2010•Journal of Sun Yat-sen UniversityRequires access

Mechanism of Growth of Human Prostate Cancer Cells Inhibited by DATS

Jianwei Hao, Shaopeng Qiu, Mao Xiaopeng, Yu Chen, Shengjie Guo, Bin Huang

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Abstract

【Objective】 This study was designed to determine growth inhibition of diallyl trisulfide (DATS) in human prostate cancer cells by inducing apoptosis and further to investigate the mechanism underlying such effect. 【Methods】 Growth inhibition by DATS was estimated by the tetrazolium (MTT) assay. Apoptosis induction in DATS-treated cells was assessed by fluorescence microscopy analysis of cells with condensed and segmented nuclei following staining with DAPI and flow cytometric analysis of cells with sub-G1 DNA content following staining with propidium iodide. Protein levels of apoptosis regulating proteins were determined using western blot. The activity of caspase-3 was measured using a colorimetric assay. 【Result】 DATS showed tumor growth inhibition in a time- and dose-dependent manner, IC50 of DATS was 14 μmol / L at 72 h. DATS evoked apoptosis as confirmed by cell morphology and by the analysis of flow cytometry. The expression of Bcl-2 and Bcl-xL, the apoptosis-suppressing proteins, was more down-regulated. The activity of caspase-3 was enhanced by DATS. 【Conclusion】 DATS inhibits growth of prostate cancer cells by inducing apoptosis in association with down-regulation of Bcl-2 and Bcl-xL and activation of caspase-3.

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What this paper is about

【Objective】 This study was designed to determine growth inhibition of diallyl trisulfide (DATS) in human prostate cancer cells by inducing apoptosis and further to investigate the mechanism underlying such effect. 【Methods】 Growth inhibition by DATS was estimated by the tetrazolium (MTT) assay. Apoptosis induction in DATS-treated cells was assessed by fluorescence microscopy analysis of cells with condensed and segmented nuclei following staining with DAPI and flow cytometric analysis of cells with sub-G1 DNA content following staining with propidium iodide. Protein levels of apoptosis regulating proteins were determined using western blot. The activity of caspase-3 was measured using a colorimetric assay. 【Result】 DATS showed tumor growth inhibition in a time- and dose-dependent manner, IC50 of DATS was 14 μmol / L at 72 h. DATS evoked apoptosis as confirmed by cell morphology and by the analysis of flow cytometry. The expression of Bcl-2 and Bcl-xL, the apoptosis-suppressing proteins, was more down-regulated. The activity of caspase-3 was enhanced by DATS. 【Conclusion】 DATS inhibits growth of prostate cancer cells by inducing apoptosis in association with down-regulation of Bcl-2 and Bcl-xL and activation of caspase-3.

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Available abstract

【Objective】 This study was designed to determine growth inhibition of diallyl trisulfide (DATS) in human prostate cancer cells by inducing apoptosis and further to investigate the mechanism underlying such effect. 【Methods】 Growth inhibition by DATS was estimated by the tetrazolium (MTT) assay. Apoptosis induction in DATS-treated cells was assessed by fluorescence microscopy analysis of cells with condensed and segmented nuclei following staining with DAPI and flow cytometric analysis of cells with sub-G1 DNA content following staining with propidium iodide. Protein levels of apoptosis regulating proteins were determined using western blot. The activity of caspase-3 was measured using a colorimetric assay. 【Result】 DATS showed tumor growth inhibition in a time- and dose-dependent manner, IC50 of DATS was 14 μmol / L at 72 h. DATS evoked apoptosis as confirmed by cell morphology and by the analysis of flow cytometry. The expression of Bcl-2 and Bcl-xL, the apoptosis-suppressing proteins, was more down-regulated. The activity of caspase-3 was enhanced by DATS. 【Conclusion】 DATS inhibits growth of prostate cancer cells by inducing apoptosis in association with down-regulation of Bcl-2 and Bcl-xL and activation of caspase-3.

Key concepts: Diallyl trisulfide, Propidium iodide, Apoptosis, DAPI, Chemistry, Flow cytometry, Molecular biology, Growth inhibition

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