The role of FAK in tumor metabolism and therapy
Focal adhesion kinase (FAK) plays a vital role in tumor cell proliferation, survival and migration. Altered metabolic pathways fuel rapid tumor growth by accelerating glucose, lipid and glutamine processing. Besides the mitogenic effects of FAK, evidence is accumulating supporting the association be...
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| Veröffentlicht in: | Pharmacology & therapeutics (Oxford) 2014-05, Vol.142 (2), p.154-163 |
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| container_title | Pharmacology & therapeutics (Oxford) |
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| creator | JIANLIANG ZHANG HOCHWALD, Steven N |
| description | Focal adhesion kinase (FAK) plays a vital role in tumor cell proliferation, survival and migration. Altered metabolic pathways fuel rapid tumor growth by accelerating glucose, lipid and glutamine processing. Besides the mitogenic effects of FAK, evidence is accumulating supporting the association between hyper-activated FAK and aberrant metabolism in tumorigenesis. FAK can promote glucose consumption, lipogenesis, and glutamine dependency to promote cancer cell proliferation, motility, and survival. Clinical studies demonstrate that FAK-related alterations of tumor metabolism are associated with increased risk of developing solid tumors. Since FAK contributes to the malignant phenotype, small molecule inhibition of FAK-stimulated bioenergetic and biosynthetic processes can provide a novel approach for therapeutic intervention in tumor growth and invasion. |
| doi_str_mv | 10.1016/j.pharmthera.2013.12.003 |
| format | Article |
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Altered metabolic pathways fuel rapid tumor growth by accelerating glucose, lipid and glutamine processing. Besides the mitogenic effects of FAK, evidence is accumulating supporting the association between hyper-activated FAK and aberrant metabolism in tumorigenesis. FAK can promote glucose consumption, lipogenesis, and glutamine dependency to promote cancer cell proliferation, motility, and survival. Clinical studies demonstrate that FAK-related alterations of tumor metabolism are associated with increased risk of developing solid tumors. 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Solid tumors. Tumors in childhood (general aspects) ; Neoplasm Invasiveness ; Neoplasms - drug therapy ; Neoplasms - enzymology ; Neoplasms - pathology ; Pharmacology. Drug treatments ; Protein Kinase Inhibitors - therapeutic use ; Signal Transduction - drug effects ; Tumors</subject><ispartof>Pharmacology & therapeutics (Oxford), 2014-05, Vol.142 (2), p.154-163</ispartof><rights>2015 INIST-CNRS</rights><rights>Copyright © 2013 Elsevier Inc. 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Altered metabolic pathways fuel rapid tumor growth by accelerating glucose, lipid and glutamine processing. Besides the mitogenic effects of FAK, evidence is accumulating supporting the association between hyper-activated FAK and aberrant metabolism in tumorigenesis. FAK can promote glucose consumption, lipogenesis, and glutamine dependency to promote cancer cell proliferation, motility, and survival. Clinical studies demonstrate that FAK-related alterations of tumor metabolism are associated with increased risk of developing solid tumors. Since FAK contributes to the malignant phenotype, small molecule inhibition of FAK-stimulated bioenergetic and biosynthetic processes can provide a novel approach for therapeutic intervention in tumor growth and invasion.