Effect of sodium aescinate in inducing human breast cancer MCF-7 cells apoptosis by inhibiting AKT, ERK and upstream signal SRC activity.
- Author:
Shi-mei QI
;
Jun LV
;
Yu MENG
;
Zhi-lin QI
;
Lie-feng LING
- Publication Type:Journal Article
- MeSH:
Antineoplastic Agents, Phytogenic;
pharmacology;
Apoptosis;
drug effects;
Breast Neoplasms;
drug therapy;
enzymology;
genetics;
physiopathology;
Down-Regulation;
drug effects;
Drugs, Chinese Herbal;
pharmacology;
Extracellular Signal-Regulated MAP Kinases;
genetics;
metabolism;
Female;
Humans;
MCF-7 Cells;
Proto-Oncogene Proteins c-akt;
genetics;
metabolism;
Saponins;
pharmacology;
Signal Transduction;
drug effects;
Triterpenes;
pharmacology;
src-Family Kinases;
genetics;
metabolism
- From:
China Journal of Chinese Materia Medica
2015;40(16):3267-3272
- CountryChina
- Language:Chinese
-
Abstract:
To study the effect of sodium aescinate in inducing human breast cancer MCF-7 cells apoptosis and its possible mechanism. MTT assay was used to detect the inhibitory effect of sodium aescinate on the proliferation of MCF-7 cells. The morphological changes were observed under inverted microscope. DAPI nuclear staining was used to detect the changes in cell nucleus. Annexin V-FITC/PI flow cytometry was adopted to test the apoptosis rate. Changes in apoptosis-related proteins (PARP, cleaved caspase-8 and pro-caspase-3), cell survival-associated signal molecules (AKT and ERK) and their common upstream kinase SRC was detected by Western blotting. The result showed that after different concentrations of sodium aescinate were used to treat breast cancer MCF-7 cells, they inhibited the proliferation of MCF-7 cells in a dose-dependent manner, induced cell apoptosis (typical morphological changes in nucleus, significant increase in cell apoptosis rate). The expressions of cleaved PARP and caspase-8 increased, while the expression of pro-caspase-3 decreased, which further verified sodium aescinate's effect in inducing cell apoptosis. Sodium aescinate significantly inhibited the phosphorylation of cell survival-related signal molecules (AKT, ERK) and down-regulate the activation of their common up-stream kinase SRC. The findings indicated that sodium aescinate can block signals transiting to downstream molecules AKT, ERK, inhibit the proliferation of breast cancer cell MCF-7 cell apoptosis and induced cell apoptosis by suppressing the activation of SRC.
