Smad4 is essential for down-regulation of E-cadherin induced by TGF-β in pancreatic cancer cell line PANC-1

被引：34
作者：
Takano, Shinichi
Kanai, Fumihiko
Jazag, Amarsanaa
Ijichi, Hideaki
Yao, Jian
Ogawa, Hideoki
Enomoto, Nobuyuki
Omata, Masao
Nakao, Atsuhito [1 ]
机构：
[1] Univ Yamanashi, Fac Med, Dept Immunol, Yamanashi 4093898, Japan
[2] Univ Yamanashi, Fac Med, Dept Med, Yamanashi 4093898, Japan
[3] Univ Tokyo, Grad Sch Med, Dept Gastroenterol, Tokyo, Japan
[4] Juntendo Univ, Sch Med, Dept Mol Signaling, Interdisciplinary Grad Sch Med & Engn, Tokyo 1138421, Japan
[5] Juntendo Univ, Sch Med, Atopy Res Ctr, Tokyo 1138421, Japan
来源：
JOURNAL OF BIOCHEMISTRY | 2007年 / 141卷 / 03期
关键词：
pancreatic cancer; E-cadherin; Smad4; TGF-beta;
D O I：
10.1093/jb/mvm039
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
Smad4 is a tumour suppressor gene frequently deleted in pancreatic cancer. To investigate the roles of Smad4 deficiency in invasive and matastatic capabilities of pancreatic cancer, we examined the effects of Smad4 deficiency on regulation of the invasion suppressor E-cadherin in pancreatic cancer cell line PANC-1. TGF-beta decreased expression of E-cadherin and beta-catenin proteins at the plasma membrane, increased Snail and Slug mRNA expression, and induced fibroblastoid morphology in PANC-1 cells. These effects of TGF-beta were abrogated in Smad4-knocked-down PANC-1 cells. We also found that TGF-beta-induced down-regulation of E-cadherin expression was partially inhibited in Snail- and Slug-knocked-down PANC-1 cells. Thus, Smad4 mediates down-regulation of E-cadherin induced by TGF-beta in PANC-1 cells, at least in part, through Snail and Slug induction. These results suggest that Smad4 deficiency observed in invasive and metastatic pancreatic cancer might not be linked to the loss of E-cadherin.
引用
收藏
页码：345 / 351
页数：7
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