doi:info:doi/10.1038/s41421-017-0001-2

TUFT1 interacts with RABGAP1 and regulates mTORC1 signaling 利用統計を見る

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アイテムタイプ	学術雑誌論文 / Journal Article
言語	英語
著者	Kawasaki Natsumi Isogaya Kazunobu Dan Shingo Yamori Takao Takano Hiroshi Yao Ryoji Morishita Yasuyuki Taguchi Luna Morikawa Masato Heldin Carl-Henrik Noda Tetsuo Ehata Shogo Miyazono Kohei Koinuma Daizo
著者所属	Department of Molecular Pathology, Graduate School of Medicine, The University of Tokyo Division of Molecular Pharmacology, Cancer Chemotherapy Center, Japanese Foundation for Cancer Research Division of Cell Biology and Director’s Room, Cancer Institute, Japanese Foundation for Cancer Research Ludwig Institute for Cancer Research, Science for Life Laboratory, Uppsala University Department of Medical Biochemistry and Microbiology, Science for Life Laboratory, Uppsala University
抄録	The mammalian target of rapamycin (mTOR) pathway is commonly activated in human cancers. The activity of mTOR complex 1 (mTORC1) signaling is supported by the intracellular positioning of cellular compartments and vesicle trafficking, regulated by Rab GTPases. Here we showed that tuftelin 1 (TUFT1) was involved in the activation of mTORC1 through modulating the Rab GTPase-regulated process. TUFT1 promoted tumor growth and metastasis. Consistently, the expression of TUFT1 correlated with poor prognosis in lung, breast and gastric cancers. Mechanistically, TUFT1 physically interacted with RABGAP1, thereby modulating intracellular lysosomal positioning and vesicular trafficking, and promoted mTORC1 signaling. In addition, expression of TUFT1 predicted sensitivity to perifosine, an alkylphospholipid that alters the composition of lipid rafts. Perifosine treatment altered the positioning and trafficking of cellular compartments to inhibit mTORC1. Our observations indicate that TUFT1 is a key regulator of the mTORC1 pathway and suggest that it is a promising therapeutic target or a biomarker for tumor progression.
内容記述	UTokyo FOCUS Articles掲載「がんの増殖・転移を促進する新規因子の同定小胞輸送を標的とする新しいがん治療戦略への可能性」 https://www.u-tokyo.ac.jp/focus/ja/articles/z0508_00119.html UTokyo FOCUS Articles "Possible target for future cancer treatment : Deregulation of system to move molecules in the cell may promote tumor growth, metastasis" https://www.u-tokyo.ac.jp/focus/en/articles/z0508_00120.html
雑誌名	Cell Discovery
巻	4
号	1
発行年	2018-01-08
ISSN	2056-5968
DOI	info:doi/10.1038/s41421-017-0001-2
権利	© The Author(s) 2018 This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any mediumor format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changesweremade. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
著者版フラグ	publisher
関係URI	https://www.u-tokyo.ac.jp/focus/ja/articles/z0508_00119.html https://www.u-tokyo.ac.jp/focus/en/articles/z0508_00120.html https://doi.org/10.1038/s41421-017-0001-2

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TUFT1 interacts with RABGAP1 and regulates mTORC1 signaling 利用統計を見る

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