Abstract
Treatment of androgen-independent prostate cancer (AIPC) remains unsatisfactory. In our present experiment, natural occurring ginsenosides (NOGs) and intestinal bacterial metabolites (IBMs) were employed to investigate their anti-AIPC cell growth activity using PC-3 cells. Our results showed that the IBMs exerted more portent anti-AIPC activity than NOGs, by decreasing survival rate, inhibiting proliferation, inducing apoptosis, and leading to cell cycle arrest in AIPC PC-3 cells. The increase of LogP and decrease of C-6 steric hindrance, which were caused by deglycosylation by intestinal bacteria, may be the reason for the higher anti-AIPC activity of IBMs.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Androgen Antagonists / pharmacology
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Antineoplastic Agents / chemistry
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Antineoplastic Agents / metabolism
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Antineoplastic Agents / pharmacology*
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Apoptosis / drug effects
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Bacteria / metabolism
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Biotransformation
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Cell Cycle / drug effects
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Cell Line, Tumor
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Cell Proliferation / drug effects*
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Cell Survival / drug effects
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Cyclin A / metabolism
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Cyclin D1 / metabolism
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Dose-Response Relationship, Drug
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Drug Resistance, Neoplasm
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Ginsenosides / chemistry
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Ginsenosides / metabolism
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Ginsenosides / pharmacology*
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Glycosylation
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Humans
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Hydrophobic and Hydrophilic Interactions
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Intestines / microbiology
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Male
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Mitochondria / drug effects
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Mitochondria / pathology
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Molecular Structure
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Prostatic Neoplasms / metabolism
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Prostatic Neoplasms / pathology*
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Structure-Activity Relationship
Substances
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Androgen Antagonists
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Antineoplastic Agents
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CCND1 protein, human
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Cyclin A
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Ginsenosides
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Cyclin D1