Cancer-derived immunoglobulin G promotes LPS-induced proinflammatory cytokine production via binding to TLR4 in cervical cancer cells.

ABSTRACT: Numerous studies have shown that various cancer cells express immunoglobulin G (IgG). However, the function of cancer-derived IgG and the underlying mechanism remain unclear. In this study, we demonstrated that IgG expression was significantly altered after exposure to LPS in cervical cancer cells, suggesting that IgG was potentially involved in regulation of TLR4 signaling. Reduction of IgG attenuated LPS-induced proinflammatory cytokine production. The phosphorylation levels of NF-κB and MAPK were consistently suppressed by knockdown of IgG, which in turn impaired NF-κB nuclear translocation and the activity of NF-κB responsive element. Furthermore, we found that IgG was recruited to TLR4 in the cytoplasm after LPS stimulation, and IgG silencing inhibited LPS-initiated proinflammatory cy

SUBMITTER: Wang J 

PROVIDER: S-EPMC4259433 | biostudies-literature | 2014 Oct

REPOSITORIES: biostudies-literature