Banxia Xiexin Decoction suppresses malignant phenotypes of colon cancer cells via PARG/PARP1/NF-κB signaling pathway.
10.19540/j.cnki.cjcmm.20240923.304
- Author:
Yu-Qing HUANG
1
;
Jia-Mei WANG
1
;
Heng-Zhou LAI
1
;
Chong XIAO
1
;
Feng-Ming YOU
2
;
Qi-Xuan KUANG
1
;
Yi-Fang JIANG
1
Author Information
1. TCM Regulating Metabolic Diseases Key Laboratory of Sichuan Province, Hospital of Chengdu University of Traditional Chinese Medicine Chengdu 610075, China.
2. TCM 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:
Banxia Xiexin Decoction;
PARG/PARP1/NF-κB signaling pathway;
colon cancer;
epithelial-mesenchymal transition(EMT)
- MeSH:
Colonic Neoplasms/pathology*;
Drugs, Chinese Herbal/pharmacology*;
Phenotype;
Signal Transduction/drug effects*;
Cell Proliferation/drug effects*;
Apoptosis;
Cell Movement/drug effects*;
Neoplasm Invasiveness;
HCT116 Cells;
Proto-Oncogene Proteins c-bcl-2/biosynthesis*;
Humans;
Poly (ADP-Ribose) Polymerase-1;
Glycoside Hydrolases;
bcl-2-Associated X Protein;
NF-kappa B p50 Subunit
- From:
China Journal of Chinese Materia Medica
2025;50(2):496-506
- CountryChina
- Language:Chinese
-
Abstract:
This study aims to delve into the influences and underlying mechanisms of Banxia Xiexin Decoction(BXD) on the proliferation, apoptosis, invasion, and migration of colon cancer cells. Firstly, the components of BXD in blood were identified by UPLC-MS/MS, and subsequently the content of these components were determined by HPLC. Then, different concentrations of BXD were used to treat both the normal intestinal epithelial cells(NCM460) and the colon cancer cells(HT29 and HCT116). The cell viability and apoptosis were examined by the cell counting kit-8(CCK-8) and flow cytometry, respectively. Western blot was employed to determine the expression of the apoptosis regulators B-cell lymphoma-2(Bcl-2) and Bcl-2-associated X(Bax). The cell wound healing assay and Transwell assay were employed to measure the cell migration and invasion, respectively. Additionally, Western blot was employed to determine the expression levels of epithelial-mesenchymal transition(EMT)-associated proteins, including epithelial cadherin(E-cadherin), neural cadherin(N-cadherin), and vimentin. The protein and mRNA levels of the factors in the poly(ADP-ribose) glycohydrolase(PARG)/poly(ADP-ribose) polymerase 1(PARP1)/nuclear factor kappa-B p65(NF-κB p65) signaling pathway were determined by Western blot and RT-qPCR, respectively. The results demonstrated that following BXD intervention, the proliferation of HT29 and HCT116 cells was significantly reduced. Furthermore, BXD promoted the apoptosis, enhanced the expression of Bcl-2, and suppressed the expression of Bax in colon cancer cells. At the same time, BXD suppressed the cell migration and invasion and augmented the expression of E-cadherin while diminishing the expression of N-cadherin and vimentin. In addition, BXD down-regulated the protein and mRNA levels of PARG, PARP1, and NF-κB p65. In conclusion, BXD may inhibit the malignant phenotypes of colon cancer cells by mediating the PARG/PARP1/NF-κB signaling pathway.
