n apoptosis in hepatoma carcinoma cells via the PI 3 K / Akt / NFk B signaling pathway

Talin1 is implicated in many cellular processes, which has been studied in various diseases using molecular biological technology. However, the detailed mechanism of talin1 in hepatocellular carcinoma (HCC) cell apoptosis remains unclear. This study was aimed at exploring the molecular mechanism mediating the effect of talin1 on the apoptosis of human HCC cells. We showed that shRNA-mediated talin1 loss led to a significant increase of apoptosis in HepG2 cells via upregulation of caspase-8, caspase-9, and PARP and downregulation of Bid protein levels. Talin1 knockdown decreased the phosphorylation of Akt and specially counteracted the effect of pCDNA-Akt in the PI3K/Akt pathway and down-regulated p50, p65, and p105 protein levels to inhibit the activation of NF-kB to promote apoptosis in HCC cells. Talin1 knockdown could enhance the inhibitory effects of IkBa on NF-kB and suppress the activation of IKKb to upregulate caspase-8, caspase-9, and PARP protein levels, thus leading to the increased apoptotic proportion in HCC cells. Moreover, talin1 could attenuate TNF-a and TRAIL-induced apoptosis, which was readily reversed by RIP. Our results demonstrated that inhibition of talin1 suppressed the HCC cell proliferation and promoted apoptosis by decreasing the activity of the PI3K/Akt/NF-kB signaling pathway. This new mechanism provides further understanding of the molecular signaling pathway in HCC cell apoptosis.