Metabolite Profiling Identifies a Key Role for Glycine in Rapid Cancer Cell Proliferation
Metabolic reprogramming has been proposed to be a hallmark of cancer, yet a systematic characterization of the metabolic pathways active in transformed cells is currently lacking. Using mass spectrometry, we measured the consumption and release (CORE) profiles of 219 metabolites from media across th...
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| Veröffentlicht in: | Science (American Association for the Advancement of Science) 2012-05, Vol.336 (6084), p.1040-1044 |
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| creator | Jain, Mohit Nilsson, Roland Sharma, Sonia Madhusudhan, Nikhil Kitami, Toshimori Souza, Amanda L. Kafri, Ran Kirschner, Marc W. Clish, Clary B. Mootha, Vamsi K. |
| description | Metabolic reprogramming has been proposed to be a hallmark of cancer, yet a systematic characterization of the metabolic pathways active in transformed cells is currently lacking. Using mass spectrometry, we measured the consumption and release (CORE) profiles of 219 metabolites from media across the NCI-60 cancer cell lines, and integrated these data with a preexisting atlas of gene expression. This analysis identified glycine consumption and expression of the mitochondrial glycine biosynthetic pathway as strongly correlated with rates of proliferation across cancer cells. Antagonizing glycine uptake and its mitochondrial biosynthesis preferentially impaired rapidly proliferating cells. Moreover, higher expression of this pathway was associated with greater mortality in breast cancer patients. Increased reliance on glycine may represent a metabolic vulnerability for selectively targeting rapid cancer cell proliferation. |
| doi_str_mv | 10.1126/science.1218595 |
| format | Article |
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Using mass spectrometry, we measured the consumption and release (CORE) profiles of 219 metabolites from media across the NCI-60 cancer cell lines, and integrated these data with a preexisting atlas of gene expression. This analysis identified glycine consumption and expression of the mitochondrial glycine biosynthetic pathway as strongly correlated with rates of proliferation across cancer cells. Antagonizing glycine uptake and its mitochondrial biosynthesis preferentially impaired rapidly proliferating cells. Moreover, higher expression of this pathway was associated with greater mortality in breast cancer patients. Increased reliance on glycine may represent a metabolic vulnerability for selectively targeting rapid cancer cell proliferation.</description><identifier>ISSN: 0036-8075</identifier><identifier>EISSN: 1095-9203</identifier><identifier>DOI: 10.1126/science.1218595</identifier><identifier>PMID: 22628656</identifier><identifier>CODEN: SCIEAS</identifier><language>eng</language><publisher>Washington, DC: American Association for the Advancement of Science</publisher><subject>biochemical pathways ; Biological and medical sciences ; Biosynthesis ; breast neoplasms ; Breast Neoplasms - genetics ; Breast Neoplasms - metabolism ; Breast Neoplasms - pathology ; Cancer ; Carcinogenesis, carcinogens and anticarcinogens ; Cell adhesion & migration ; Cell Cycle ; Cell growth ; Cell Line ; Cell Line, Tumor ; Cell lines ; Cell Proliferation ; Cell Transformation, Neoplastic ; Cellular metabolism ; Chromatography, Liquid ; Culture Media ; Enzymes ; Gene Expression ; Gene Expression Profiling ; General aspects ; Glycine - biosynthesis ; Glycine - metabolism ; Humans ; Mass spectrometry ; Medical sciences ; Metabolic Networks and Pathways - genetics ; Metabolites ; Metabolome ; Mitochondria ; Mitochondria - enzymology ; Mitochondria - metabolism ; mortality ; neoplasm cells ; Neoplasms - genetics ; Neoplasms - metabolism ; Neoplasms - pathology ; patients ; Purines ; Purines - biosynthesis ; Stem cells ; Tandem Mass Spectrometry ; Transformed cell line ; Tumor cell line ; Tumors</subject><ispartof>Science (American Association for the Advancement of Science), 2012-05, Vol.336 (6084), p.1040-1044</ispartof><rights>Copyright © 2012 American Association for the Advancement of Science</rights><rights>2015 INIST-CNRS</rights><rights>Copyright © 2012, American Association for the Advancement of