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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Antineoplastic Agents, Phytogenic, Apoptosis, Carcinoma, Hepatocellular, Cell Survival, DNA Fragmentation, Diterpenes, Humans, Inhibitor of Apoptosis Proteins, Liver Neoplasms, Microtubule-Associated Proteins, Neoplasm Proteins, Proto-Oncogene Proteins c-bcl-2, Survivin, Tumor Cells, Cultured, bcl-2-Associated X Protein.
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Does ponicidin inhibit cell growth on hepatocellular carcinoma cells by induction of apoptosis? Context: Ponicidin is recently reported to have anti-tumour effects on a large variety of cancers. The present study was undertaken to investigate the anti-proliferation effects of ponicidin on hepatocellular carcinoma cells and its mechanism. Two hepatocellular carcinoma cell lines, QGY-7701 and HepG-2 cells, were used. Cell viability was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Cell apoptosis was assessed by flow cytometry and deoxyribonucleic acid fragmentation analysis. Cell morphology was observed by Hoechst 33258 staining. Reverse transcriptase-polymerase chain reaction and Western blot analysis were used to detect Survivin as well as Bax and Bcl-2 expressions. Ponicidin could inhibit the growth of QGY-7701 and HepG-2 cells significantly by induction of apoptosis. Marked morphological changes of apoptosis were observed clearly. Both Survivin and Bcl-2 expressions were down-regulated remarkably while Bax expression up-regulated when apoptosis occurred.
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Ponicidin has significant anti-proliferation effects by inducing apoptosis on hepatocellular carcinoma cells in vitro, down regulation of Survivin and Bcl-2 as well as upregualation of Bax expressions may be the important apoptotic inducing mechanisms. Final Decision: yes