Growth inhibitory and apoptosis-inducing effects of xanthohumol, a prenylated chalone present in hops, in human prostate cancer cells.

Abstract

Promotion of apoptosis in cancer cells could potentially lead to the regression and improved prognosis of hormone-refractory prostate cancer. Xanthohumol (XN), a prenylated chalcone-derived from hops, has shown strong antitumorigenic activity towards diverse types of cancer cells. In the present study, the growth-inhibitory and apoptosis-inducing activity of XN was tested in hormone-sensitive and hormone-refractory human prostate cancer cells lines. Cell growth/viability assay (MTS) demonstrated that prostate cancer cells are highly sensitive to XN at a concentration range of 20-40 μM. The primary mode of tumor cell destruction was apoptosis as demonstrated by the binding of annexin V-FITC, cleavage of PARP-1, activation of procaspases -3, -8, and -9, mitochondrial depolarization and release of cytochrome c from mitochondria. Induction of apoptosis by XN was associated with the inhibition of prosurvival Akt, NF-κB and mTOR signaling proteins and NF-κB-regulated anti-apoptotic Bcl-2 and survivin. These studies provide a rationale for clinical evaluation of XN for the treatment of hormone-refractory metastatic prostate cancer.

• Authors: D Deeb, X Gao, H Jiang, A S Arbab, S A Dulchavsky, S C Gautam
• Journal: Anticancer research (Anticancer Res) Vol. 30 Issue 9 Pg. 3333-9 (Sep 2010) ISSN: 1791-7530 [Electronic] Greece
• PMID: 20944105 (Publication Type: Journal Article, Research Support, N.I.H., Extramural)

Chemical References

• Antineoplastic Agents
• Flavonoids
• Plant Extracts
• Propiophenones
• xanthohumol

Topics

• Antineoplastic Agents (pharmacology)
• Apoptosis (drug effects)
• Blotting, Western
• Cell Line, Tumor
• Cell Proliferation (drug effects)
• Flavonoids (pharmacology)
• Humans
• Humulus (chemistry)
• Male
• Membrane Potential, Mitochondrial (drug effects)
• Phytotherapy (methods)
• Plant Extracts (pharmacology)
• Propiophenones (pharmacology)
• Prostatic Neoplasms (metabolism)
• Signal Transduction (drug effects)