अमूर्त
Research on the mechanisms of zerumbone in inhibition of proliferation and induction of apoptosis in human esophageal cancer cell line Eca-109
Changjiang Lei, Manli Yan, Bin Wang, Hong Ren, Yuan Li, Qingyun Pan
Objective: To investigate the mechanisms of zerumbone in proliferation and inducing effect on apoptosis of human esophageal cancer cell line Eca-109.
Methods: Eca-109 cell lines were divided into two zerumbone treatment groups (10 μmol/L and 20 μmol/L) and one blank control group (0 μmol/L). Thereafter, MTT assay was performed to observe the inhibitory effect of zerumbone on the in-vitro growth of Eca-109 cells; flow cytometry was performed for detecting the distribution of cell cycles; inverted phase contrast microscope was used to observe the morphology of Eca-109 cells; RT-PCR and Western blotting assay were carried out for detecting the changes in mRNA and protein expressions of CXCR4.
Results: Zerumbone had a significant inhibitory effect on the growth of Eca-109 cells, and the inhibitory effect was continuously elevated with an increase in concentration (p<0.05). Besides, zerumbone could induce the apoptosis of Eca-109 cells, and the apoptotic rate was increased in a concentration-dependent manner (p<0.05). After 48 h and 72 h of treatment with zerumbone in different concentrations, we found that the incidence of poor adhesive growth and cell death was increased against the augmentation in concentration of zerumbone; with the time extension, the quantity of Eca-109 cells would be decreased gradually after treatment with zerumbone in a certain concentration. The results of RT-PCR and Western blotting assay also showed that compared with the control group, the mRNA and protein expressions of CXCR4 in 10 μmol/L and 20 μmol/L groups were significantly decreased (p<0.05), in which the decrease in 20 μmol/L group was more significant.
Conclusion: Zerumbone can inhibit the growth of Eca-109 cells with a promoting effect on apoptosis, and the mechanism might be correlated with the downregulation of CXCR4.