共查询到20条相似文献,搜索用时 15 毫秒
1.
Prunier C Ferrand N Frottier B Pessah M Atfi A 《Molecular and cellular biology》2001,21(10):3302-3313
2.
3.
4.
5.
6.
RUNX3 suppresses gastric epithelial cell growth by inducing p21(WAF1/Cip1) expression in cooperation with transforming growth factor {beta}-activated SMAD 总被引:3,自引:0,他引:3 下载免费PDF全文
Chi XZ Yang JO Lee KY Ito K Sakakura C Li QL Kim HR Cha EJ Lee YH Kaneda A Ushijima T Kim WJ Ito Y Bae SC 《Molecular and cellular biology》2005,25(18):8097-8107
7.
8.
9.
10.
11.
Min B Kim MK Zhang JW Kim J Chung KC Oh BC Stein GS Lee YH van Wijnen AJ Bae SC 《Journal of cellular physiology》2012,227(2):839-849
Recent genetic screens of fly mutants and molecular analysis have revealed that the Hippo (Hpo) pathway controls both cell proliferation and cell death. Deregulation of its human counterpart (the MST pathway) has been implicated in human cancers. However, how this pathway is linked with the known tumor suppressor network remains to be established. RUNX3 functions as a tumor suppressor of gastric cancer, lung cancer, bladder cancer, and colon cancer. Here, we show that RUNX3 is a principal and evolutionarily conserved component of the MST pathway. SAV1/WW45 facilitates the close association between MST2 and RUNX3. MST2, in turn, stimulates the SAV1-RUNX3 interaction. In addition, we show that siRNA-mediated RUNX3 knockdown abolishes MST/Hpo-mediated cell death. By establishing that RUNX3 is an endpoint effector of the MST pathway and that RUNX3 is capable of inducing cell death in cooperation with MST and SAV1, we define an evolutionarily conserved novel regulatory mechanism loop for tumor suppression in human cancers. 相似文献
12.
13.
14.
Activation of transforming growth factor-beta signaling by SUMO-1 modification of tumor suppressor Smad4/DPC4 总被引:15,自引:0,他引:15
Lin X Liang M Liang YY Brunicardi FC Melchior F Feng XH 《The Journal of biological chemistry》2003,278(21):18714-18719
15.
16.
Xie S Sukkar MB Issa R Oltmanns U Nicholson AG Chung KF 《American journal of physiology. Lung cellular and molecular physiology》2005,288(1):L68-L76
Transforming growth factor (TGF)-beta may play an important role in airway remodeling, and the fibrogenic effect of TGF-beta may be mediated through connective tissue growth factor (CTGF) release. We investigated the role of MAPKs and phosphatidylinositol 3-kinase (PI3K) and the effects of inflammatory cytokines on TGF-beta-induced CTGF expression in human airway smooth muscle cells (ASMC). We examined whether Smad signal was involved in the regulatory mechanisms. TGF-beta 1 induced a time- and concentration-dependent expression of CTGF gene and protein as analyzed by real-time RT-PCR and Western blot. Inhibition of ERK and c-jun NH(2)-terminal kinase (JNK), but not of p38 MAPK and PI3K, blocked the effect of TGF-beta 1 on CTGF mRNA and protein expression and on Smad2/3 phosphorylation. T helper lymphocyte 2-derived cytokines, IL-4 and IL-13, attenuated TGF-beta 1-stimulated mRNA and protein expression of CTGF and inhibited TGF-beta 1-stimulated ERK1/2 and Smad2/3 activation in ASMC. The proinflammatory cytokines tumor necrosis factor-alpha and IL-1 beta reduced TGF-beta 1-stimulated mRNA expression of CTGF but did not inhibit TGF-beta-induced Smad2/3 phosphorylation. TGF-beta 1-stimulated CTGF expression is mediated by mechanisms involving ERK and JNK pathways and is downregulated by IL-4 and IL-13 through modulation of Smad and ERK signals. 相似文献
17.
Peron P Rahmani M Zagar Y Durand-Schneider AM Lardeux B Bernuau D 《The Journal of biological chemistry》2001,276(13):10524-10531
18.
Ungefroren H Lenschow W Chen WB Faendrich F Kalthoff H 《The Journal of biological chemistry》2003,278(13):11041-11049
19.
20.