MyD88 mediates colorectal cancer cell proliferation, migration and invasion via NF-κB/AP-1 signaling pathway

The role of myeloid differentiation factor 88 (MyD88) in malignant tumors is largely unknown. Therefore, in this study, we aimed to examine the function and underlying mechanism of MyD88 in colorectal carcinoma in vitro using SW480 and HCT116 cell lines and in vivo using a nude mouse model. SW480 and HCT116 cells were infected with a lentiviral-based effective MyD88 siRNA virus. CCK-8 and colony formation assay were used to assess cell proliferation. Transwell and scratch assays were used to test the migration of colorectal cancer cells, and the Transwell assay was further used to analyze the invasiveness of colorectal cancer cells. Western blotting was performed to analyze the underlying mechanism of MyD88 regulation. In vitro experiments demonstrated that silencing MyD88 in SW480 and HCT116 cells markedly suppressed growth and invasion. Furthermore, MyD88 knockdown affected the MyD88-NF-kappa B/AP-1 signaling pathways in SW480 and HCT116 cells. In vivo, MyD88 knockdown inhibited tumor growth in a HCT116 cell subcutaneous nude model. We found that knockdown of the MyD88 gene can affect proliferation, invasion, and migration of colorectal cancer cells. We further verified that MyD88 knockdown can reduce the activity of NF-kappa B and AP-1 pathways. These results show that MyD88 gene plays an important role in promoting colorectal cancer, and thus can be exploited as a potential diagnostic and prognostic biomarker for colorectal cancer.