Innate immunity and hepatocarcinoma: Can toll-like receptors open the door to oncogenesis?

Figure 2 Toll-like receptor 2’s signalling pathways contributing to hepatocarcinoma. In the absence of TLR2, cells are incapable of responding to an increasing ROS when submitted to DEN. This is the result of an absence of MAPK/NF-κB pathway and an up-regulation of the UPR-JNK pathway. Consequently, cells containing higher ROS and DNA damages have more chances to survive and, HCC develops. In a second stage, where HCC is already established, HMGB1 and HSPA1A released by tumour’s dying cells, through TLR2 stimulation, lead to an NF-κB up-regulation which, in this contest, seems to contribute to tumour’s growth. HCC: Hepatocarcinoma; TLR2: Toll-like receptor 2; ROS: Reactive oxigen species; DEN: Diethylnitrosamine; MAPK: Mitogen-activated protein kinase; NF-κB: Nuclear transcription factor kappa B; UPR: Unfold protein response; JNK: Junamino-terminal kinase; HMGB1: High mobility group box 1; HSPA1A: Heat shock protein A1A.