These results suggest that TLR/MyD88/NF-kappaB signaling pathway plays a significant role in connecting inflammation and cancer invasion and progression.
Both nonneoplastic colon epithelium and colon carcinoma cells in situ are continuously exposed to lipopolysaccharide (LPS). Few reports have addressed possible direct e ects of LPS in promotion of colon carcinoma and underlying mechanisms. We found evidence that LPS directly stimulated growth of the human colon carcinoma cell line CE-1 through an increase in the production of prostaglandin E 2 (PGE 2 ) as a result of cyclo-oxygenase-2 (COX-2) expression. LPS induced signi®cant increases in PGE 2 production in CE-1 cells, which were found to express a high-a nity LPS receptor, CD14. Positive correlations were found between PGE 2 production and activation of nuclear factor (NF)-kB as well as expression of both COX-2 mRNA and protein in LPSstimulated CE-1 cells. When CE-1 cells were exposed to exogenous PGE 2 , DNA synthesis increased. These results indicate that LPS may stimulate DNA synthesis in certain colon carcinoma cells as a result of PGE 2 production involving increased COX-2 expression that might result in turn from activation of NF-kB by LPS. Further investigation of the pathways mediating LPSinduced stimulation of colon carcinoma cells may provide insights into LPS e ects in in vivo tumor biology.
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