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|Title:||Molecular targets of apigenin in colorectal cancer cells: Involvement of p21, NAG-1 and p53|
protein kinase C gamma
protein nag 1
in vitro study
reverse transcription polymerase chain reaction
Cyclin-Dependent Kinase Inhibitor p21
Growth Differentiation Factor 15
Tumor Cells, Cultured
Tumor Suppressor Protein p53
|Abstract:||Persuasive epidemiological and experimental evidence suggests that dietary flavonoids have anti-cancer activity. Since conventional therapeutic and surgical approaches have not been able to fully control the incidence and outcome of most cancer types, including colorectal neoplasia, there is an urgent need to develop alternative approaches for the management of cancer. We sought to develop the best flavonoids for the inhibition of cell growth, and apigenin (flavone) proved to be the most promising compound in colorectal cancer cell growth arrest. Subsequently, we found that pro-apoptotic proteins (NAG-1 and p53) and cell cycle inhibitor (p21) were induced in the presence of apigenin, and kinase pathways, including PKCδ and ataxia telangiectasia mutated (ATM), play an important role in activating these proteins. The data generated by in vitro experiments were confirmed in an animal study using APC MIN+ mice. Apigenin is able to reduce polyp numbers, accompanied by increasing p53 activation through phosphorylation in animal models. Our data suggest apparent beneficial effects of apigenin on colon cancer. © 2010 Elsevier Ltd. All rights reserved.|
|Appears in Collections:||Scopus 1983-2021|
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