Pu X, et al. - Given the implication of Toll-like receptor 4 (TLR4) in the inflammation in liver cancer and a common prevalence of high-expressed stomatin-like protein 2 (SLP-2) in many cancer types, researchers focused on the functions of SLP-2 in TLR4-mediated inflammatory responses and tumor progression of liver cancer. They found that the cell proliferation of SK-Hep1 and generation of tumor necrosis factor-α (TNF-α) and IL-6 were promoted by lipopolysaccharide (LPS). Remarkable reversal of proapoptotic ability of SLP-2 silencing as well as the promotion of the expression of Cdc42 and generation of TNF-α and IL-6 were shown to be induced by overexpressed CD14, which also caused a notable reversal of the inhibitory influences on the malignant abilities of SK-Hep1 cells by SLP-2 silencing. Overall, findings revealed the ability of SLP-2 silencing in significantly reducing the inflammatory responses and tumor progression of liver cancer by inhibiting LPS/TLR4 signal transduction through the repression of CD14.