Research Papers:
RNF4-mediated SUMOylation is essential for NDRG2 suppression of lung adenocarcinoma
Metrics: PDF 1630 views | HTML 1864 views | ?
Abstract
Jicheng Tantai1, Xufeng Pan1, Dingzhong Hu1
1Department of Thoracic Surgery, Shanghai Chest Hospital, Shanghai Jiao Tong University, Shanghai, China
Correspondence to:
Dingzhong Hu, e-mail: [email protected]
Keywords: NDRG2, RNF4, SUMOylation, tumorigenesis, STUbL
Received: October 27, 2015 Accepted: March 06, 2016 Published: April 09, 2016
ABSTRACT
N-Myc downstream-regulated gene 2 (NDRG2) protein is a tumor suppressor that inhibits cancer growth, metastasis and invasion. The ubiquitin ligase RNF4 integrates signaling by SUMO and ubiquitin through its selective recognition and ubiquitination of SUMO-modified proteins. We evaluated NDRG2 SUMOylation in lung adenocarcinoma cells and its underlying molecular mechanism. The results showed that NDRG2 is covalently modified by SUMO1 at K333, which suppressed anchorage independent adenocarcinoma cell proliferation and tumor growth. In human lung adenocarcinomas cells, RNF4 targeted NDRG2 to proteasomal degradation by stimulating its SUMOylation. Endogenous RNF4 expression was increased in human lung adenocarcinomas cells, and there was a concomitant upregulation of SUMO. These findings indicate that SUMOylation of NDRG2 is necessary for its tumor suppressor function in lung adenocarcinoma and that RNF4 increases the efficiency of this process.
![Creative Commons License](/images/80x15.png)
PII: 8663