p53 Is a Key Regulator for Osthole-Triggered

ASIAIR > College of Medical and Health Science > Department of Biotechnology > Journal Article > Item 310904400/79916

Please use this identifier to cite or link to this item: http://asiair.asia.edu.tw/ir/handle/310904400/79916

Title:	p53 Is a Key Regulator for Osthole-Triggered
Authors:	蔡政芳;Tsai, Cheng-Fang
Contributors:	生物科技學系
Date:	2014-06
Issue Date:	2014-07-03 07:43:35 (UTC+0)
Abstract:	Osthole has been reported to have antitumor activities via the induction of apoptosis and inhibition of cancer cell growth and metastasis. However, the detailed molecular mechanisms underlying the anticancer effects of osthole in human colon cancer remain unclear. In the present study, we have assessed osthole-induced cell death in two different human colon cancer cell lines, HCT116 and SW480. Our results also showed that osthole activated proapoptotic signaling pathways in human colon cancer cells. By using cell culture insert system, osthole reduced cell motility in both human colon cancer cell lines. This study also provides evidence supporting the potential of osthole in p53 activation. Expression of p53, an apoptotic protein, was remarkably upregulated in cells treated with osthole. Importantly, the levels of phosphorylation of p53 on Ser15 (p-p53) and acetylation of p53 on Lys379 (acetyl-p53) were increased under osthole treatment. Our results also demonstrated that p53 was activated followed by generation of reactive oxygen species (ROS) and activation of c-Jun N-terminal kinase (JNK). Our study provides novel insights of p53-mediated responses under osthole treatment. Taken together, we concluded that osthole induces cancer cell death and inhibits migratory activity in a controlled manner and is a promising candidate for antitumor drug development.
Relation:	BioMed Research International
Appears in Collections:	[Department of Biotechnology] Journal Article

Files in This Item:

File	Size	Format
index.html	0Kb	HTML	431	View/Open

Loading...