Eleutheroside B induces apoptosis and autophagy of lung cancer cells by regulating PI3K/Akt/mTOR pathway.
10.19540/j.cnki.cjcmm.20230804.401
- Author:
Xue-Ting CAO
1
;
Bo-Ya WU
1
;
Jing CHEN
2
Author Information
1. Tangshan Key Laboratory for Preclinical and Basic Research on Chronic Diseases, Hebei Key Laboratory for Chronic Diseases, School of Basic Medical Sciences, North China University of Science and Technology Tangshan 063210, China.
2. College of Life Sciences, North China University of Science and Technology Tangshan 063210, China.
- Publication Type:Journal Article
- Keywords:
PI3K/Akt/mTOR pathway;
apoptosis;
autophagy;
eleutheroside B;
lung cancer
- MeSH:
Humans;
Lung Neoplasms/metabolism*;
Proto-Oncogene Proteins c-akt/metabolism*;
Phosphatidylinositol 3-Kinases/metabolism*;
Signal Transduction;
TOR Serine-Threonine Kinases/metabolism*;
Apoptosis;
Apoptosis Regulatory Proteins;
Autophagy;
Cell Proliferation;
Cell Line, Tumor;
Glucosides;
Phenylpropionates
- From:
China Journal of Chinese Materia Medica
2023;48(24):6693-6701
- CountryChina
- Language:Chinese
-
Abstract:
This study investigated the effect of eleutheroside B on apoptosis and autophagy of lung cancer A549 and H460 cells and its molecular mechanism. MTT assay was used to detect the cytotoxicity of eleutheroside B at 5, 10, 15, 20, 25, 30, 35, 40, and 45 mmol·L~(-1) on lung cancer cells. Trypan blue exclusion assay was used to detect the effect of eleutheroside B on the survival rate of lung cancer A549 and H460 cells at different time. Colony formation assay was used to detect the effect of eleutheroside B on the proliferation of lung cancer A549 and H460 cells. AO/EB fluorescence double staining and Hoechst 33342 fluorescence staining were used to detect the effect of eleutheroside B on apoptosis of lung cancer A549 and H460 cells, and Western blot was used to detect apoptosis-related proteins to explore the apoptosis-related molecular mechanism. AO fluorescence staining and Western blot were used to detect the expression of autophagic vesicles and autophagy-related proteins P62 and LC3. The results showed that compared with the control group, eleutheroside B inhibited the growth of lung cancer A549 and H460 cells in a concentration-dependent manner. The optimal effect time of eleutheroside B on lung cancer A549 and H460 cells was 24 h, and the optimal concentrations were 28.64 and 22.16 mmol·L~(-1), respectively. Eleutheroside B could inhibit the colony formation of A549 and H460 cells. Compared with the control group, eleutheroside B could promote the formation of apoptotic bodies and induce cell apoptosis, as well as induce the expression of mitochondrial pathway-related proteins. Under the effect of eleutheroside B, the acidic autophagy vacuole in lung cancer cells increased, LC3Ⅱ expression increased, P62 protein expression decreased, and PI3K, p-Akt, and p-mTOR protein expression decreased in the PI3K/Akt/mTOR pathway. Studies have shown that eleutheroside B can inhibit the growth of lung cancer cells, reduce colony formation, induce apoptosis of lung cancer cells through mitochondrial pathway, and induce autophagy. The mechanism may be related to the PI3K/Akt/mTOR pathway.
