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Enterolactone induces apoptosis in human prostate carcinoma LNCaP cells via a mitochondrial-mediated, caspase-dependent pathway.
| Content Provider | Semantic Scholar |
|---|---|
| Author | Chen, Li-Hua Fang, Jing Li, Huaixing Demark-Wahnefried, Wendy Lin, Xu |
| Copyright Year | 2007 |
| Abstract | The mammalian lignan enterolactone is a major metabolite of plant-based lignans that has been shown to inhibit the growth and development of prostate cancer. However, little is known about the mechanistic basis for its anticancer activity. In this study, we report that enterolactone selectively suppresses the growth of LNCaP prostate cancer cells by triggering apoptosis. Mechanistic studies showed that enterolactone-induced apoptosis was characterized by a dose-dependent loss of mitochondrial membrane potential, release of cytochrome c and cleavage of procaspase-3 and poly(ADP-ribose)-polymerase (PARP). Caspase dependence was indicated by the ability of the pan-caspase inhibitor z-VAD-fmk to attenuate enterolactone-mediated apoptosis. Mechanistic studies suggested roles for Akt, GSK-3beta, MDM2, and p53 in enterolactone-dependent apoptosis. Our findings encourage further studies of enterolactone as a promising chemopreventive agent against prostate cancer. |
| Starting Page | 244 |
| Ending Page | 247 |
| Page Count | 4 |
| File Format | PDF HTM / HTML |
| Alternate Webpage(s) | http://mct.aacrjournals.org/content/molcanther/6/9/2581.full.pdf |
| PubMed reference number | 17876055v1 |
| Volume Number | 6 |
| Issue Number | 9 |
| Journal | Molecular cancer therapeutics |
| Language | English |
| Access Restriction | Open |
| Subject Keyword | Adenosine Diphosphate Apoptosis Caspase Inhibitors Lignans MDM2 protein, human Malignant neoplasm of prostate Mammals Membrane Potentials Mitochondrial Inheritance Mitochondrial Membranes Prostate carcinoma Prostatic Neoplasms Proto-Oncogene Proteins c-akt Teniposide VAD I protocol benzyloxycarbonyl-Phe-Ala-fluormethylketone cancer cell glycogen synthase kinase 3 beta |
| Content Type | Text |
| Resource Type | Article |