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Background Cigarette smoking has been verified as the risk factor of esophageal squamous cell carcinoma(ESCC).Overexpression of cyclooxygenase 2(COX-2)is shown in ESCC.The objective of this study was to investigate theeffects of cigarette smoking ethanol extract(EE)on the proliferation of the human ESCC cell lines,and to explore thecorrelation between the proliferation rate of human ESCC cell lines and the expression pattern of COX-2.Whether aspirincan inhibit the proliferation of the ESCC cell lines pretreated with EE,and regulate the mRNA expression levels of COX-2are also examined.Methods Two human ESCC cell lines were selected.EC109 was poorly differentiated and EC9706 was highlydifferentiated.EC109 and EC9706 were treated with EE and aspirin for different time course.The cell growth of ESCCwas measured by MTT reduction assay and the expression of COX-2 was measured by RT-PCR and Western blotanalysis.Results EE promoted the proliferation of EC109 and EC9706 in dose-and time-dependent manners.In theconcentration range(10-100 μg/ml for EE)and in the time range(24-72 hours)after addition of EE,the cell proliferationwas prominent in an up-scaled manner respectively.Aspirin could inhibit the proliferation of cell lines EC109 and EC9706pretreated with EE for 5 hours,in a dose-dependent manner.In the concentration range(0.5-8.0 mmol/L for aspirin),thecell growth inhibition was prominent in an up-scaled manner accordingly(P<0.05).The effect of EE on cell proliferationwas correlated with the up-regulation of COX-2 gene.However,the cell growth inhibition of aspirin was correlated withthe down-regulation of COX-2 gene.Conclusions EE can stimulate the proliferation of human ESCC cell lines EC109 and EC9706,most likely throughup-regulating the expression of COX-2.Aspirin can inhibit the proliferation of ESCC cell lines induced by EE,whichsuggests it may be advantageous in the chemoprevention and therapy of human tobacco-related ESCC.And its effect islikely to be related with modulating COX-2 activity.
Background Cigarette smoking has been verified as the risk factor of esophageal squamous cell carcinoma (ESCC). Overexpression of cyclooxygenase 2 (COX-2) is shown in ESCC. The objective of this study was to investigate the effects of cigarette smoking ethanol extract (EE) on the proliferation of the human ESCC cell lines, and to explore thecorrelation between the proliferation rate of human ESCC cell lines and the expression pattern of COX-2.Whether aspirincan inhibit the proliferation of the ESCC cell lines pretreated with EE, and regulate the mRNA Expression levels of COX-2are also examined. Two Human ESCC cell lines were selected. EC109 was poorly differentiated and EC9706 was highly differentiated. EC109 and EC9706 were treated with EE and aspirin for different time course. The cell growth of ESCC was measured by MTT reduction assay and the expression of COX-2 was measured by RT-PCR and Western blot analysis. Results EE promoted the proliferation of EC109 and EC9706 in dose-and time-depende nt manners. In the range of concentration (10-100 μg / ml for EE) and in the time range (24-72 hours) after addition of EE, the cell proliferation was prominent in an up-scaled manner respectively. Aspirin could inhibit the proliferation of cell lines EC109 and EC9706pretreated with EE for 5 hours in a dose-dependent manner.In the concentration range (0.5-8.0 mmol / L for aspirin), thecell growth inhibition was significantly in an up-scaled manner accordingly (P <0.05) The effect of EE on cell proliferation is correlated with the up-regulation of COX-2 gene. However, the cell growth inhibition of aspirin was correlated with the down-regulation of COX-2 gene. Conclusions EE can stimulate the proliferation of human ESCC cell lines EC109 and EC9706, most likely throughup-regulating the expression of COX-2.Aspirin can inhibit the proliferation of ESCC cell lines induced by EE, whichsuggests it may be advantageous in the chemoprevention and therapy of human tobacco-related ESCC. And its its effect islikely to be related with modulating COX-2 activity.