PT - JOURNAL ARTICLE AU - ARNATCHAI MAIUTHED AU - TATCHAKORN PINKHIEN AU - SUPAKARN CHAMNI AU - KHANIT SUWANBORIRUX AU - NAOKI SAITO AU - NAREERAT PETPIROON AU - PITHI CHANVORACHOTE TI - Apoptosis-inducing Effect of Hydroquinone 5-<em>O</em>-Cinnamoyl Ester Analog of Renieramycin M on Non-small Cell Lung Cancer Cells DP - 2017 Nov 01 TA - Anticancer Research PG - 6259--6267 VI - 37 IP - 11 4099 - http://ar.iiarjournals.org/content/37/11/6259.short 4100 - http://ar.iiarjournals.org/content/37/11/6259.full SO - Anticancer Res2017 Nov 01; 37 AB - Background: A newly-synthesized derivative of renieramycin M (RM), an anticancer lead compound isolated from the blue sponge Xestospongia sp., hydroquinone 5-O-cinnamoyl ester (CIN-RM), was investigated here for its activity against non-small cell lung cancer cells. Materials and Methods: Cytotoxicity effects of CIN-RM and RM on H292 lung cancer cells were determined by the MTT assay. We also investigated the mechanism of CIN-RM-mediated apoptosis and mechanism of action of this compound by western blotting. Results: CIN-RM showed more potent cytotoxicity than its parental compound (RM) against H292 lung cancer cells. At concentrations of 15-60 μM, CIN-RM significantly induced apoptosis by increasing expression of apoptosis-inducing factor (AIF) and activation of caspase-3 and -9. For up-stream mechanism, CIN-RM mediated apoptosis through a p53-dependent mechanism, that consequently down-regulated anti-apoptotic B-cell lymphoma 2 (BCL2), while increasing the level of pro-apoptotic BCL2-associated X (BAX). In addition, phosphorylation of pro-survival protein AKT was found to be dramatically reduced. Conclusion: This study revealed the potential of CIN-RM for apoptosis induction and in the development of a novel anticancer agent.