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LPS can induce TACE upregulation via signaling from TLR4-derived EGFR activationin tumor cells. The regulation and activity of TACE have been investigated withthe observation that gene expression is upregulated in response to LPS followedby EGFR activation, however, the process remains poorly understood. In this study,we examined the effects of LPS on H22 hepatocarcinoma cells that displayed constitutivelyactive TLR4 expression. Upon TLR4 shRNA transfection into H22 cells, HSP70 expressionsignificantly increased. However, LPS induced early phosphorylation of EGFR inH22 cells, which reached maximum levels within 30 min. Inhibition of TLR4 in H22cells resulted in a significant rise in both EGFR phosphorylation and TACE upregulation24 h after exposure to LPS. Exogenous HSP70 also induced rapid phosphorylationof EGFR, upregulated the expression of COX-2 via a signaling pathway that involvedTACE-dependent TGF-α release. Furthermore, inhibition of EGFR activation and reductionof COX-2 expression by COX-2 inhibitor prevented HSP70-induced cell invasion invitro. These findings demonstrate that the biological importance of HSP70/COX-2is crucial to the second, but not the first, phase of EGFR phosphorylation intumor cells. The growth of tumor cells by inserting shRNA plasmid TLR4 combinationwith COX-2 inhibitor could be effectively reduced in LPS stimulation. We concludedthat LPS triggered a bypass feedback loop of EGFR activation and involved HSP70/COX-2in H22 cells by inhibition of TLR4 and that EGFR phosphorylation is implicatedin tumor growth by LPS stimulation.

Lipopolysaccharide initiates a bypass feedback loop of epidermal growth factor receptor signaling by HPS70-induced COX-2 in H22 hepatocarcinoma cells