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Chalcones Enhance TRAIL-Induced Apoptosis in Prostate Cancer Cells
Chair and Department of Microbiology and Immunology, Medical University of Silesia in Katowice, Jordana 19, 41 808 Zabrze, Poland
Chair and Department of Pediatric Hematology and Oncology, Medical University of Silesia in Katowice, 3-go Maja 13, 41 800 Zabrze, Poland
Chair and Department of Urology, Medical University of Silesia in Katowice, 3-go Maja 13, 41 800 Zabrze, Poland
* Author to whom correspondence should be addressed.
Received: 28 October 2009; in revised form: 23 November 2009 / Accepted: 23 December 2009 / Published: 24 December 2009
Abstract: Chalcones exhibit chemopreventive and antitumor effects. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a naturally occurring anticancer agent that induces apoptosis in cancer cells and is not toxic to normal cells. We examined the cytotoxic and apoptotic effect of five chalcones in combination with TRAIL on prostate cancer cells. The cytotoxicity was evaluated by the MTT and LDH assays. The apoptosis was determined using flow cytometry with annexin V-FITC. Our study showed that all five tested chalcones: chalcone, licochalcone-A, isobavachalcone, xanthohumol, butein markedly augmented TRAIL-mediated apoptosis and cytotoxicity in prostate cancer cells and confirmed the significant role of chalcones in chemoprevention of prostate cancer.
Keywords: chalcones; TRAIL (tumor necrosis factor-related apoptosis-inducing ligand); apoptosis; chemoprevention; prostate cancer
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Szliszka, E.; Czuba, Z.P.; Mazur, B.; Sedek, L.; Paradysz, A.; Krol, W. Chalcones Enhance TRAIL-Induced Apoptosis in Prostate Cancer Cells. Int. J. Mol. Sci. 2010, 11, 1-13.
Szliszka E, Czuba ZP, Mazur B, Sedek L, Paradysz A, Krol W. Chalcones Enhance TRAIL-Induced Apoptosis in Prostate Cancer Cells. International Journal of Molecular Sciences. 2010; 11(1):1-13.
Szliszka, Ewelina; Czuba, Zenon P.; Mazur, Bogdan; Sedek, Lukasz; Paradysz, Andrzej; Krol, Wojciech. 2010. "Chalcones Enhance TRAIL-Induced Apoptosis in Prostate Cancer Cells." Int. J. Mol. Sci. 11, no. 1: 1-13.