Author/Authors :
Chen، Xiaoguang G. نويسنده , , Lv، Qiongxia نويسنده Animal Science and Technology School, Henan University of Science and Technology, Luoyang, China , , Liu، Yumei نويسنده Animal Science and Technology School, Henan University of Science and Technology, Luoyang, China , , Deng، Wen نويسنده Animal Science and Technology School, Henan University of Science and Technology, Luoyang, China ,
Abstract :
Objective: Today, esophageal cancer (EC) has become one of the most common cancer
types in China. Therefore, new drug and therapeutic strategies are urgently needed to
improve postoperative survival rate of patients with EC. As a food additive, several lines
of evidence have shown that citric acid can be served as glycolysis suppressor to inhibit
growth of some tumor cells. However, little is known about the effect of this organic acid
on the growth of human esophageal carcinoma cell line, EC109.
Materials and Methods: In this experimental study, cell proliferation rate was determined
using MTT assay. Apoptotic morphological changes were evaluated by fluorescent microscopy
using Hoechst 33258 staining. Cell apoptosis rate and mitochondrial membrane
potential (MMP) were detected using flow-cytometry. Effect of citric acid on cellular membrane
permeability was assessed by measuring lactate dehydrogenase (LDH) activity,
using LDH assay kit.
Results: Compared to the control group, there was a marked decrease in cells proliferation
when the cells were treated with higher citric acid concentrations (800, 1600 ?g/ml).
Typical apoptotic morphology of EC109 cells was observed upon treatment with citric acid,
such as chromatin condensation and appearance of apoptotic body. Cell apoptotic indexes
were significantly increased (P < 0.01) after treatment with citric acid at the concentration
of 400-1600 ?g/ml. Extracellular LDH activity and loss of MMP in all of the treated
groups were significantly higher than control (P < 0.05), in a dose-dependent manner.
Conclusion: These results suggest that citric acid prevents EC109 cell growth by inhibiting
cell proliferation and inducing apoptosis, which perhaps offers some theoretical guidance
for its application in EC treatment.
