|Title:||Induction of apoptosis by hydroxydibenzoylmethane through coordinative modulation of cyclin D3, Bcl-X L , and Bax, release of cytochrome c, and sequential activation of caspases in human colorectal carcinoma cells||Authors:||Pan M.-H.
|Keywords:||Apoptosis;Caspase-2;Caspase-3;Caspase-9;Caspase-activated deoxyribonuclease;Cytochrome c;DBM;DNA fragmentation factor;HDB;HMDB;Poly-(ADP-ribose) polymerase||Issue Date:||2003||Journal Volume:||51||Journal Issue:||14||Start page/Pages:||3977-3984||Source:||Journal of Agricultural and Food Chemistry||Abstract:||
DBM (dibenzoylmethane) is a minor constituent of licorice that has antimutagenic activity. However, its other biological activities are not well-known. The structurally related £]-diketones hydroxydibenzoylmethane (HDB) and hydroxymethyldibenzoylmethane (HMDB) were able to induce apoptosis in colorectal carcinoma COLO 205 cells. Thus, the effect of structurally related £]-diketones on cell viability, DNA fragmentation, and caspase activity was assessed. The potency of these compounds on these features of apoptosis were in the order of HDB > HMDB > DBM in colorectal carcinoma COLO 205 cells. Here, we found that HDB-induced apoptotic cell death was accompanied by upregulation of cyclin D3, Bax, and p21 and down-regulation of Bcl-X L , while HDB had no effect on the levels of Bcl-2 and Bad protein. These results indicate that HDB allows caspase-activated deoxyribonuclease to enter the nucleus and degrade chromosomal DNA and induces DFF-45 degradation. It is suggested that HDB-induced apoptosis is triggered by the release of cytochrome c into cytosol, procaspase-9 processing, activation of caspase-3 and caspase-2, degradation of PARP, and DNA fragmentation caused by the caspase-activated deoxyribonuclease through the digestion of DFF-45. The induction of apoptosis by HDB may provide a pivotal mechanism for its cancer chemopreventive action.
|Appears in Collections:||食品科技研究所|
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