Decursin affects proliferation, apoptosis, and migration of colorectal cancer cells through PI3K/Akt signaling pathway.
10.19540/j.cnki.cjcmm.20230117.703
- Author:
Yi YANG
1
;
Yan-E HU
1
;
Mao-Yuan ZHAO
1
;
Yi-Fang JIANG
1
;
Xi FU
1
;
Feng-Ming YOU
2
Author Information
1. Traditional Chinese Medicine Regulating Metabolic Diseases Key Laboratory of Sichuan Province,Hospital of Chengdu University of Traditional Chinese Medicine Chengdu 610075, China.
2. Traditional Chinese Medicine Regulating Metabolic Diseases Key Laboratory of Sichuan Province,Hospital of Chengdu University of Traditional Chinese Medicine Chengdu 610075, China Cancer Institute, Chengdu University of Traditional Chinese Medicine Chengdu 610072, China.
- Publication Type:Journal Article
- Keywords:
PI3K/Akt signaling pathway;
apoptosis;
colorectal cancer;
decursin;
migration;
proliferation
- MeSH:
Humans;
Proto-Oncogene Proteins c-akt/metabolism*;
Phosphatidylinositol 3-Kinases/metabolism*;
bcl-2-Associated X Protein;
Vimentin/metabolism*;
Cell Proliferation;
Signal Transduction;
Apoptosis;
Cell Line, Tumor;
Colorectal Neoplasms/genetics*;
Cadherins/genetics*;
Cell Movement
- From:
China Journal of Chinese Materia Medica
2023;48(9):2334-2342
- CountryChina
- Language:Chinese
-
Abstract:
We investigated the effects of decursin on the proliferation, apoptosis, and migration of colorectal cancer HT29 and HCT116 cells through the phosphatidylinositol 3-kinase(PI3K)/serine-threonine kinase(Akt) pathway. Decursin(10, 30, 60, and 90 μmol·L~(-1)) was used to treat HT29 and HCT116 cells. The survival, colony formation ability, proliferation, apoptosis, wound hea-ling area, and migration of the HT29 and HCT116 cells exposed to decursin were examined by cell counting kit-8(CCK8), cloning formation experiments, Ki67 immunofluorescence staining, flow cytometry, wound healing assay, and Transwell assay, respectively. Western blot was employed to determine the expression levels of epithelial cadherin(E-cadherin), neural cadherin(N-cadherin), vimentin, B-cell lymphoma/leukemia-2(Bcl-2), Bcl-2-associated X protein(Bax), tumor suppressor protein p53, PI3K, and Akt. Compared with the control group, decursin significantly inhibited the proliferation and colony number and promoted the apoptosis of HT29 and HCT116 cells, and it significantly down-regulated the expression of Bcl-2 and up-regulated the expression of Bax. Decursin inhibited the wound healing and migration of the cells, significantly down-regulated the expression of N-cadherin and vimentin, and up-regulated the expression of E-cadherin. In addition, it significantly down-regulated the expression of PI3K and Akt and up-regulated that of p53. In summary, decursin may regulate epithelial-mesenchymal transition(EMT) via the PI3K/Akt signaling pathway, thereby affecting the proliferation, apoptosis, and migration of colorectal cancer cells.
