MyD88 Regulates LPS-induced NF-κB/MAPK Cytokines and Promotes Inflammation and Malignancy in Colorectal Cancer Cells.

Background/Aim: Inflammation may play a role in cancer initiation and progression. The molecular mechanisms by which inflammation causes colorectal cancer, remains unclear. The present study investigated a signaling pathway that affects inflammation in colorectal cancer. Materials and Methods: SW480 cells, HCT116 cells, and cells with knockdown of myeloid differentiation 88 (MyD88), and forced expression of MyD88 were treated with lipopolysaccharide (LPS; 1 ƒÊg/ml). Inflammation-related mRNA expression was analyzed by the quantitative reverse transcription polymerase chain reaction and inflammatory cytokines were detected by western blotting. The enzymelinked immunosorbent assay (ELISA) was used to quantify inflammation-related cytokines in colorectal cancer cells. Cancer cell properties were evaluated using the woundhealing assay, transwell migration assay, transwell invasion assay, colony-formation assay, and CCK-8 assay. Results: LPS up-regulated mRNA and protein levels of inflammatory factors in colorectal cancer cells. Knockdown of MyD88 inhibited LPS-induced mRNA expression and inflammatory protein expression in colorectal cancer cells. Similarly, silencing of MyD88 expression suppressed LPS-induced changes in the biological behavior of colorectal cancer cells. Silencing of MyD88 expression down-regulated expression of proteins of the LPS/nuclear factor kappa-light-chainenhancer of activated B-cells (NF-.B)/mitogen-activated protein kinase (MAPK) signaling pathway. Restoration of the expression of MyD88 reversed the effects in LPS-treated HCT116 cells. Conclusion: MyD88-regulated LPS/NF.B/MAPK signaling pathway affects the inflammatory and biological behavior of LPS-induced colorectal cancer cells. [ABSTRACT FROM AUTHOR]