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Effect And Mechanism Of Bifidobacterial Lipoteichoic Acid On Inhibiting Metastasis Of Colon Carcinoma Cell Lines

Posted on:2008-08-27Degree:MasterType:Thesis
Country:ChinaCandidate:J L LiuFull Text:PDF
GTID:2144360218459173Subject:Clinical Laboratory Science
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ObjectiveBifidobacterium is an important normal physiological bacterium in human and animal colon. Lipoteichoic acid(LTA)of Bifidobacterium is able to induce tumor cells apoptosis and differentiation in vivo and in vitro, but the effects of LTA on the metastasis of colon carcinoma are still unclear. In order to explore the effects of LTA on metastasis of colon carcinoma, the study investigated the ability of adhere, invasion and metastasis and the changes of vascular endothelial growth factor (VEGF),CD44v6 and matrix metalloproteinase-2 (MMP-2 ) in colon carcinoma LoVo cells and HT-29 cells treated with LTA.Methods1. The effects of LTA on adhesion of human colon carcinoma cell lines LoVo and HT-29 in vitro were explored by MTT colorimetric. The effects of LTA on invasion and metastasis of these two carcinoma cells were explored by transwell chamber.2. Changes of the mRNA expression of VEGF,CD44v6 and MMP-2 in two colon carcinoma cells treated with LTA were detected by RT-PCR; Changes of the protein expression of VEGF,CD44v6 and MMP-2 in two colon carcinoma cells treated with LTA were detected by Western blot or immunocytochemistry.Results1. The adhesion, invasion and metastasis of colon carcinoma cells were inhibited after treated with proper dose of LTA.2. The mRNA and protein of VEGF,CD44v6 and MMP-2 were decreased in colon carcinoma cells after treated with LTA. Conclusions1. LTA of Bifidobacterium can inhibit the adhesion, invasion and metastasis of colon carcinoma cells LoVo and HT-29.2. LTA can down regulate the mRNA and protein expression of VEGF,CD44v6 and MMP-2 in colon carcinoma cells LoVo and HT-29.
Keywords/Search Tags:Lipoteichoic acid, colon carcinoma, metastasis, vascular endothelial growth factor, CD44, matrix metalloproteinase-2
PDF Full Text Request
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