Ursolic acid overcomes Bcl-2-mediated resistance to apoptosis in prostate cancer cells involving activation of JNK-induced Bcl-2 phosphorylation and degradation
| Autor: | Chuanliang Xu, Yuxi Zhang, Xian-kui Liu, Yinghao Sun, Lin-hui Wang, Jin-yi Li, Chui-Ze Kong, Bin Xu |
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| Rok vydání: | 2010 |
| Předmět: |
Male
Apoptosis Biology urologic and male genital diseases Biochemistry chemistry.chemical_compound Prostate cancer Ursolic acid Prostate Cell Line Tumor LNCaP medicine Humans Phosphorylation Molecular Biology Kinase JNK Mitogen-Activated Protein Kinases Prostatic Neoplasms Cell Biology medicine.disease Antineoplastic Agents Phytogenic Caspase 9 Triterpenes medicine.anatomical_structure chemistry Proto-Oncogene Proteins c-bcl-2 Cell culture Cancer research |
| Zdroj: | Journal of cellular biochemistry. 109(4) |
| ISSN: | 1097-4644 |
| Popis: | Androgen-independent prostate cancers express high levels of Bcl-2, and this over-expression of Bcl-2 protects prostate cancer cells from undergoing apoptosis. Ursolic acid (UA) has demonstrated an anti-proliferative effect in various tumor types. The aim of this study is to evaluate the difference between UA-induced apoptosis in androgen-dependent prostate cancer cell line LNCaP cells and androgen-independent prostate cancer cell line LNCaP-AI cells and to reveal the molecular mechanisms underlying the apoptosis. We found that UA treatment in vitro can effectively induce apoptosis in LNCaP and LNCaP-AI cells. UA can overcome Bcl-2-mediated resistance to apoptosis in LNCaP-AI cells. Intrinsic apoptotic pathways can be triggered by UA treatment because c-Jun N-terminal kinase (JNK) is activated and subsequently provokes Bcl-2 phosphorylation and degradation, inducing activation of caspase-9. Although further evaluation is clearly needed, the present results suggest the potential utility of UA as a novel therapeutic agent in advanced prostate cancer. |
| Databáze: | OpenAIRE |
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