2012Journal of Jilin UniversityRequires access

Inhibitory effects of celecoxib on expressions of VEGF and MMP-9 in human medullary thyroid TT cells and their mechanisms

Qun Li

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Abstract

Objective To discuss the effect of cyclooxegenase-2(COX-2) selective suppressor celecoxib on the expressions of vascular endothelial growth factor(VEGF) mRNA and matrix metalloproteinases-9(MMP-9) mRNA in human medullary thyroid TT cells,and to approach the anticancer mechanism of celecoxib.Methods The TT cells of human medullary thyroid carcinoma were divided into control group and different concertrations of celecoxib groups,and the cells in celecoxib groups were treated with different concentrations of celecoxib(20,40 and 80 μmol·L-1),the cells in control group were treated with F12K culture fluid.The expressions of VEGF mRNA and MMP-9 mRNA in each group were detected by RT-PCR 72 h after treatment.Results the RT-PCR results showed that the expressions of VEGF mRNA and MMP-9 mRNA in TT cells were decreased after treated with 20,40 and 80 μmol·L-1 celecoxib.There was significance difference of the VEGF/GAPDH and MMP-9/GAPDH of TT cells between 40,80 μmol·L-1 celecoxib groups and control group(P0.05).Conclusion The secretion of VEGF mRNA and MMP-9 mRNA is decreased obviously when the concentration of celecoxib is above 40 μmol·L-1,which may inhibit the growth of tumor.

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Objective To discuss the effect of cyclooxegenase-2(COX-2) selective suppressor celecoxib on the expressions of vascular endothelial growth factor(VEGF) mRNA and matrix metalloproteinases-9(MMP-9) mRNA in human medullary thyroid TT cells,and to approach the anticancer mechanism of celecoxib.Methods The TT cells of human medullary thyroid carcinoma were divided into control group and different concertrations of celecoxib groups,and the cells in celecoxib groups were treated with different concentrations of celecoxib(20,40 and 80 μmol·L-1),the cells in control group were treated with F12K culture fluid.The expressions of VEGF mRNA and MMP-9 mRNA in each group were detected by RT-PCR 72 h after treatment.Results the RT-PCR results showed that the expressions of VEGF mRNA and MMP-9 mRNA in TT cells were decreased after treated with 20,40 and 80 μmol·L-1 celecoxib.There was significance difference of the VEGF/GAPDH and MMP-9/GAPDH of TT cells between 40,80 μmol·L-1 celecoxib groups and control group(P0.05).Conclusion The secretion of VEGF mRNA and MMP-9 mRNA is decreased obviously when the concentration of celecoxib is above 40 μmol·L-1,which may inhibit the growth of tumor.

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Available abstract

Objective To discuss the effect of cyclooxegenase-2(COX-2) selective suppressor celecoxib on the expressions of vascular endothelial growth factor(VEGF) mRNA and matrix metalloproteinases-9(MMP-9) mRNA in human medullary thyroid TT cells,and to approach the anticancer mechanism of celecoxib.Methods The TT cells of human medullary thyroid carcinoma were divided into control group and different concertrations of celecoxib groups,and the cells in celecoxib groups were treated with different concentrations of celecoxib(20,40 and 80 μmol·L-1),the cells in control group were treated with F12K culture fluid.The expressions of VEGF mRNA and MMP-9 mRNA in each group were detected by RT-PCR 72 h after treatment.Results the RT-PCR results showed that the expressions of VEGF mRNA and MMP-9 mRNA in TT cells were decreased after treated with 20,40 and 80 μmol·L-1 celecoxib.There was significance difference of the VEGF/GAPDH and MMP-9/GAPDH of TT cells between 40,80 μmol·L-1 celecoxib groups and control group(P0.05).Conclusion The secretion of VEGF mRNA and MMP-9 mRNA is decreased obviously when the concentration of celecoxib is above 40 μmol·L-1,which may inhibit the growth of tumor.

Key concepts: Celecoxib, Medullary cavity, Internal medicine, Endocrinology, Matrix metalloproteinase, Glyceraldehyde 3-phosphate dehydrogenase, Messenger RNA, Vascular endothelial growth factor

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Inhibitory effects of celecoxib on expressions of VEGF and MMP-9 in human medullary thyroid TT cells and their mechanisms — Research Paper | ScholarLens