Ran GTPase: A Key Player in Tumor Progression and Metastasis
Ran (Ras-related nuclear protein) GTPase is a member of the Ras superfamily. Like all the GTPases, Ran cycles between an active (GTP-bound) and inactive (GDP-bound) state. However, Ran lacks the CAAX motif at its C-terminus, a feature of other small GTPases that ensures a plasma membrane localizatio...
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Published in | Frontiers in cell and developmental biology Vol. 8; p. 345 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
Frontiers Media S.A
26.05.2020
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Subjects | |
Online Access | Get full text |
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Summary: | Ran (Ras-related nuclear protein) GTPase is a member of the Ras superfamily. Like all the GTPases, Ran cycles between an active (GTP-bound) and inactive (GDP-bound) state. However, Ran lacks the CAAX motif at its C-terminus, a feature of other small GTPases that ensures a plasma membrane localization, and largely traffics between the nucleus and the cytoplasm. Ran regulates nucleo-cytoplasmic transport of molecules through the nuclear pore complex and controls cell cycle progression through the regulation of microtubule polymerization and mitotic spindle formation. The disruption of Ran expression has been linked to cancer at different levels – from cancer initiation to metastasis. In the present review, we discuss the contribution of Ran in the acquisition of three hallmarks of cancer, namely, proliferative signaling, resistance to apoptosis, and invasion/metastasis, and highlight its prognostic value in cancer patients. In addition, we discuss the use of this GTPase as a therapeutic target in cancer. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-3 content type line 23 ObjectType-Review-1 Reviewed by: Kamalakannan Rajasekaran, Genentech, Inc., United States; Lu-Shiun Her, National Cheng Kung University, Taiwan Edited by: Uday Kishore, Brunel University London, United Kingdom This article was submitted to Signaling, a section of the journal Frontiers in Cell and Developmental Biology |
ISSN: | 2296-634X 2296-634X |
DOI: | 10.3389/fcell.2020.00345 |