</description><subject>Animals</subject><subject>Antineoplastic agents</subject><subject>Antineoplastic Agents - therapeutic use</subject><subject>Biological and medical sciences</subject><subject>Cell Movement - drug effects</subject><subject>Cell Proliferation - drug effects</subject><subject>Cell Survival - drug effects</subject><subject>Drug Design</subject><subject>Energy Metabolism - drug effects</subject><subject>Focal Adhesion Protein-Tyrosine Kinases - antagonists & inhibitors</subject><subject>Focal Adhesion Protein-Tyrosine Kinases - metabolism</subject><subject>General aspects</subject><subject>Humans</subject><subject>Medical sciences</subject><subject>Molecular Targeted Therapy</subject><subject>Multiple tumors. Solid tumors. Tumors in childhood (general aspects)</subject><subject>Neoplasm Invasiveness</subject><subject>Neoplasms - drug therapy</subject><subject>Neoplasms - enzymology</subject><subject>Neoplasms - pathology</subject><subject>Pharmacology. Drug treatments</subject><subject>Protein Kinase Inhibitors - therapeutic use</subject><subject>Signal Transduction - drug effects</subject><subject>Tumors</subject><issn>0163-7258</issn><issn>1879-016X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkT1v2zAQhokiReOk_QsBlwBZJPN4_NJSwAjqNmiALh66EbRE1TIk0SHlAP73oRM3aadMN9xzL3n3EEKBlcBAzbflbuPiMG18dCVngCXwkjH8QGZgdFVk5vcZmeWChebSnJOLlLaMMSEY_0TOuUBEyXBG5quNpzH0noaWLhc_aTfSaT-ESAc_uXXouzRQNzb0-a3d4TP52Lo--S-neklWy2-r2x_F_a_vd7eL-6KWopoK1UALFWjZMmAcuFEKFRij2lYKCQ6VFrryvtIaDatFs26EN6ZBJWAtPV6Sry-xu_168E3txym63u5iN7h4sMF19v_O2G3sn_BoFYqKS5EDbk4BMTzsfZrs0KXa970bfdgnCwY1ci04vo9KyJGVEiyj5gWtY0gp-vb1R8Ds0Yzd2jcz9mjGArfZTB69-nej18G_KjJwfQJcql3fRjfWXXrjDEqZ74hPzUqYXw</recordid><startdate>20140501</startdate><enddate>20140501</enddate><creator>JIANLIANG ZHANG</creator><creator>HOCHWALD, Steven N</creator><general>Elsevier</general><scope>IQODW</scope><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>7X8</scope><scope>7U7</scope><scope>C1K</scope><scope>5PM</scope></search><sort><creationdate>20140501</creationdate><title>The role of FAK in tumor metabolism and therapy</title><author>JIANLIANG ZHANG ; HOCHWALD, Steven N</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c549t-6d1f19175f010212866361886ff5451a367479ee977380c4dbd4e88d3641b5e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Animals</topic><topic>Antineoplastic agents</topic><topic>Antineoplastic Agents - therapeutic use</topic><topic>Biological and medical sciences</topic><topic>Cell Movement - drug effects</topic><topic>Cell Proliferation - drug effects</topic><topic>Cell Survival - drug effects</topic><topic>Drug Design</topic><topic>Energy Metabolism - drug effects</topic><topic>Focal Adhesion Protein-Tyrosine Kinases - antagonists & inhibitors</topic><topic>Focal Adhesion Protein-Tyrosine Kinases - metabolism</topic><topic>General aspects</topic><topic>Humans</topic><topic>Medical sciences</topic><topic>Molecular Targeted Therapy</topic><topic>Multiple tumors. 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| ispartof | Pharmacology & therapeutics (Oxford), 2014-05, Vol.142 (2), p.154-163 |
| issn | 0163-7258 1879-016X |
| language | eng |
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| source | MEDLINE; Access via ScienceDirect (Elsevier) |
| subjects | Animals Antineoplastic agents Antineoplastic Agents - therapeutic use Biological and medical sciences Cell Movement - drug effects Cell Proliferation - drug effects Cell Survival - drug effects Drug Design Energy Metabolism - drug effects Focal Adhesion Protein-Tyrosine Kinases - antagonists & inhibitors Focal Adhesion Protein-Tyrosine Kinases - metabolism General aspects Humans Medical sciences Molecular Targeted Therapy Multiple tumors. Solid tumors. Tumors in childhood (general aspects) Neoplasm Invasiveness Neoplasms - drug therapy Neoplasms - enzymology Neoplasms - pathology Pharmacology. Drug treatments Protein Kinase Inhibitors - therapeutic use Signal Transduction - drug effects Tumors |
| title | The role of FAK in tumor metabolism and therapy |
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