Suppression of β-catenin Signaling Pathway in Human Prostate Cancer PC3 Cells by Delphinidin.
10.15430/JCP.2016.21.2.110
- Author:
Wooje LEE
1
;
Jung Mi YUN
Author Information
1. National Research Center for Dementia, Chosun University, Gwangju, Korea.
- Publication Type:Brief Communication
- Keywords:
Beta-catenin;
Prostate neoplasms;
Delphinidin;
Anthocyanidins
- MeSH:
Adenomatous Polyposis Coli;
Anthocyanins;
Axin Protein;
beta Catenin;
Chemoprevention;
Cyclin D1;
Cytoplasm;
Glycogen Synthase Kinases;
Humans*;
Phosphorylation;
Prostate*;
Prostatic Neoplasms*;
Serine;
Threonine
- From:Journal of Cancer Prevention
2016;21(2):110-114
- CountryRepublic of Korea
- Language:English
-
Abstract:
Delphinidin possesses strong anti-oxidant, anti-inflammatory, and anti-cancer properties. Suppression of the Wnt/β-catenin signaling pathway is a potential strategy for chemoprevention and therapy. As aberrant activation of the β-catenin signaling pathway contributes to prostate cancer progression, we evaluated the effect of delphinidin on this pathway in human PC3 prostate cancer cells. An MTT assay showed that treatment with delphinidin (15-180 μM, 72 hours) resulted in a dose-dependent growth inhibition of cells. Treatment with delphinidin increased the phosphorylation of serine or threonine residues on β-catenin and decreased the levels of cytoplasmic β-catenin. Moreover, treatment with delphinidin inhibited the nuclear translocation of β-catenin and the expression of β-catenin target genes such as cyclin D1, c-myc, Axin-2, and T cell factor-1. Delphinidin also induced the phosphorylation of glycogen synthase kinase 3β and the expression of adenomatous polyposis coli and Axin proteins. Our results indicate that inhibition of cell growth by delphinidin is mediated, at least in part, through modulation of the β-catenin signaling pathway. We suggest that delphinidin is a potent inhibitor of Wnt/β-catenin signaling in prostate cancer cells.
