JOURNAL ARTICLE

Over-expression of Smac promotes TRAIL-induced cell death in human hepatocellular carcinoma

Hiroshi Okano, Katsuya Shiraki, Hidekazu Inoue, Tomoyuki Kawakita, Yukiko Saitou, Naoyuki Enokimura, Norihiko Yamamoto, Kazushi Sugimoto, Katsuhiko Fujikawa, Kazumoto Murata, Takeshi Nakano
International Journal of Molecular Medicine 2003, 12 (1): 25-8
12792804
The second mitochondria-derived activator of caspase, Smac, is an apoptosis-related protein. Smac releases inhibition of the IAP family from caspase-3 to induce apoptosis. Smac is expressed in some malignant tumor cells and is released from mitochondria into the cytosol after death receptor stimulation to promote apoptosis of tumor cells. In this study, we found down-regulated Smac protein expression in hepatocellular carcinoma (HCC) tissues, compared to that in non-tumor hepatic tissues. Simultaneously, caspase-3 expression also decreased in HCC tissues. HCC cell lines did not undergo apoptosis after TRAIL stimulation, although Smac was expressed in these HCC cells. Ectopic Smac alone did not induce cell death, but could sensitize HCC cells to TRAIL stimulation. With over-expression of Smac in HCC cells, TRAIL induced by 10% HCC cell death. The role of Smac in apoptosis signaling pathway in HCC cells warrants further study.

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