Role of p21 as a determinant of 1,6-Bis[4-(4-amino-3-hydroxyphenoxy)phenyl] diamantane response in human HCT-116 colon carcinoma cells

CCUR > College of Environmental Planning & Bioresources > College of Agriculture > Department of Horticulture > journal articles > Item 987654321/24285

Please use this identifier to cite or link to this item: https://irlib.pccu.edu.tw/handle/987654321/24285

Title:	Role of p21 as a determinant of 1,6-Bis[4-(4-amino-3-hydroxyphenoxy)phenyl] diamantane response in human HCT-116 colon carcinoma cells
Authors:	Wang, JJ (Wang, Jane-Jen) Hung, HF (Hung, Hui-Fang) Huang, ML (Huang, Min-Li) Lee, HJ (Lee, Hui-Ju) Chern, YT (Chern, Yaw-Terng) Chang, YF (Chang, Yuh-Fang) Chi, CW (Chi, Chin-Wen) Hsu, YC (Hsu, Yi-Chiung)
Contributors:	Dept Hort & Biotechnol
Keywords:	colorectal carcinoma cell cycle p21 anti-proliferation anti-migration diamantane
Date:	2012-03
Issue Date:	2013-02-22 16:16:36 (UTC+8)
Abstract:	1,6-Bis[4-(4-amino-3-hydroxyphenoxy)phenyl] diamantane (DPD) induces growth inhibition in human cancer cells. In our previous study, we discovered that DPD irreversibly inhibits the growth of Colo 205 colon cancer cells at the G(0)/G(1) phase and induces cell differentiation. However, the detailed mechanism is still unknown. In this study, we examined the functional importance of p21 and p53 in DPD-induced anticancer effects. We used three isogenic cell lines, HCT-116, HCT-116 p53(-/-) and HCT-116 p21(-/-), to evaluate the roles of p21 and p53 in the in vitro anticancer effects of DPD. The in vivo anti-proliferative effect of DPD was demonstrated by HCT-116 and HCT-116 p21(-/-) xenograft models. DPD significantly inhibited the growth as well as increased the number of HCT-116 cells in the G(0)/G(1), phase, but not in HCT-116 p53(-/-) and HCT-116 p21 cells examined by flow cytometry. Additionally, Western blot analysis showed that DPD treatment induced p21, but not p53 protein expression in HCT-116 cells. The p21-associated cell cycle regulated proteins, such as cyclin D, CDK4 and pRb were decreased after DPD treatment in HCT-116 cells. The DPD-increased G(0)/G(1), phase and induced cell cycle regulated protein expression were not observed in HCT-116 p21(-/-) and HCT-116 p53(-/-) cells. DPD decreased cell migration in HCT-116 and HCT-116 p53(-/-) but not in HCT-116 p21(-/-) cells. p21 was required for the DPD-induced in vitro anti-colon cancer effect. The in vivo study also showed that DPD significantly inhibited tumor growth through p21 signaling. Our results clearly demonstrate that DPD-induced in vitro and in vivo anticancer effects through the activation of p21 in HCT-116 cells.
Relation:	ONCOLOGY REPORTS 卷: 27 期: 2 頁數: 529-534
Appears in Collections:	[Department of Horticulture] journal articles

Files in This Item:

File	Description	Size	Format
index.html		0Kb	HTML	394	View/Open

View Licence

Loading...