Ubiquitin-specific protease 11 functions as a tumor suppressor by modulating Mgl-1 protein to regulate cancer cell growthopen access
- Authors
- Lim, Key-Hwan; Suresh, Bharathi; Park, Jung-Hyun; Kim, Young-Soo; Ramakrishna, Suresh; Baek, Kwang-Hyun
- Issue Date
- Mar-2016
- Publisher
- IMPACT JOURNALS LLC
- Keywords
- deubiquitinating enzyme; RanBPM; UAF1; ubiquitin; USP11
- Citation
- ONCOTARGET, v.7, no.12, pp.14441 - 14457
- Indexed
- SCIE
SCOPUS
- Journal Title
- ONCOTARGET
- Volume
- 7
- Number
- 12
- Start Page
- 14441
- End Page
- 14457
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/154910
- DOI
- 10.18632/oncotarget.7581
- Abstract
- The Lethal giant larvae (Lgl) gene encodes a cortical cytoskeleton protein, Lgl, and is involved in maintaining cell polarity and epithelial integrity. Previously, we observed that Mgl-1, a mammalian homologue of the Drosophila tumor suppressor protein Lgl, is subjected to degradation via ubiquitin-proteasome pathway, and scaffolding protein RanBPM prevents the turnover of the Mgl-1 protein. Consequently, overexpression of RanBPM enhances Mgl-1-mediated cell proliferation and migration. Here, we analyzed the ability of ubiquitin-specific protease 11 (USP11) as a novel regulator of Mgl-1 and it requires RanBPM to regulate proteasomal degradation of Mgl-1. USP11 showed deubiquitinating activity and stabilized Mgl-1 protein. However, USP11-mediated Mgl-1 stabilization was inhibited in RanBPMknockdown cells. Furthermore, in the cancer cell migration, the regulation of Mgl-1 by USP11 required RanBPM expression. In addition, an in vivo study revealed that depletion of USP11 leads to tumor formation. Taken together, the results indicated that USP11 functions as a tumor suppressor through the regulation of Mgl-1 protein degradation via RanBPM.
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