A Thirty-year quest for a role of R-Ras in cancer: from an oncogene to a multitasking GTPase
Abstract Since the identification of R-Ras, which is the first Ras-related GTPase isolated based on sequence similarity to the classical RAS oncogene, more than 160 members of the Ras superfamily of GTPases have been identified and classified into the Ras, Rho, Rap, Rab, Ran, Arf, Rheb, RGK, Rad, Ri...
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description | Abstract Since the identification of R-Ras, which is the first Ras-related GTPase isolated based on sequence similarity to the classical RAS oncogene, more than 160 members of the Ras superfamily of GTPases have been identified and classified into the Ras, Rho, Rap, Rab, Ran, Arf, Rheb, RGK, Rad, Rit, and Miro subfamilies. R-Ras belongs to the Ras subfamily of small G-proteins, which are frequently implicated in cell growth and differentiation. Although the roles of R-Ras in cellular transformation and integrin-mediated cell adhesion have been extensively studied, the physiological function of this enigmatic G-protein was only revealed when a mouse strain deficient in R-Ras was generated. In parallel, a plethora of research findings also linked R-Ras with processes including tumor angiogenesis, axon guidance, and immune cell trafficking. Several upstream factors that modulate R-Ras GTP-binding were identified including Notch, semaphorin, and chemokine C-C motif ligand 21. A review of our evolving understanding of the role of R-Ras in oncogenesis is timely, as this year marks the 30th anniversary of the publication describing the cloning of R-Ras. |
doi_str_mv | 10.1016/j.canlet.2017.06.003 |
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R-Ras belongs to the Ras subfamily of small G-proteins, which are frequently implicated in cell growth and differentiation. Although the roles of R-Ras in cellular transformation and integrin-mediated cell adhesion have been extensively studied, the physiological function of this enigmatic G-protein was only revealed when a mouse strain deficient in R-Ras was generated. In parallel, a plethora of research findings also linked R-Ras with processes including tumor angiogenesis, axon guidance, and immune cell trafficking. Several upstream factors that modulate R-Ras GTP-binding were identified including Notch, semaphorin, and chemokine C-C motif ligand 21. A review of our evolving understanding of the role of R-Ras in oncogenesis is timely, as this year marks the 30th anniversary of the publication describing the cloning of R-Ras.</description><identifier>ISSN: 0304-3835</identifier><identifier>EISSN: 1872-7980</identifier><identifier>DOI: 10.1016/j.canlet.2017.06.003</identifier><identifier>PMID: 28610953</identifier><language>eng</language><publisher>Ireland: Elsevier B.V</publisher><subject>Angiogenesis ; Animals ; Axon guidance ; Biomarkers, Tumor - genetics ; Biomarkers, Tumor - history ; Biomarkers, Tumor - metabolism ; Biomedical Research - history ; Biomedical Research - methods ; Breast cancer ; Cancer ; Cell adhesion ; Cell adhesion & migration ; Cell Adhesion Molecules - metabolism ; Cell Communication ; Cell Transformation, Neoplastic - genetics ; Cell Transformation, Neoplastic - metabolism ; Cell Transformation, Neoplastic - pathology ; Cloning ; Deoxyribonucleic acid ; DNA ; Enzyme Activation ; Gene expression ; Genetic Predisposition to Disease ; GTPase ; Guanosine triphosphatases ; Guanosine triphosphate ; Hematology, Oncology and Palliative Medicine ; History, 20th Century ; History, 21st Century ; Humans ; Integrins ; Kinases ; Multitasking ; Mutation ; Neoplasms - enzymology ; Neoplasms - genetics ; Neoplasms - history ; Neoplasms - pathology ; Nerve Tissue Proteins - metabolism ; Notch protein ; Oncogene ; Oncogenes ; Phenotype ; Prostate ; Proteins ; R-Ras ; Ras ; Ras protein ; ras Proteins - genetics ; ras Proteins - history ; ras Proteins - metabolism ; Semaphorins - metabolism ; Signal Transduction ; Tumorigenesis ; Zebrafish</subject><ispartof>Cancer letters, 2017-09, Vol.403, p.59-65</ispartof><rights>Elsevier B.V.