Abstract | PURPOSE: METHODS:
Prostate cancer (PC-3) cells were treated with either apigenin or bortezomib, and proliferation inhibition was correlated with proteasomal biochemistry, ER-degradation and cell apoptosis. RESULTS: CONCLUSIONS:
Apigenin selectively inhibits proteasomal degradation of tumor suppressor ER-β by specifically inhibiting chymotrypsin-like activity of proteasome, preventing its assembly via PSMA5 and inhibiting USP14 enzyme activity in prostate cancer cells, resulting in cancer cell apoptosis. Unlike bortezomib, apigenin's actions are subtle, precise, mechanistically distinct and capable of abstaining drug resistance.
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Authors | Vishal Singh, Vikas Sharma, Vikas Verma, Deepti Pandey, Santosh K Yadav, Jagdamba P Maikhuri, Gopal Gupta |
Journal | European journal of nutrition
(Eur J Nutr)
Vol. 54
Issue 8
Pg. 1255-67
(Dec 2015)
ISSN: 1436-6215 [Electronic] Germany |
PMID | 25408199
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- ESR1 protein, human
- Estrogen Receptor alpha
- Estrogen Receptor beta
- Proteasome Inhibitors
- USP14 protein, human
- Ubiquitin
- Bortezomib
- Apigenin
- UBE3A protein, human
- Ubiquitin-Protein Ligases
- Ubiquitin Thiolesterase
- CASP3 protein, human
- CASP8 protein, human
- Caspase 3
- Caspase 8
- PSMA5 protein, human
- PSMB1 protein, human
- PSMB2 protein, human
- Proteasome Endopeptidase Complex
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Topics |
- Apigenin
(pharmacology)
- Apoptosis
(drug effects)
- Bortezomib
(pharmacology)
- Caspase 3
(genetics, metabolism)
- Caspase 8
(genetics, metabolism)
- Cell Line, Tumor
(drug effects)
- Cell Proliferation
(drug effects)
- Down-Regulation
- Estrogen Receptor alpha
(genetics, metabolism)
- Estrogen Receptor beta
(genetics, metabolism)
- Humans
- Male
- Prostatic Neoplasms
(pathology)
- Proteasome Endopeptidase Complex
(genetics, metabolism)
- Proteasome Inhibitors
(pharmacology)
- Ubiquitin
(genetics, metabolism)
- Ubiquitin Thiolesterase
(genetics, metabolism)
- Ubiquitin-Protein Ligases
(genetics, metabolism)
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