Shenbai Jiedu Prescription Inhibits Proliferation of Colorectal Cancer Cells by Regulating PTEN/PI3K/Akt Signaling Pathway
10.13422/j.cnki.syfjx.20220721
- VernacularTitle: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
- Author:
Jianrong LIU
1
;
Min HUANG
1
;
Minmin FAN
1
;
Haibo CHENG
1
;
Weixing SHEN
1
;
Jun XIAO
2
;
Changliang XU
1
;
Jiani TAN
1
;
Yueyang LAI
1
;
Chengtao YU
1
;
Dongdong SUN
1
;
Liu LI
1
Author Information
1. The First School of Clinical Medical， Nanjing University of Chinese Medicine， Nanjing 210023， China
2. Affiliated Hospital of Nanjing University of Chinese Medicine， Jiangsu Province Hospital of China Medicine， Nanjing 210029， China
- Publication Type:Journal Article
- Keywords:
Shenbai Jiedu prescription;
colorectal cancer;
cell proliferation;
phosphatase and tensin homolog deleted on chromosome ten （PTEN）/phosphatidylinositol 3-kinase （PI3K）/protein kinase B （Akt） signaling pathway;
β-catenin nuclear import
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2022;28(14):36-43
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo 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. MethodShenbai 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-3β （GSK-3β）， c-Myc， survivin and Cyclin D1. Western blot was employed to measure the protein expression levels of PTEN， phosphorylated PTEN （p-PTEN）， PI3K， Akt， phosphorylated Akt （p-Akt）， GSK-3β， phosphorylated GSK-3β （p-GSK-3β）， c-Myc， survivin and Cyclin D1， β-catenin nuclear import was explored by immunofluorescence assay. ResultCompared with the control group， Shenbai Jiedu prescription inhibited the proliferation of HCT116 cells in a dose-dependent manner （P<0.01）. Compared with the control group， the mRNA expression levels of PTEN and GSK-3β were up-regulated whereas those of PI3K， Akt， c-Myc， survivin and CyclinD1 were down-regulated after treatment with Shenbai Jiedu prescription （P<0.01）. The protein expression levels of PTEN， p-PTEN and GSK-3β were up-regulated whereas those of PI3K， Akt， p-Akt， GSK-3β， p-GSK-3β， c-Myc， survivin and CyclinD1 were down-regulated （P<0.05， P<0.01）. Immunofluorescence assay showed that Shenbai Jiedu prescription suppressed β-catenin nuclear import in HCT116 cells. ConclusionShenbai Jiedu prescription inhibited the proliferation of HCT116 cells via the mechanism of regulating the PTEN/PI3K/Akt signaling pathway.