</rights><rights>2017 Elsevier B.V.</rights><rights>Copyright © 2017 Elsevier B.V. All rights reserved.</rights><rights>Copyright Elsevier Limited Sep 10, 2017</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c511t-a605fa0a07744d2cd64d4407d0e27440953ae176e8e71bba4cc8a8501b3dc99b3</citedby><cites>FETCH-LOGICAL-c511t-a605fa0a07744d2cd64d4407d0e27440953ae176e8e71bba4cc8a8501b3dc99b3</cites><orcidid>0000-0002-4323-4566</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.canlet.2017.06.003$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>315,781,785,3551,27929,27930,46000</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28610953$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, Wai Nam</creatorcontrib><creatorcontrib>Yan, Mingfei</creatorcontrib><creatorcontrib>Chan, Andrew M</creatorcontrib><title>A Thirty-year quest for a role of R-Ras in cancer: from an oncogene to a multitasking GTPase</title><title>Cancer letters</title><addtitle>Cancer Lett</addtitle><description>Abstract Since the identification of R-Ras, which is the first Ras-related GTPase isolated based on sequence similarity to the classical RAS oncogene, more than 160 members of the Ras superfamily of GTPases have been identified and classified into the Ras, Rho, Rap, Rab, Ran, Arf, Rheb, RGK, Rad, Rit, and Miro subfamilies. R-Ras belongs to the Ras subfamily of small G-proteins, which are frequently implicated in cell growth and differentiation. Although the roles of R-Ras in cellular transformation and integrin-mediated cell adhesion have been extensively studied, the physiological function of this enigmatic G-protein was only revealed when a mouse strain deficient in R-Ras was generated. In parallel, a plethora of research findings also linked R-Ras with processes including tumor angiogenesis, axon guidance, and immune cell trafficking. Several upstream factors that modulate R-Ras GTP-binding were identified including Notch, semaphorin, and chemokine C-C motif ligand 21. A review of our evolving understanding of the role of R-Ras in oncogenesis is timely, as this year marks the 30th anniversary of the publication describing the cloning of R-Ras.</description><subject>Angiogenesis</subject><subject>Animals</subject><subject>Axon guidance</subject><subject>Biomarkers, Tumor - genetics</subject><subject>Biomarkers, Tumor - history</subject><subject>Biomarkers, Tumor - metabolism</subject><subject>Biomedical Research - history</subject><subject>Biomedical Research - methods</subject><subject>Breast cancer</subject><subject>Cancer</subject><subject>Cell adhesion</subject><subject>Cell adhesion & migration</subject><subject>Cell Adhesion Molecules - metabolism</subject><subject>Cell Communication</subject><subject>Cell Transformation, Neoplastic - genetics</subject><subject>Cell Transformation, Neoplastic - metabolism</subject><subject>Cell Transformation, Neoplastic - pathology</subject><subject>Cloning</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>Enzyme Activation</subject><subject>Gene expression</subject><subject>Genetic Predisposition to Disease</subject><subject>GTPase</subject><subject>Guanosine triphosphatases</subject><subject>Guanosine triphosphate</subject><subject>Hematology, Oncology and Palliative Medicine</subject><subject>History, 20th Century</subject><subject>History, 21st