Isofebrifuzine regulates energy metabolism of EC9706 cells based on AMPK/mTOR signaling pathway
10.7501/j.issn.0253-2670.2020.17.016
- VernacularTitle: 基于AMPK/mTOR信号通路研究异常山碱对EC9706细胞能量代谢的调控机制
- Author:
Dan-Hua MENG
1
Author Information
1. Henan Key Laboratory of Signal Transduction, Henan University of Traditional Chinese Medicine
- Publication Type:Journal Article
- Keywords:
AMPK/mTOR pathway;
Apoptosis;
Cycle;
EC9706 cells;
Energy metabolism;
Isofebrifuzine;
Proliferation
- From:
Chinese Traditional and Herbal Drugs
2020;51(17):4482-4488
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To investigate the molecular mechanism of isofebrifuzine in the treatment of esophageal cancer by observing the effects of isofebrifuzine on proliferation, apoptosis, cycle, energy metabolism and protein expression related to energy metabolism pathway in EC9706 cells. Methods: ECC9706 cells were routinely cultured, cell activity was detected by MTT method, drug concentration was screened, and two concentrations of 1 μg/mL and 2 μg/mL were selected, the effect of isofebrifuzine on apoptosis and cycle of esophageal cancer cells EC9706 was detected by flow cytometry. The effect of isofebrifuzine on energy metabolism of EC9706 cells was detected by energy metabolism detection system, and the protein expressions of mTOR, p-mTOR, p-ACC and AMPK in cells were detected by Western blotting. Results: The proliferation of EC9706 cells was effectively inhibited in a dose-dependent manner (P < 0.01) after 48 h of treatment with different concentrations of isofebrifuzine, which could arrest EC9706 cells in S phase and G2/M phase (P < 0.05), effectively promote cell apoptosis (P < 0.05), and significantly inhibit cell glycolysis and mitochondrial metabolism (P < 0.01). Compared with the control group, AMPK expression was increased and mTOR, p-mTOR, p-ACC expression was decreased in the treatment group (P < 0.05). Conclusion: These results indicated that isofebrifuzine may regulate the cycle and apoptosis of EC9706 cells and inhibit the proliferation of EC9706 cells in esophageal cancer through energy metabolism.
