| Literature DB >> 24746703 |
Taoyong Chen1, Mingjin Yang1, Zhou Yu2, Songqing Tang2, Chen Wang3, Xuhui Zhu3, Jun Guo3, Nan Li3, Weiping Zhang3, Jin Hou3, Haibo Liu3, Chaofeng Han3, Qiuyan Liu3, Yan Gu3, Cheng Qian3, Tao Wan3, Long Cui4, Minghua Zhu5, Weiqiang Zheng5, Xuetao Cao6.
Abstract
Ras-related small GTPases play important roles in cancer. However, the roles of RBJ, a representative of the sixth subfamily of Ras-related small GTPases, in tumorigenesis and tumor progression remain unknown. Here, we report that RBJ is dysregulated in human gastrointestinal cancers and can promote carcinogenesis and tumor progression via nuclear entrapment of mitogen-activated protein/extracellular signal-regulated kinase (ERK) kinase (MEK)1/MEK2 and activation of ERK1/ERK2. Nucleus-localized RBJ interacts with MEK/ERK and prolongs the duration of MEK/ERK activation. Rbj deficiency abrogates nuclear accumulation of MEK1/MEK2, attenuates ERK1/ERK2 activation, and impairs AOM/DSS-induced colonic carcinogenesis. Moreover, Rbj knockdown inhibits growth of established tumors. Our data suggest that RBJ may be an oncogenic Ras-related small GTPase mediating nuclear accumulation of active MEK1/MEK2 in tumor progression.Entities:
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Year: 2014 PMID： 24746703 DOI： 10.1016/j.ccr.2014.03.009
Source DB: PubMed Journal: Cancer Cell ISSN： 1535-6108 Impact factor: 31.743