(13)C and (15)N natural isotope abundance reflects breast cancer cell metabolism.
Identifieur interne : 001856 ( PubMed/Corpus ); précédent : 001855; suivant : 001857(13)C and (15)N natural isotope abundance reflects breast cancer cell metabolism.
Auteurs : Illa Tea ; Estelle Martineau ; Ingrid Antheaume ; Julie Lalande ; Caroline Mauve ; Francoise Gilard ; Sophie Barillé-Nion ; Anneke C. Blackburn ; Guillaume TcherkezSource :
- Scientific reports [ 2045-2322 ] ; 2016.
Abstract
Breast cancer is the most common cancer in women worldwide. Despite the information provided by anatomopathological assessment and molecular markers (such as receptor expression ER, PR, HER2), breast cancer therapies and prognostics depend on the metabolic properties of tumor cells. However, metabolomics have not provided a robust and congruent biomarker yet, likely because individual metabolite contents are insufficient to encapsulate all of the alterations in metabolic fluxes. Here, we took advantage of natural (13)C and (15)N isotope abundance to show there are isotopic differences between healthy and cancer biopsy tissues or between healthy and malignant cultured cell lines. Isotope mass balance further suggests that these differences are mostly related to lipid metabolism, anaplerosis and urea cycle, three pathways known to be impacted in malignant cells. Our results demonstrate that the isotope signature is a good descriptor of metabolism since it integrates modifications in C partitioning and N excretion altogether. Our present study is thus a starting point to possible clinical applications such as patient screening and biopsy characterization in every cancer that is associated with metabolic changes.
DOI: 10.1038/srep34251
PubMed: 27678172
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Blackburn</name><affiliation><nlm:affiliation>Cancer Metabolism and Genetics Group, The John Curtin School of Medical Research, The Australian National University, Canberra 2601 ACT, Australia.</nlm:affiliation></affiliation></author><author><name sortKey="Tcherkez, Guillaume" sort="Tcherkez, Guillaume" uniqKey="Tcherkez G" first="Guillaume" last="Tcherkez">Guillaume Tcherkez</name><affiliation><nlm:affiliation>Research School of Biology, The Australian National University, Canberra 2601 ACT, Australia.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Scientific reports</title><idno type="eISSN">2045-2322</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Breast cancer is the most common cancer in women worldwide. Despite the information provided by anatomopathological assessment and molecular markers (such as receptor expression ER, PR, HER2), breast cancer therapies and prognostics depend on the metabolic properties of tumor cells. However, metabolomics have not provided a robust and congruent biomarker yet, likely because individual metabolite contents are insufficient to encapsulate all of the alterations in metabolic fluxes. Here, we took advantage of natural (13)C and (15)N isotope abundance to show there are isotopic differences between healthy and cancer biopsy tissues or between healthy and malignant cultured cell lines. Isotope mass balance further suggests that these differences are mostly related to lipid metabolism, anaplerosis and urea cycle, three pathways known to be impacted in malignant cells. Our results demonstrate that the isotope signature is a good descriptor of metabolism since it integrates modifications in C partitioning and N excretion altogether. Our present study is thus a starting point to possible clinical applications such as patient screening and biopsy characterization in every cancer that is associated with metabolic changes.</div></front></TEI><pubmed><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">27678172</PMID><DateCreated><Year>2016</Year><Month>09</Month><Day>28</Day></DateCreated><DateRevised><Year>2017</Year><Month>02</Month><Day>20</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">2045-2322</ISSN><JournalIssue CitedMedium="Internet"><Volume>6</Volume><PubDate><Year>2016</Year><Month>Sep</Month><Day>28</Day></PubDate></JournalIssue><Title>Scientific reports</Title><ISOAbbreviation>Sci Rep</ISOAbbreviation></Journal><ArticleTitle>(13)C and (15)N natural isotope abundance reflects breast cancer cell metabolism.</ArticleTitle><Pagination><MedlinePgn>34251</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1038/srep34251</ELocationID><Abstract><AbstractText>Breast cancer is the most common cancer in women worldwide. Despite the information provided by anatomopathological assessment and molecular markers (such as receptor expression ER, PR, HER2), breast cancer therapies and prognostics depend on the metabolic properties of tumor cells. However, metabolomics have not provided a robust and congruent biomarker yet, likely because individual metabolite contents are insufficient to encapsulate all of the alterations in metabolic fluxes. Here, we took advantage of natural (13)C and (15)N isotope abundance to show there are isotopic differences between healthy and cancer biopsy tissues or between healthy and malignant cultured cell lines. Isotope mass balance further suggests that these differences are mostly related to lipid metabolism, anaplerosis and urea cycle, three pathways known to be impacted in malignant cells. Our results demonstrate that the isotope signature is a good descriptor of metabolism since it integrates modifications in C partitioning and N excretion altogether. Our present study is thus a starting point to possible clinical applications such as patient screening and biopsy characterization in every cancer that is associated with metabolic changes.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Tea</LastName><ForeName>Illa</ForeName><Initials>I</Initials><AffiliationInfo><Affiliation>EBSI team, CEISAM, University of Nantes-CNRS UMR 6230, 2 rue de la Houssinière BP 92208, F-44322 Nantes, France.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Cancer Metabolism and Genetics Group, The John Curtin School of Medical Research, The Australian National University, Canberra 2601 ACT, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Martineau</LastName><ForeName>Estelle</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>EBSI team, CEISAM, University of Nantes-CNRS UMR 6230, 2 rue de la Houssinière BP 92208, F-44322 Nantes, France.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Spectromaitrise, CAPACITÉS SAS, 26 Bd Vincent Gâche, 44200 Nantes, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Antheaume</LastName><ForeName>Ingrid</ForeName><Initials>I</Initials><AffiliationInfo><Affiliation>EBSI team, CEISAM, University of Nantes-CNRS UMR 6230, 2 rue de la Houssinière BP 92208, F-44322 Nantes, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lalande</LastName><ForeName>Julie</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>EBSI team, CEISAM, University of Nantes-CNRS UMR 6230, 2 rue de la Houssinière BP 92208, F-44322 Nantes, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mauve</LastName><ForeName>Caroline</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Plateforme Métabolisme-Métabolome, Bâtiment 630 IPS2, Université Paris-Sud, 91405 Orsay cedex, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gilard</LastName><ForeName>Francoise</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Plateforme Métabolisme-Métabolome, Bâtiment 630 IPS2, Université Paris-Sud, 91405 Orsay cedex, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Barillé-Nion</LastName><ForeName>Sophie</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>CRCNA, UMR INSERM U892/CNRS 6299/Université de Nantes, Team 8 «Cell survival and tumor escape in breast cancers», Institut de Recherche en Santé de l'Université de Nantes, 8 quai Moncousu, BP 70721, 44 007 Nantes cedex 1, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Blackburn</LastName><ForeName>Anneke C</ForeName><Initials>AC</Initials><AffiliationInfo><Affiliation>Cancer Metabolism and Genetics Group, The John Curtin School of Medical Research, The Australian National University, Canberra 2601 ACT, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tcherkez</LastName><ForeName>Guillaume</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Research School of Biology, The Australian National University, Canberra 2601 ACT, Australia.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2016</Year><Month>09</Month><Day>28</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Sci Rep</MedlineTA><NlmUniqueID>101563288</NlmUniqueID><ISSNLinking>2045-2322</ISSNLinking></MedlineJournalInfo><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Phys Med Biol. 2007 Oct 21;52(20):6093-115</RefSource><PMID Version="1">17921574</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Nutr. 2005 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