A central role for vesicle trafficking in epithelial neoplasia: intracellular highways to carcinogenesis
This Opinion article outlines the roles of vesicle trafficking pathways in various phenotypes shown by cancer cells, especially loss of polarity and invasion, and argues that although these proteins are not drivers of transformation, they are integral to maintaining neoplastic phenotypes. Epithelial...
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| Veröffentlicht in: | Nature reviews. Cancer 2013-11, Vol.13 (11), p.813-820 |
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| description | This Opinion article outlines the roles of vesicle trafficking pathways in various phenotypes shown by cancer cells, especially loss of polarity and invasion, and argues that although these proteins are not drivers of transformation, they are integral to maintaining neoplastic phenotypes.
Epithelial cell carcinogenesis involves the loss of cell polarity, alteration of polarized protein presentation, dynamic cell morphology changes, increased proliferation, and increased cell motility and invasion. Membrane vesicle trafficking underlies all of these processes. Specific membrane trafficking regulators, including RAB small GTPases, through the coordinated dynamics of intracellular trafficking along cytoskeletal pathways, determine the cell surface presentation of proteins and the overall function of both differentiated and neoplastic cells. Although mutations in vesicle trafficking proteins may not be direct drivers of transformation, components of the machinery of vesicle movement have crucial roles in the phenotypes of neoplastic cells. Therefore, the regulators of membrane vesicle trafficking decisions are essential mediators of the full range of cell physiologies that drive cancer cell biology, including initial loss of cell polarity, invasion and metastasis. Targeting of these fundamental intracellular processes may permit the manipulation of cancer cell behaviour. |
| doi_str_mv | 10.1038/nrc3601 |
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Epithelial cell carcinogenesis involves the loss of cell polarity, alteration of polarized protein presentation, dynamic cell morphology changes, increased proliferation, and increased cell motility and invasion. Membrane vesicle trafficking underlies all of these processes. Specific membrane trafficking regulators, including RAB small GTPases, through the coordinated dynamics of intracellular trafficking along cytoskeletal pathways, determine the cell surface presentation of proteins and the overall function of both differentiated and neoplastic cells. Although mutations in vesicle trafficking proteins may not be direct drivers of transformation, components of the machinery of vesicle movement have crucial roles in the phenotypes of neoplastic cells. Therefore, the regulators of membrane vesicle trafficking decisions are essential mediators of the full range of cell physiologies that drive cancer cell biology, including initial loss of cell polarity, invasion and metastasis. Targeting of these fundamental intracellular processes may permit the manipulation of cancer cell behaviour.</description><identifier>ISSN: 1474-175X</identifier><identifier>EISSN: 1474-1768</identifier><identifier>DOI: 10.1038/nrc3601</identifier><identifier>PMID: 24108097</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>631/67/70 ; 631/80/313 ; 631/80/85 ; Biomedicine ; Cancer Research ; Carcinogenesis ; Cell Membrane - metabolism ; Cell Movement ; Cell Polarity ; Cell Proliferation ; Cell Transformation, Neoplastic ; Development and progression ; Epithelial Cells - cytology ; Epithelial tumors ; G proteins ; Genetic aspects ; GTP Phosphohydrolases - metabolism ; Humans ; Mutation ; Neoplasm Invasiveness ; Neoplasm Metastasis ; Neoplasms, Glandular and Epithelial - metabolism ; opinion-2 ; Phenotype ; Physiological aspects ; Protein Transport ; Risk factors ; Transport Vesicles - metabolism</subject><ispartof>Nature reviews. Cancer, 2013-11, Vol.13 (11), p.813-820</ispartof><rights>Springer Nature Limited 2013</rights><rights>COPYRIGHT 2013 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Nov 2013</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c627t-e88f1f951a760fe957c7507951c48d2e4798fbe6e66567079e3735c89024f2653</citedby><cites>FETCH-LOGICAL-c627t-e88f1f951a760fe957c7507951c48d2e4798fbe6e66567079e3735c89024f2653</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/nrc3601$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/nrc3601$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>230,314,777,781,882,27905,27906,41469,42538,51300</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24108097$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Goldenring, James R.</creatorcontrib><title>A central role for vesicle trafficking in epithelial neoplasia: intracellular highways to carcinogenesis</title><title>Nature reviews. Cancer</title><addtitle>Nat Rev Cancer</addtitle><addtitle>Nat Rev Cancer</addtitle><description>This Opinion article outlines the roles of vesicle trafficking pathways in various phenotypes shown by cancer cells, especially loss of polarity and invasion, and argues that although these proteins are not drivers of transformation, they are integral to maintaining neoplastic phenotypes.
