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Inhibitory effects of extracellular adenosine triphosphate on growth of esophageal carcinoma cells

Inhibitory effects of extracellular adenosine triphosphate on growth of esophageal carcinoma cells

作     者:Ming-Xia Wang Lei-Ming Ren Bao-En Shan 

作者机构:the Fourth Affiliated Hospital of Hebei Medical University Shijiazhuang 050011 Hebei ProvinceChina School of Pharmacy Hebei Medical UniversityShijiazhuang 050017 Hebei Province China 

出 版 物:《World Journal of Gastroenterology》 (世界胃肠病学杂志(英文版))

年 卷 期:2005年第11卷第38期

页      面:5915-5919页

核心收录:

学科分类:1002[医学-临床医学] 100201[医学-内科学(含:心血管病、血液病、呼吸系病、消化系病、内分泌与代谢病、肾病、风湿病、传染病)] 10[医学] 

基  金:Supported by the Science and Technology Development Project of Hebei Province  No. 032761192 

主  题:Extracellular adenosine triphosphate Esophageal carcinoma cells Apoptosis Growth inhibition 

摘      要:AIM: To study the growth inhibitory effects of ATP on TE-13 human squamous esophageal carcinoma cellsin vitro. METHODS: NTT assay was used to determine the inhibition of proliferation of ATP or adenosine (ADO) on TE-13 cell line. The morphological changes of TE-13 cells induced by ATP or ADO were observed under fluorescence light microscope by acridine orange (AO)/ethidium bromide (EB) double stained cells. The intemudeosomal fragmentation of genomic DNA was detected by agarose gel electrophoresis. The apoptotic rate and cell cycle after treatment with ATP or ADO were determined by flow cytometry. RESULTS: ATP and ADO produced inhibitory effects on TE-13 cells at the concentration between 0.01 and 1.0 mmol/L. The ICs0 of TE-13 cells exposed to ATP or ADO for 48 and 72 h was 0.71 or 1.05, and 0.21 or 0.19 mmol/L, respectively. The distribution of cell cycle phase and proliferation index (PI) value of TE-13 cells changed, when being exposed to ATP or ADO at the concentrations of 0.01, 0.1, and 1 mmol/L for 48 h. ATP and ADO inhibited the cell proliferation by changing the distribution of cell cycle phase via either G0/G1 phase (ATP or ADO, 1 mmol/L) or S phase (ATP, 0.1 mmol/L) arrest. Under light microscope, the tumor cells exposed to 0.3 mmol/L ATP or ADO displayed morphological changes of apoptosis. A ladder-like pattern of DNA fragmentation was obtained from TE-13 cells treated with 0.1-1 mmol/L ATP or ADO in agarose gel electrophoresis. ATP and ADO induced apoptosis of TE-13 cells in a dose-dependent manner at the concentration between 0.03 and 1 mmol/L. The maximum apoptotic rate of TE-13 cells exposed to ATP or ADO for 48 h was 16.63% or 16.9%, respectively. CONCLUSION: ATP and ADO inhibit cell proliferation, arrest cell cycle, and induce apoptosis of TE-13 cell line.

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