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Apigenin potentiates the growth inhibitory effects by IKK-β-mediated NF-κB activation in pancreatic cancer cells.

Toxicology letters (2013-10-24)
Ding-Guo Wu, Peng Yu, Jian-Wei Li, Peng Jiang, Jing Sun, Huai-Zhi Wang, Lei-Da Zhang, Ming-Bo Wen, Ping Bie
ABSTRACT

Apigenin is a potential chemopreventive agent for cancer prevention. Because of the central role of transcription factor nuclear factor-κB (NF-κB) in pancreatic cancer, we investigated the roles of NF-κB in apigenin-induced growth inhibition in pancreatic cancer cells. It showed that apigenin reduced cell growth and induced apoptosis in the cells. Apigenin treatment down-regulated not only basal but also TNF-α-induced NF-κB DNA binding activity, NF-κB transcription activity, inhibitor of κB (IκB)-α phosphorylation together with translocation of p65 and p50, and it accompanied with the blockade of IκB kinase (IKK)-β activity. Moreover, IKK blockage potentiated the anticancer efficacy of apigenin and IKK-β overexpression attenuated the apigenin-induced cell growth inhibition. Additionally, apigenin (30 mg/kg) administration suppressed pancreatic cancer growth and IKK-β activation in nude mice xenograft. These results indicated that apigenin had a potential to inhibit IKK-β-mediated NF-κB activation, and was a valuable agent for the pancreatic cancer treatment.

MATERIALS
Product Number
Brand
Product Description

Sigma-Aldrich
Apigenin, ≥95.0% (HPLC)
Supelco
Apigenin, analytical standard
Apigenin, primary reference standard