Science</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c610t-bf145b0c0caf596f54e126518630e4c4e613ccffef45c4470b56af9197be0183</citedby><cites>FETCH-LOGICAL-c610t-bf145b0c0caf596f54e126518630e4c4e613ccffef45c4470b56af9197be0183</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/41584914$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/41584914$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>230,314,550,776,780,799,881,2871,2872,27901,27902,57992,58225</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=25949300$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22628656$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttp://kipublications.ki.se/Default.aspx?queryparsed=id:124628100$$DView record from Swedish Publication Index$$Hfree_for_read</backlink></links><search><creatorcontrib>Jain, Mohit</creatorcontrib><creatorcontrib>Nilsson, Roland</creatorcontrib><creatorcontrib>Sharma, Sonia</creatorcontrib><creatorcontrib>Madhusudhan, Nikhil</creatorcontrib><creatorcontrib>Kitami, Toshimori</creatorcontrib><creatorcontrib>Souza, Amanda L.</creatorcontrib><creatorcontrib>Kafri, Ran</creatorcontrib><creatorcontrib>Kirschner, Marc W.</creatorcontrib><creatorcontrib>Clish, Clary B.</creatorcontrib><creatorcontrib>Mootha, Vamsi K.</creatorcontrib><title>Metabolite Profiling Identifies a Key Role for Glycine in Rapid Cancer Cell Proliferation</title><title>Science (American Association for the Advancement of Science)</title><addtitle>Science</addtitle><description>Metabolic reprogramming has been proposed to be a hallmark of cancer, yet a systematic characterization of the metabolic pathways active in transformed cells is currently lacking. Using mass spectrometry, we measured the consumption and release (CORE) profiles of 219 metabolites from media across the NCI-60 cancer cell lines, and integrated these data with a preexisting atlas of gene expression. This analysis identified glycine consumption and expression of the mitochondrial glycine biosynthetic pathway as strongly correlated with rates of proliferation across cancer cells. Antagonizing glycine uptake and its mitochondrial biosynthesis preferentially impaired rapidly proliferating cells. Moreover, higher expression of this pathway was associated with greater mortality in breast cancer patients. Increased reliance on glycine may represent a metabolic vulnerability for selectively targeting rapid cancer cell proliferation.</description><subject>biochemical pathways</subject><subject>Biological and medical sciences</subject><subject>Biosynthesis</subject><subject>breast neoplasms</subject><subject>Breast Neoplasms - genetics</subject><subject>Breast Neoplasms - metabolism</subject><subject>Breast Neoplasms - pathology</subject><subject>Cancer</subject><subject>Carcinogenesis, carcinogens and anticarcinogens</subject><subject>Cell adhesion & migration</subject><subject>Cell Cycle</subject><subject>Cell growth</subject><subject>Cell Line</subject><subject>Cell Line, Tumor</subject><subject>Cell lines</subject><subject>Cell Proliferation</subject><subject>Cell Transformation, Neoplastic</subject><subject>Cellular metabolism</subject><subject>Chromatography, Liquid</subject><subject>Culture Media</subject><subject>Enzymes</subject><subject>Gene Expression</subject><subject>Gene Expression Profiling</subject><subject>General aspects</subject><subject>Glycine - biosynthesis</subject><subject>Glycine - metabolism</subject><subject>Humans</subject><subject>Mass spectrometry</subject><subject>Medical sciences</subject><subject>Metabolic Networks and Pathways - genetics</subject><subject>Metabolites</subject><subject>Metabolome</subject><subject>Mitochondria</subject><subject>Mitochondria - enzymology</subject><subject>Mitochondria - metabolism</subject><subject>mortality</subject><subject>neoplasm cells</subject><subject>Neoplasms - genetics</subject><subject>Neoplasms - metabolism</subject><subject>Neoplasms - pathology</subject><subject>patients</subject><subject>Purines</subject><subject>Purines - biosynthesis</subject><subject>Stem cells</subject><subject>Tandem Mass Spectrometry</subject><subject>Transformed cell line</subject><subject>Tumor cell line</subject><subject>Tumors</subject><issn>0036-8075</issn><issn>1095-9203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>D8T</sourceid><recordid>eNpdkc1vEzEQxS1ERUPgzAlkCSFx2dbfWV-QUFRK1SJQ1Qsny-uMi4OzTu0NVf57HGUbaE-2_H4znjcPoTeUnFDK1GlxAXoHJ5TRVmr5DE0o0bLRjPDnaEIIV01LZvIYvSxlSUjVNH-BjhlTrFVSTdDPbzDYLsUwAP6Rkw8x9Lf4YgH9EHyAgi2-hC2-ThGwTxmfx60LPeDQ42u7Dgs8t_X_jOcQ465BDB6yHULqX6Ejb2OB1-M5RTdfzm7mX5ur7-cX889XjVOUDE3nqZAdccRZL7XyUkA1JmmrOAHhBCjKnfMevJBOiBnppLJeUz3rgNCWT1Gzb1vuYb3pzDqHlc1bk2ww49PvegMjuWq1rvynPV-VFSxcNZptfFT2WOnDL3Ob_hgumaLtrsHHsUFOdxsog1mF4qp920PaFMPqmrmYMc4q-v4Jukyb3NdtGEqobGs8jFbqdE-5nErJ4A_DUGJ2KZsxZTOmXCve_e_hwD_EWoEPI2CLs9HnGlIo_zipheZ1zCl6u-eWZUj5oIs6m9BU8L-itLt3</recordid><startdate>20120525</startdate><enddate>20120525</enddate><creator>Jain, Mohit</creator><creator>Nilsson, Roland</creator><creator>Sharma, Sonia</creator><creator>Madhusudhan, Nikhil</creator><creator>Kitami, Toshimori</creator><creator>Souza, Amanda L.