Cancer has the ability of over-proliferation. The antiproliferative effects of berry anthocyanin-rich extracts and pure anthocyanins from variable berries have been studied on multiple cancer cell types. Among the berries studied are raspberry, strawberry, black chokeberry, black currant, bilberry, cranberry, blueberry.
Although difficult to compare due to the differences in the experimental approaches, it can be observed that different species and cultivars of berries show different cell antiproliferative activity. The ethanol anthocyanin-rich extract from bilberry was found to be more effective than those from lowbush blueberry, highbush blueberry, cranberry, raspberry, strawberry, black currant, red currant, cowberry, etc.
The bilberry anthocyanin-rich extract inhibited the growth of HL60 cells and HCT116 cells by 84 and 97% respectively at 4 mg dry wt/mL. Different cultivars of blueberries were also tested for their inhibitory effects on HT-29 and CaCo-2 cells. As a result, the cultivar Briteblue showed the highest potential inhibition than Tifblue and Powderblue.
Selective carcinoma cell antiproliferation of anthocyanins has been shown in a few studies. Several studies have shown that the inhibition of cell proliferation by anthocyanins or anthocyanin-rich extracts was more pronounced on carcinoma cells than on immortalized normal cells. It was found that anthocyaninrich extracts inhibited the growth of HT29 cells with little or no effects on normal colonic cell growth when added to the media in the same concentrations. Flavonoid fractions of a red grape wine showed their selective cytotoxicity on MCF-7 cells with relatively low effect towards normal human mammary epithelial cells (HMEC) and non-tumorigenic MCF-10A cells.
It was proposed that the mechanism was related to the interference of flavonoids with calcium second messenger function since the efficiency of cell antiproliferation by flavonoid fractions was associated with their inhibition of calcium and calmodulin-promoted phosphodiesterase activity. Stoner and coworkers found that the ethanol extract of black rasberries selectively inhibited the growth and stimulated apoptosis of a tumor rat esophageal epithelial cells but not the low tumorigenic precursor line. They also found that the uptake of anthocyanins was 100-fold higher in the highly tumorigenic cells than in the low tumorigenic precursor line and remained at steady state levels for 12 h.
The mechanisms behind those chemopreventive effects of anthocyanins need to be considered at the molecular level. Anthocyanin inhibition of cancer cell growth involve blockage of various stages of the cell cycle, which are related to variable cell cycle regulator proteins.
The human HT-29 colon cancer cells treated with anthocyanin-rich extract from chokeberries (Aronia meloncarpa E.) showed a blockage at G1/G0 and G2/M phases of the cell cycle through an increased expression of the p21WAF1 and p27KIP1 genes and decreased expression of cyclin A and B genes.
Besides targeting cell cycle arrest, inhibition of cancer cell growth could also be evaluated by blocking other signal transduction pathways such as epidermal growth factor receptor (EGFR) and the mitogen activation protein kinases (MAPK). The transcription factor activator protein 1 (AP-1) plays an important role in carcinogenesis by activating transcription of genes involved in cell proliferation.
Lingonberry anthocyanin extracts effectively targeted signaling transduction pathways by blocking phosphorylation of the MAPK signaling members ERK1, ERK2 p38, and MEK1/2 induced by either 12-O-tetradecanoylphorbol-13-acetate or ultraviolet-B and as a result suppressed the activation of AP-1 and nuclear factor- KB (NF-KB) in JB6 mouse epidermal cells. Anthocyanidins contributed to the inhibition of tumorigenesis by blocking activation of the MAPK pathway.
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