Epithelial cell carcinogenesis involves the loss of cell polarity, alteration of polarized protein presentation, dynamic cell morphology changes, increased proliferation, and increased cell motility and invasion. Membrane vesicle trafficking underlies all of these processes. Specific membrane trafficking regulators, including RAB small GTPases, through the coordinated dynamics of intracellular trafficking along cytoskeletal pathways, determine the cell surface presentation of proteins and the overall function of both differentiated and neoplastic cells. Although mutations in vesicle trafficking proteins may not be direct drivers of transformation, components of the machinery of vesicle movement have crucial roles in the phenotypes of neoplastic cells. Therefore, the regulators of membrane vesicle trafficking decisions are essential mediators of the full range of cell physiologies that drive cancer cell biology, including initial loss of cell polarity, invasion and metastasis. Targeting of these fundamental intracellular processes may permit the manipulation of cancer cell behaviour.</description><subject>631/67/70</subject><subject>631/80/313</subject><subject>631/80/85</subject><subject>Biomedicine</subject><subject>Cancer Research</subject><subject>Carcinogenesis</subject><subject>Cell Membrane - metabolism</subject><subject>Cell Movement</subject><subject>Cell Polarity</subject><subject>Cell Proliferation</subject><subject>Cell Transformation, Neoplastic</subject><subject>Development and progression</subject><subject>Epithelial Cells - cytology</subject><subject>Epithelial tumors</subject><subject>G proteins</subject><subject>Genetic aspects</subject><subject>GTP Phosphohydrolases - metabolism</subject><subject>Humans</subject><subject>Mutation</subject><subject>Neoplasm Invasiveness</subject><subject>Neoplasm Metastasis</subject><subject>Neoplasms, Glandular and Epithelial - metabolism</subject><subject>opinion-2</subject><subject>Phenotype</subject><subject>Physiological aspects</subject><subject>Protein Transport</subject><subject>Risk factors</subject><subject>Transport Vesicles - 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metabolism</topic><topic>Cell Movement</topic><topic>Cell Polarity</topic><topic>Cell Proliferation</topic><topic>Cell Transformation, Neoplastic</topic><topic>Development and progression</topic><topic>Epithelial Cells - cytology</topic><topic>Epithelial tumors</topic><topic>G proteins</topic><topic>Genetic aspects</topic><topic>GTP Phosphohydrolases - metabolism</topic><topic>Humans</topic><topic>Mutation</topic><topic>Neoplasm Invasiveness</topic><topic>Neoplasm Metastasis</topic><topic>Neoplasms, Glandular and Epithelial - metabolism</topic><topic>opinion-2</topic><topic>Phenotype</topic><topic>Physiological aspects</topic><topic>Protein Transport</topic><topic>Risk factors</topic><topic>Transport Vesicles - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Goldenring, James R.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>Consumer Health Database (Alumni Edition)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Biological Science Collection</collection><collection>Consumer Health Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Genetics Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Nature reviews. Cancer</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Goldenring, James R.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A central role for vesicle trafficking in epithelial neoplasia: intracellular highways to carcinogenesis</atitle><jtitle>Nature reviews. Cancer</jtitle><stitle>Nat Rev Cancer</stitle><addtitle>Nat Rev Cancer</addtitle><date>2013-11-01</date><risdate>2013</risdate><volume>13</volume><issue>11</issue><spage>813</spage><epage>820</epage><pages>813-820</pages><issn>1474-175X</issn><eissn>1474-1768</eissn><abstract>This Opinion article outlines the roles of vesicle trafficking pathways in various phenotypes shown by cancer cells, especially loss of polarity and invasion, and argues that although these proteins are not drivers of transformation, they are integral to maintaining neoplastic phenotypes.
Epithelial cell carcinogenesis involves the loss of cell polarity, alteration of polarized protein presentation, dynamic cell morphology changes, increased proliferation, and increased cell motility and invasion. Membrane vesicle trafficking underlies all of these processes. Specific membrane trafficking regulators, including RAB small GTPases, through the coordinated dynamics of intracellular trafficking along cytoskeletal pathways, determine the cell surface presentation of proteins and the overall function of both differentiated and neoplastic cells. Although mutations in vesicle trafficking proteins may not be direct drivers of transformation, components of the machinery of vesicle movement have crucial roles in the phenotypes of neoplastic cells. Therefore, the regulators of membrane vesicle trafficking decisions are essential mediators of the full range of cell physiologies that drive cancer cell biology, including initial loss of cell polarity, invasion and metastasis. Targeting of these fundamental intracellular processes may permit the manipulation of cancer cell behaviour.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>24108097</pmid><doi>10.1038/nrc3601</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Nature reviews. Cancer, 2013-11, Vol.13 (11), p.813-820 |
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| subjects | 631/67/70 631/80/313 631/80/85 Biomedicine Cancer Research Carcinogenesis Cell Membrane - metabolism Cell Movement Cell Polarity Cell Proliferation Cell Transformation, Neoplastic Development and progression Epithelial Cells - cytology Epithelial tumors G proteins Genetic aspects GTP Phosphohydrolases - metabolism Humans Mutation Neoplasm Invasiveness Neoplasm Metastasis Neoplasms, Glandular and Epithelial - metabolism opinion-2 Phenotype Physiological aspects Protein Transport Risk factors Transport Vesicles - metabolism |
| title | A central role for vesicle trafficking in epithelial neoplasia: intracellular highways to carcinogenesis |
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