Metabolic reprogramming during TGFβ1-induced epithelial-to-mesenchymal transition
Metastatic progression, including extravasation and micrometastatic outgrowth, is the main cause of cancer patient death. Recent studies suggest that cancer cells reprogram their metabolism to support increased proliferation through increased glycolysis and biosynthetic activities, including lipogen...
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| Veröffentlicht in: | Oncogene 2015-07, Vol.34 (30), p.3908-3916 |
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| creator | Jiang, L Xiao, L Sugiura, H Huang, X Ali, A Kuro-o, M Deberardinis, R J Boothman, D A |
| description | Metastatic progression, including extravasation and micrometastatic outgrowth, is the main cause of cancer patient death. Recent studies suggest that cancer cells reprogram their metabolism to support increased proliferation through increased glycolysis and biosynthetic activities, including lipogenesis pathways. However, metabolic changes during metastatic progression, including alterations in regulatory gene expression, remain undefined. We show that transforming growth factor beta 1 (TGFβ1)-induced epithelial-to-mesenchymal transition (EMT) is accompanied by coordinately reduced enzyme expression required to convert glucose into fatty acids, and concomitant enhanced respiration. Overexpressed Snail1, a transcription factor mediating TGFβ1-induced EMT, was sufficient to suppress carbohydrate-responsive-element-binding protein (ChREBP, a master lipogenic regulator), and fatty acid synthase (FASN), its effector lipogenic gene. Stable FASN knockdown was sufficient to induce EMT, stimulate migration and extravasation
in vitro
. FASN silencing enhanced lung metastasis and death
in vivo
. These data suggest that a metabolic transition that suppresses lipogenesis and favors energy production is an essential component of TGFβ1-induced EMT and metastasis. |
| doi_str_mv | 10.1038/onc.2014.321 |
| format | Article |
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in vitro
. FASN silencing enhanced lung metastasis and death
in vivo
. These data suggest that a metabolic transition that suppresses lipogenesis and favors energy production is an essential component of TGFβ1-induced EMT and metastasis.</description><identifier>ISSN: 0950-9232</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/onc.2014.321</identifier><identifier>PMID: 25284588</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>631/80/84/2176 ; 631/80/86 ; 692/4028/67/2327 ; 692/4028/67/322 ; Animals ; Apoptosis ; Carbohydrate Metabolism ; Cell Biology ; Cell Line, Tumor ; Cell Movement ; Cell proliferation ; Development and progression ; Enzyme Repression ; Epithelial cells ; Epithelial-Mesenchymal Transition ; Extravasation ; Fatty Acid Synthase, Type I - genetics ; Fatty Acid Synthase, Type I - metabolism ; Fatty acids ; Fatty-acid synthase ; Female ; Gene Expression ; Gene Expression Regulation, Enzymologic ; Gene Expression Regulation, Neoplastic ; