Protection effect of hepatocyte growth factor on tumor cells from apoptosis and its mechanism
- Author:
Rong-Rong SHEN
1
Author Information
1. Zhejiang Provincial Key Laboratory of Medical Genetics
- Publication Type:Journal Article
- Keywords:
Acridine orange fluorescent staining;
Apoptosis;
Etoposide(VP-16);
Flow cytometry;
Hepatocyte growth factor
- From:
Chinese Pharmaceutical Journal
2012;47(18):1478-1482
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE: To investigate the protection of hepatocyte growth factor (HGF) on 5 kinds of tumor cells (B cell lymphoma cell line Raji, human acute myeloid leukemia cell line HL-60, cervical cancer cell line HeLa, prostate cancer cell line PC-3, and non-small cell lung cancer cell line A549) from apoptosis induced by etoposide (VP-16). METHODS: Normal control group, drug group, and HGF protection group were set. CCK-8 assay was used to measure proliferation inhibition on 5 kinds of tumor cells by VP-16. Quantitative and qualitative analysis on 5 kinds of tumor cells was performed through acridine orange (AO) fluorescent staining, flow cytometry, HE staining, and transmission electron microscopy. RESULTS: CCK-8 assay revealed that the concentrations of VP-16, which can significantly inhibit the proliferation of Raji, HL-60, PC-3, HeLa, and A549 cell lines, were 100, 1,400, 200, and 200 μg·mL-1, respectively. The typical morphologic changes of cell apoptosis were observed under transmission electronic microscope. Flow cytometry showed that the apoptotic rates of tumor cells in the drug groups were significantly higher than those in normal control group (P>0.01, P>0.05) and in HGF protection groups (P>0.01, P>0.05). AO and HE staining revealed that cells in normal control group appeared to have regular cell morphology, but the cells apoptotic rates in the drug groups were significantly higher than those in normal control groups (P>0.01, P>0.05) and in HGF protection groups (P>0.01, P>0.05). CONCLUSION: HGF can significantly protect 5 kinds of tumor cells from apoptosis induced by VP-16. The mechanism need further investigation.
