α-Hederin Regulates SREBP1/FASN Pathway and Inhibits Malignant Phenotype of Non-small Cell Lung Cancer
10.3971/j.issn.1000-8578.2023.22.1503
- VernacularTitle:α-常春藤皂苷调控SREBP1/FASN通路抑制非小细胞肺癌的恶性表型
- Author:
Yuzhen CHANG
1
;
Hao YANG
;
Gang HUANG
Author Information
1. Shanghai University of Traditional Chinese Medicine, Shanghai 200120, China
- Publication Type:Research Article
- Keywords:
α-Hederin;
NSCLC;
SREBP1;
FASN;
Lipid accumulation
- From:
Cancer Research on Prevention and Treatment
2023;50(8):745-752
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the regulative effect of α-Hederin on the proliferation and invasion of NSCLC and investigate its related molecular mechanism. Methods After A549 and HCC-1833 cells were treated with a concentration gradient of α-Hederin for 24 and 48 h, the OD450nm was detected by using CCK8 assays, and the IC50 was calculated.The A549 and HCC-1833 cells were divided into the blank control and α-Hederin groups in accordance with IC50 values.Cell proliferation was detected by EdU assays, and cell cycle transformation and cell apoptosis were detected by flow cytometry.Cell mobility was detected by using Transwell and scratch assays.SREBP1 and FASN protein expression levels were detected through Western blot analysis, and cell lipid accumulation was detected via oil red O staining. Results The survival rate of lung cancer cells decreased significantly with the increase of α-Hederin concentration, and the IC50 values of A549 and HCC-1833 cells at 48 h were 15 and 25 μg/ml, respectively.Compared with the blank control group, cells proliferation and migration were significantly inhibited, cells were blocked in the G1/S phase, the apoptosis rate increased, and the protein expression and lipid accumulation of SREBP1/FASN significantly reduced after α-Hederin treatment. Conclusion α-Hederin can inhibit the proliferation and migration, G1/S phase transition and induce the apoptosis of NSCLC cells and hinder the malignant progression of NSCLC by downregulating the expression of SREBP1 and FASN and reducing the accumulation of cell lipids.
