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Natural compounds from soft corals have been increasingly used for their antitumor therapeutic properties. This study examined 11- epi -sinulariolide acetate (11- epi -SA), an active compound isolated from the cultured soft coral Sinularia flexibilis , to determine its potential antitumor effect on four hepatocellular carcinoma cell lines. Cell viability was investigated using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, and the results demonstrated that 11- epi -SA treatment showed more cytotoxic effect toward HA22T cells. Protein profiling of the 11- epi -SA-treated HA22T cells revealed substantial protein alterations associated with stress response and protein synthesis and folding, suggesting that the mitochondria and endoplasmic reticulum (ER) play roles in 11- epi -SA-initiated apoptosis. Moreover, 11- epi -SA activated caspase-dependent apoptotic cell death, suggesting that mitochondria-related apoptosis genes were involved in programmed cell death. The unfolded protein response signaling pathway-related proteins were also activated on 11- epi -SA treatment, and these changes were accompanied by the upregulated expression of growth arrest and DNA damage-inducible protein ( GADD153 ) and CCAAT/enhancer binding protein ( C/EBP ) homologous protein ( CHOP ), the genes encoding transcription factors associated with growth arrest and apoptosis under prolonged ER stress. Two inhibitors, namely salubrinal (Sal) and SP600125, partially abrogated 11- epi -SA-related cell death, implying that the protein kinase R (PKR)-like endoplasmic reticulum kinase (PERK)-activating transcription factor (ATF) 6-CHOP or the inositol-requiring enzyme 1 alpha (IRE1α)-c-Jun N-terminal kinase (JNK)-cJun signal pathway was activated after 11- epi -SA treatment. In general, these results suggest that 11- epi -SA exerts cytotoxic effects on HA22T cells through mitochondrial dysfunction and ER stress cell death pathways.

international journal of molecular sciences

Cytotoxicity of 11-epi-Sinulariolide Acetate Isolated from Cultured Soft Corals on HA22T Cells through the Endoplasmic Reticulum Stress Pathway and Mitochondrial Dysfunction