The metastatic suppressor NDRG1 inhibits EMT, migration and invasion through interaction and promotion of caveolin-1 ubiquitylation in human colorectal cancer cells.
The metastatic suppressor NDRG1 inhibits EMT, migration and invasion through interaction and promotion of caveolin-1 ubiquitylation in human colorectal cancer cells.
复制标题
转移抑制因子 NDRG1 通过相互作用和促进人结直肠癌细胞中的 Caveolin-1 泛素化来抑制 EMT、迁移和侵袭
作者：
Mi L;Zhu F;Yang X;Lu J;Zheng Y;Zhao Q;Wen X;Lu A;Wang M;Zheng M;Ji J;Sun J
N-myc下游调节基因1（NDRG 1）是肿瘤进展相关信号通路中的关键调节分子，尤其是在肿瘤转移过程中。然而，相关的机制尚未完全发现。在此，我们证明了细胞迁移和侵袭的新分子，小窝蛋白-1，在人结直肠癌（CRC）细胞中与NDRG 1有直接的相互作用。此外，我们发现NDRG 1通过促进其泛素化和随后的降解，通过蛋白酶体在CRC细胞中减少小窝蛋白-1的蛋白表达。此外，caveolin-1介导NDRG 1在上皮-间质转化、体外迁移和侵袭以及体内转移中的抑制功能。这些结果有助于实现NDRG 1在人类结直肠癌抗转移治疗中的潜在机制。
N-myc downstream-regulated gene 1 (NDRG1) has been reported to act as a key regulatory molecule in tumor progression-related signaling pathways, especially in tumor metastasis. However, the related mechanism has not been fully discovered yet. Herein we demonstrated that the novel molecule of cell migration and invasion, caveolin-1, has direct interaction with NDRG1 in human colorectal cancer (CRC) cells. Moreover, we discovered that NDRG1 reduces caveolin-1 protein expression through promoting its ubiquitylation and subsequent degradation via the proteasome in CRC cells. In addition, caveolin-1 mediates the suppressive function of NDRG1 in epithelial–mesenchymal transition, migration and invasion in vitro and metastasis in vivo. These results help to fulfill the potential mechanisms of NDRG1 in anti-metastatic treatment for human colorectal cancer.
登录
查看更多内容
DOI：
10.1083/jcb.201003086
发表时间：
2010-11-01
期刊：
The Journal of cell biology
影响因子：
--
作者：
Hayer A;Stoeber M;Ritz D;Engel S;Meyer HH;Helenius A
通讯作者：
Helenius A
影响因子：
8
作者：
Lee, SW;Reimer, CL;Schnitzer, JE
通讯作者：
Schnitzer, JE
影响因子：
6
作者：
Kai, WC;Diatchenko, L;Sers, C
通讯作者：
Sers, C
影响因子：
11.2
作者：
Joshi, Bharat;Strugnell, Scott S.;Nabi, Ivan R.
通讯作者：
Nabi, Ivan R.
影响因子：
4
作者：
Jin, Runsen;Liu, Wensheng;Richardson, Des R.
通讯作者：
Richardson, Des R.