Century</subject><subject>Humans</subject><subject>Integrins</subject><subject>Kinases</subject><subject>Multitasking</subject><subject>Mutation</subject><subject>Neoplasms - enzymology</subject><subject>Neoplasms - genetics</subject><subject>Neoplasms - history</subject><subject>Neoplasms - pathology</subject><subject>Nerve Tissue Proteins - metabolism</subject><subject>Notch protein</subject><subject>Oncogene</subject><subject>Oncogenes</subject><subject>Phenotype</subject><subject>Prostate</subject><subject>Proteins</subject><subject>R-Ras</subject><subject>Ras</subject><subject>Ras protein</subject><subject>ras Proteins - genetics</subject><subject>ras Proteins - history</subject><subject>ras Proteins - metabolism</subject><subject>Semaphorins - metabolism</subject><subject>Signal Transduction</subject><subject>Tumorigenesis</subject><subject>Zebrafish</subject><issn>0304-3835</issn><issn>1872-7980</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkl9L3TAYh8PYmGe6byAjsJvdtHvTpE27i4GIcwNB0eOdENL0rebYJi5phfPtl-44BW92FQjP--_hR8ghg5wBq75ucqPdgFNeAJM5VDkAf0NWrJZFJpsa3pIVcBAZr3m5Rz7EuAGAUsjyPdkr6opBU_IVuTmi6zsbpm22RR3o7xnjRHsfqKbBD0h9Ty-zSx2pdTTNMxi-0T74kWpHvTP-Fh3SySd8nIfJTjreW3dLT9cXOuIBedfrIeLHp3efXP84WR__zM7OT38dH51lpmRsynQFZa9Bg5RCdIXpKtEJAbIDLNLPsqhGJiusUbK21cKYWtclsJZ3pmlavk--7Po-BP_3AjXaaHAYtEM_R8UaaKQoWSUT-vkVuvFzcGm7RBWJkQUTiRI7ygQfY8BePQQ76rBVDNRiX23Uzr5a7CuoVLKfyj49NZ_bEbvnon-6E_B9B2Cy8WgxqGgsJqudDWgm1Xn7vwmvG5jBOmv0cI9bjC-3qFgoUFdLApYAMMmBp1TwP89Bqfw</recordid><startdate>20170910</startdate><enddate>20170910</enddate><creator>Liu, Wai Nam</creator><creator>Yan, Mingfei</creator><creator>Chan, Andrew M</creator><general>Elsevier B.V</general><general>Elsevier Limited</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TO</scope><scope>7U9</scope><scope>H94</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-4323-4566</orcidid></search><sort><creationdate>20170910</creationdate><title>A Thirty-year quest for a role of R-Ras in cancer: from an oncogene to a multitasking GTPase</title><author>Liu, Wai Nam ; Yan, Mingfei ; Chan, Andrew M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c511t-a605fa0a07744d2cd64d4407d0e27440953ae176e8e71bba4cc8a8501b3dc99b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Angiogenesis</topic><topic>Animals</topic><topic>Axon guidance</topic><topic>Biomarkers, Tumor - genetics</topic><topic>Biomarkers, Tumor - history</topic><topic>Biomarkers, Tumor - metabolism</topic><topic>Biomedical Research - history</topic><topic>Biomedical Research - methods</topic><topic>Breast cancer</topic><topic>Cancer</topic><topic>Cell adhesion</topic><topic>Cell adhesion & migration</topic><topic>Cell Adhesion Molecules - metabolism</topic><topic>Cell Communication</topic><topic>Cell Transformation, Neoplastic - genetics</topic><topic>Cell Transformation, Neoplastic - metabolism</topic><topic>Cell Transformation, Neoplastic - pathology</topic><topic>Cloning</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>Enzyme Activation</topic><topic>Gene expression</topic><topic>Genetic Predisposition to Disease</topic><topic>GTPase</topic><topic>Guanosine triphosphatases</topic><topic>Guanosine triphosphate</topic><topic>Hematology, Oncology and Palliative Medicine</topic><topic>History, 20th Century</topic><topic>History, 21st Century</topic><topic>Humans</topic><topic>Integrins</topic><topic>Kinases</topic><topic>Multitasking</topic><topic>Mutation</topic><topic>Neoplasms - enzymology</topic><topic>Neoplasms - genetics</topic><topic>Neoplasms - history</topic><topic>Neoplasms - pathology</topic><topic>Nerve Tissue Proteins - metabolism</topic><topic>Notch