</creator><creator>Kafri, Ran</creator><creator>Kirschner, Marc W.</creator><creator>Clish, Clary B.</creator><creator>Mootha, Vamsi K.</creator><general>American Association for the Advancement of Science</general><general>The American Association for the Advancement of Science</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>7QF</scope><scope>7QG</scope><scope>7QL</scope><scope>7QP</scope><scope>7QQ</scope><scope>7QR</scope><scope>7SC</scope><scope>7SE</scope><scope>7SN</scope><scope>7SP</scope><scope>7SR</scope><scope>7SS</scope><scope>7T7</scope><scope>7TA</scope><scope>7TB</scope><scope>7TK</scope><scope>7TM</scope><scope>7U5</scope><scope>7U9</scope><scope>8BQ</scope><scope>8FD</scope><scope>C1K</scope><scope>F28</scope><scope>FR3</scope><scope>H8D</scope><scope>H8G</scope><scope>H94</scope><scope>JG9</scope><scope>JQ2</scope><scope>K9.</scope><scope>KR7</scope><scope>L7M</scope><scope>L~C</scope><scope>L~D</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>7S9</scope><scope>L.6</scope><scope>5PM</scope><scope>ADTPV</scope><scope>AOWAS</scope><scope>D8T</scope><scope>ZZAVC</scope></search><sort><creationdate>20120525</creationdate><title>Metabolite Profiling Identifies a Key Role for Glycine in Rapid Cancer Cell Proliferation</title><author>Jain, Mohit ; Nilsson, Roland ; Sharma, Sonia ; Madhusudhan, Nikhil ; Kitami, Toshimori ; Souza, Amanda L. ; Kafri, Ran ; Kirschner, Marc W. ; Clish, Clary B. ; Mootha, Vamsi K.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c610t-bf145b0c0caf596f54e126518630e4c4e613ccffef45c4470b56af9197be0183</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>biochemical pathways</topic><topic>Biological and medical sciences</topic><topic>Biosynthesis</topic><topic>breast neoplasms</topic><topic>Breast Neoplasms - 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Using mass spectrometry, we measured the consumption and release (CORE) profiles of 219 metabolites from media across the NCI-60 cancer cell lines, and integrated these data with a preexisting atlas of gene expression. This analysis identified glycine consumption and expression of the mitochondrial glycine biosynthetic pathway as strongly correlated with rates of proliferation across cancer cells. Antagonizing glycine uptake and its mitochondrial biosynthesis preferentially impaired rapidly proliferating cells. Moreover, higher expression of this pathway was associated with greater mortality in breast cancer patients. Increased reliance on glycine may represent a metabolic vulnerability for selectively targeting rapid cancer cell proliferation.</abstract><cop>Washington, DC</cop><pub>American Association for the Advancement of Science</pub><pmid>22628656</pmid><doi>10.1126/science.1218595</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | biochemical pathways Biological and medical sciences Biosynthesis breast neoplasms Breast Neoplasms - genetics Breast Neoplasms - metabolism Breast Neoplasms - pathology Cancer Carcinogenesis, carcinogens and anticarcinogens Cell adhesion & migration Cell Cycle Cell growth Cell Line Cell Line, Tumor Cell lines Cell Proliferation Cell Transformation, Neoplastic Cellular metabolism Chromatography, Liquid Culture Media Enzymes Gene Expression Gene Expression Profiling General aspects Glycine - biosynthesis Glycine - metabolism Humans Mass spectrometry Medical sciences Metabolic Networks and Pathways - genetics Metabolites Metabolome Mitochondria Mitochondria - enzymology Mitochondria - metabolism mortality neoplasm cells Neoplasms - genetics Neoplasms - metabolism Neoplasms - pathology patients Purines Purines - biosynthesis Stem cells Tandem Mass Spectrometry Transformed cell line Tumor cell line Tumors |
| title | Metabolite Profiling Identifies a Key Role for Glycine in Rapid Cancer Cell Proliferation |
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