J Cancer Prev.  2016 Jun;21(2):110-114. 10.15430/JCP.2016.21.2.110.

Suppression of β-catenin Signaling Pathway in Human Prostate Cancer PC3 Cells by Delphinidin

• Lee W
• Yun JM

• KMID: 2353811
• DOI: http://doi.org/10.15430/JCP.2016.21.2.110

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.

Keyword

Beta-catenin; Prostate neoplasms; Delphinidin; Anthocyanidins

MeSH Terms

Adenomatous Polyposis Coli
Anthocyanins
Axin Protein
beta Catenin
Chemoprevention
Cyclin D1
Cytoplasm
Glycogen Synthase Kinases
Humans*
Phosphorylation
Prostate*
Prostatic Neoplasms*
Serine
Threonine
Anthocyanins
Axin Protein
Cyclin D1
Glycogen Synthase Kinases
Serine
Threonine
beta Catenin