Cancer Cells by Regulating PTEN/PI3K/Akt Signaling Pathway

更新时间：2022-09-01

- Shenbai Jiedu Prescription Inhibits Proliferation of Colorectal Cancer Cells by Regulating PTEN/PI3K/Akt Signaling Pathway
- Chinese Journal of Experimental Traditional Medical Formulae Vol. 28, Issue 14, Pages: 36-43(2022)
- 作者机构：
  
  1.南京中医药大学第一临床医学院，南京 210023
  2.南京市中医院，南京 210012
  3.江苏省中医药防治肿瘤协同创新中心，南京 210023
  4.南京中医药大学附属医院江苏省中医院，南京 210029
- 作者简介：
- 基金信息：
- DOI：10.13422/j.cnki.syfjx.20220721
  CLC： R22;R242;R2-031;R285.5
- Published：20 July 2022，
  
  Published Online：29 January 2022，
  
  Received：20 October 2021，
- 稿件说明：
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刘见荣,黄敏,范旻旻等.参白解毒方通过调控PTEN/PI3K/Akt信号通路抑制结直肠癌细胞增殖[J].中国实验方剂学杂志,2022,28(14):36-43.

LIU Jianrong,HUANG Min,FAN Minmin,et al.Shenbai Jiedu Prescription Inhibits Proliferation of Colorectal Cancer Cells by Regulating PTEN/PI3K/Akt Signaling Pathway[J].Chinese Journal of Experimental Traditional Medical Formulae,2022,28(14):36-43.
刘见荣,黄敏,范旻旻等.参白解毒方通过调控PTEN/PI3K/Akt信号通路抑制结直肠癌细胞增殖[J].中国实验方剂学杂志,2022,28(14):36-43. DOI： 10.13422/j.cnki.syfjx.20220721.

LIU Jianrong,HUANG Min,FAN Minmin,et al.Shenbai Jiedu Prescription Inhibits Proliferation of Colorectal Cancer Cells by Regulating PTEN/PI3K/Akt Signaling Pathway[J].Chinese Journal of Experimental Traditional Medical Formulae,2022,28(14):36-43. DOI： 10.13422/j.cnki.syfjx.20220721.

摘要

目的

研究参白解毒方基于磷酸酶及张力蛋白同源物（PTEN）/磷脂酰肌醇-3激酶（PI3K）/蛋白激酶B（Akt）信号通路抑制结直肠癌细胞HCT116增殖的作用机制。

方法

采用水提醇沉法提取参白解毒方有效部位进行冻干粉制备；体外培养HCT116细胞，用参白解毒方（2、4、8、16 g·L

-1

）对HCT116细胞进行处理，采用噻唑蓝（MTT）比色法检测参白解毒方对HCT116细胞增殖的抑制作用；实时荧光定量聚合酶链式反应（Real-time PCR）检测细胞PTEN、PI3K、Akt、糖原合成酶激酶-3

（GSK-3

）、c-核蛋白类基因（c-Myc）、生存素（Survivin）和细胞周期蛋白D

（CyclinD

）mRNA表达水平；蛋白免疫印迹法（Western blot）检测PTEN、磷酸化磷酸酶及张力蛋白同源物（p-PTEN）、PI3K、Akt、磷酸化蛋白激酶B（p-Akt）、GSK-3

、磷酸化糖原合成酶激酶-3（p-GSK-3

）、c-Myc、Survivin、CyclinD

的蛋白表达水平；免疫荧光检测

-连环蛋白（

-catenin）入核情况。

结果

与空白组比较，参白解毒方各质量浓度均可以显著抑制HCT116细胞的增殖（

0.01），且具有浓度依赖性。与空白组比较，参白解毒方处理细胞后PTEN、GSK-3

mRNA表达水平均上调，PI3K、Akt、c-Myc、Survivin、CyclinD

mRNA表达水平均下调（

0.01）；细胞PTEN、p-PTEN和GSK-3

蛋白表达水平上调，PI3K、Akt、p-Akt、GSK-3

、p-GSK-3

、c-Myc、Survivin、CyclinD

蛋白表达水平均下调（

0.05，

0.01）。免疫荧光结果显示参白解毒方可以抑制结直肠癌细胞HCT116中

-catenin的入核。

结论

参白解毒方可以抑制结直肠癌细胞HCT116的增殖，其作用机制可能是通过调节PTEN/PI3K/Akt信号通路。

Abstract

Objective

To study the mechanism of Shenbai Jiedu prescription inhibiting the proliferation of HCT116 colorectal cancer （CRC） cells by regulating the phosphatase and tensin homolog deleted on chromosome ten （PTEN）/phosphatidylinositol 3-kinase （PI3K）/ protein kinase B （Akt） signaling pathway.

Method

Shenbai Jiedu prescription was extracted by water extraction and alcohol precipitation to prepare freeze-dried powder. HCT116 cells were cultured

in vitro

， and treated with different concentrations of Shenbai Jiedu prescription （2， 4， 8， 16 g·L

-1

）. The inhibitory effect of Shenbai Jiedu prescription on the proliferation of HCT116 cells was tested by methyl thiazolyl tetrazolium （MTT）. Real-time quantitative PCR was used to detect the mRNA expression levels of PTEN， PI3K， Akt， glycogen synthase kinase-3

（GSK-3

）， c-Myc， survivin and Cyclin D

. Western blot was employed to measure the protein expression levels of PTEN， phosphorylated PTEN （p-PTEN）， PI3K， Akt， phosphorylated Akt （p-Akt）， GSK-3

， phosphorylated GSK-3

（p-GSK-3

β）

， c-Myc， survivin and Cyclin D

，

-catenin nuclear import was explored by immunofluorescence assay.

Result

Compared with the control group， Shenbai Jiedu prescription inhibited the proliferation of HCT116 cells in a dose-dependent manner （

0.01）. Compared with the control group， the mRNA expression levels of PTEN and GSK-3

were up-regulated whereas those of PI3K， Akt， c-Myc， survivin and CyclinD

were down-regulated after treatment with Shenbai Jiedu prescription （

0.01）. The protein expression levels of PTEN， p-PTEN and GSK-3

were up-regulated whereas those of PI3K， Akt， p-Akt， GSK-3

， p-GSK-3

， c-Myc， survivin and CyclinD

were down-regulated （

0.05，

0.01）. Immunofluorescence assay showed that Shenbai Jiedu prescription suppressed

-catenin nuclear import in HCT116 cells.

Conclusion

Shenbai Jiedu prescription inhibited the proliferation of HCT116 cells via the mechanism of regulating the PTEN/PI3K/Akt signaling pathway.

关键词

参白解毒方结直肠癌细胞增殖磷酸酶及张力蛋白同源物（PTEN）/磷脂酰肌醇-3激酶（PI3K）/蛋白激酶B（PKB/Akt）信号通路β-连环蛋白（β-catenin）入核

Keywords

Shenbai Jiedu prescriptioncolorectal cancercell proliferationphosphatase and tensin homolog deleted on chromosome ten （PTEN）/phosphatidylinositol 3-kinase （PI3K）/protein kinase B （Akt） signaling pathwayβ-catenin nuclear import

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