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J Med Food. 2014 Aug;17(8):842-8. doi: 10.1089/jmf.2013.0159. Epub 2014 Apr 8.

Anticancer activity of protocatechualdehyde in human breast cancer cells.

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1
Department of Nutrition and Food Science, College of Agriculture and Natural Resources, University of Maryland , College Park, Maryland, USA .

Abstract

Protocatechualdehyde (PCA) is a natural polyphenol compound isolated from the root of the herb S. miltiorrhiza and barley tea plants. PCA possesses antiproliferative and pro-apoptotic properties in human colorectal cancer cells. However, the cellular mechanism has not been fully understood. β-catenin and cyclin D1 are proto-oncogene that is overexpressed in many types of cancers and leads to cancer development. The present study was performed to elucidate the molecular mechanism by which PCA stimulates cell growth arrest and apoptosis in human breast cancer cells. PCA repressed cell proliferation and induced apoptosis in dose-dependent manner. PCA suppressed the expression of β-catenin and cyclin D1 with no changes in mRNA levels. Inhibition of proteosomal degradation using MG-132 and Ada-(Ahx)3-(Leu)3-vinyl sulfone ameliorates PCA-induced downregulation of β-catenin and cyclin D1. PCA treatment decreased the half-life of β-catenin and cyclin D1. PCA-mediated β-catenin downregulation depends on GSK3β. We further provide the evidence that PCA increased nuclear translocation of nuclear factor kappa-B (NF-κB) and the blockage of NF-κB using Bay11-7082 inhibited PCA-mediated β-catenin downregulation. The current study demonstrates that PCA suppress β-catenin expression through GSK3β- and NF-κB-mediated proteosomal degradation. In addition, PCA decreased cyclin D1 expression independent to β-catenin through proteosomal degradation.

KEYWORDS:

breast cancer; cyclin D1; protocatechualdehyde; β-catenin

PMID:
24712725
DOI:
10.1089/jmf.2013.0159
[Indexed for MEDLINE]

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