Nudix-type motif 2 contributes to cancer proliferation through the regulation of Rag GTPase-mediated mammalian target of rapamycin complex 1 localization
SCIE
SCOPUS
- Title
- Nudix-type motif 2 contributes to cancer proliferation through the regulation of Rag GTPase-mediated mammalian target of rapamycin complex 1 localization
- Authors
- Kwon, O.; Kwak, D.; Ha, S.H.; Jeon, H.; Park, M.; Chang, Y.; Suh, Pann-Ghill; Ryu, S.H.
- Date Issued
- 2017-04
- Publisher
- ELSEVIER SCIENCE INC
- Abstract
- Lysosomal localization of mammalian target of rapamycin complex 1 (mTORC1) is a critical step for activation of the molecule. Rag GTPases are essential for this translocation. Here, we demonstrate that Nudix-type motif 2 (NUDT2) is a novel positive regulator of mTORC1 activation. Activation of mTORC1 is impaired in NUDT2-silenced cells. Mechanistically, NUDT2 binds to Rag GTPase and controls mTORC1 translocation to the lysosomal membrane. Furthermore, NUDT2-dependent mTORC1 regulation is critical for proliferation of breast cancer cells, as NUDT2-silenced cells arrest in G0/G1 phases. Taken together, these results show that NUDT2 is a novel complex formation enhancing factor regulating mTORC1-Rag GTPase signaling that is crucial for cell growth control. ? 2017 Elsevier Inc.
- Keywords
- heterodimer; mammalian target of rapamycin complex 1; membrane protein; nucleic acid binding protein; nudix type motif 2; Rag guanosine triphosphatase; unclassified drug; Article; breast cancer; breast carcinogenesis; cancer growth; cell cycle checkpoint; cell growth; cell proliferation; colony forming cell; complex formation; controlled study; down regulation; G0 phase cell cycle checkpoint; G1 phase cell cycle checkpoint; gene expression regulation; gene silencing; gene translocation; lysosome membrane; protein function; protein localization; protein protein interaction; signal transduction
- URI
- https://oasis.postech.ac.kr/handle/2014.oak/50419
- DOI
- 10.1016/j.cellsig.2017.01.015
- ISSN
- 0898-6568
- Article Type
- Article
- Citation
- CELLULAR SIGNALLING, vol. 32, page. 24 - 35, 2017-04
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