Dihydromyricetin inhibits proliferation and migration of gastric cancer cells through regulating Akt/STAT3 signaling pathways and HMGB1 expression.
10.12122/j.issn.1673-4254.2021.01.12
- Author:
Shengnan WANG
1
;
Fei GE
2
;
Tianyu CAI
3
;
Shimei QI
1
;
Zhilin QI
1
Author Information
1. Department of Biochemistry and Molecular Biology, Wannan Medical College, Wuhu 241002, China.
2. School of Pharmacy, Wannan Medical College, Wuhu 241002, China.
3. Anhui Provincial Key Laboratory of Active Biological Macro-molecules, Wannan Medical College, Wuhu 241002, China.
- Publication Type:Journal Article
- Keywords:
Akt/stat3 signaling pathways;
HMGB1;
dihydromyricetin;
gastric cancer;
migration;
proliferation
- MeSH:
Cell Line, Tumor;
Cell Movement;
Cell Proliferation;
Flavonols;
HMGB1 Protein/metabolism*;
Humans;
Proto-Oncogene Proteins c-akt/metabolism*;
STAT3 Transcription Factor;
Stomach Neoplasms
- From:
Journal of Southern Medical University
2021;41(1):87-92
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To investigate the inhibitory effects of dihydromyricetin on the proliferation and migration of gastric cancer BGC-823 cells and explore the molecular mechanisms.
METHODS:BGC-823 cells in routine culture were treated with different concentrations of dihydromyricetin (0, 40, 60, 80, 100, and 120 μg/mL) for 24 h, and the changes in cell viability were detected using CCK-8 assay; colony forming assay and Transwell assay were performed to assess the changes in colonyforming and migration abilities of the cells, respectively. The levels of MMP-2 and MMP-9 in the treated cells were determined using ELISA, and Western blotting was used to detect the expressions of E-cadherin, N-cadherin, cyclin D1, cyclin E1, HSP70 and HMGB1 and the phosphorylation levels of Akt and Stat3.
RESULTS:CCK-8 assay showed that dihydromyricetin treatment dose-dependently inhibited the viability of BGC-823 cells (
CONCLUSIONS:Dihydromyricetin inhibits the proliferation and migration of BGC-823 cells through suppressing the activation of Akt/stat3 signaling pathways and HMGB1 expression.