protein</topic><topic>Oncogene</topic><topic>Oncogenes</topic><topic>Phenotype</topic><topic>Prostate</topic><topic>Proteins</topic><topic>R-Ras</topic><topic>Ras</topic><topic>Ras protein</topic><topic>ras Proteins - genetics</topic><topic>ras Proteins - history</topic><topic>ras Proteins - metabolism</topic><topic>Semaphorins - metabolism</topic><topic>Signal Transduction</topic><topic>Tumorigenesis</topic><topic>Zebrafish</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, Wai Nam</creatorcontrib><creatorcontrib>Yan, Mingfei</creatorcontrib><creatorcontrib>Chan, Andrew M</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>Cancer letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, Wai Nam</au><au>Yan, Mingfei</au><au>Chan, Andrew M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A Thirty-year quest for a role of R-Ras in cancer: from an oncogene to a multitasking GTPase</atitle><jtitle>Cancer letters</jtitle><addtitle>Cancer Lett</addtitle><date>2017-09-10</date><risdate>2017</risdate><volume>403</volume><spage>59</spage><epage>65</epage><pages>59-65</pages><issn>0304-3835</issn><eissn>1872-7980</eissn><abstract>Abstract Since the identification of R-Ras, which is the first Ras-related GTPase isolated based on sequence similarity to the classical RAS oncogene, more than 160 members of the Ras superfamily of GTPases have been identified and classified into the Ras, Rho, Rap, Rab, Ran, Arf, Rheb, RGK, Rad, Rit, and Miro subfamilies. R-Ras belongs to the Ras subfamily of small G-proteins, which are frequently implicated in cell growth and differentiation. Although the roles of R-Ras in cellular transformation and integrin-mediated cell adhesion have been extensively studied, the physiological function of this enigmatic G-protein was only revealed when a mouse strain deficient in R-Ras was generated. In parallel, a plethora of research findings also linked R-Ras with processes including tumor angiogenesis, axon guidance, and immune cell trafficking. Several upstream factors that modulate R-Ras GTP-binding were identified including Notch, semaphorin, and chemokine C-C motif ligand 21. A review of our evolving understanding of the role of R-Ras in oncogenesis is timely, as this year marks the 30th anniversary of the publication describing the cloning of R-Ras.</abstract><cop>Ireland</cop><pub>Elsevier B.V</pub><pmid>28610953</pmid><doi>10.1016/j.canlet.2017.06.003</doi><tpages>7</tpages><orcidid>https://orcid.org/0000-0002-4323-4566</orcidid></addata></record> |
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subjects | Angiogenesis Animals Axon guidance Biomarkers, Tumor - genetics Biomarkers, Tumor - history Biomarkers, Tumor - metabolism Biomedical Research - history Biomedical Research - methods Breast cancer Cancer Cell adhesion Cell adhesion & migration Cell Adhesion Molecules - metabolism Cell Communication Cell Transformation, Neoplastic - genetics Cell Transformation, Neoplastic - metabolism Cell Transformation, Neoplastic - pathology Cloning Deoxyribonucleic acid DNA Enzyme Activation Gene expression Genetic Predisposition to Disease GTPase Guanosine triphosphatases Guanosine triphosphate Hematology, Oncology and Palliative Medicine History, 20th Century History, 21st Century Humans Integrins Kinases Multitasking Mutation Neoplasms - enzymology Neoplasms - genetics Neoplasms - history Neoplasms - pathology Nerve Tissue Proteins - metabolism Notch protein Oncogene Oncogenes Phenotype Prostate Proteins R-Ras Ras Ras protein ras Proteins - genetics ras Proteins - history ras Proteins - metabolism Semaphorins - metabolism Signal Transduction Tumorigenesis Zebrafish |
title | A Thirty-year quest for a role of R-Ras in cancer: from an oncogene to a multitasking GTPase |
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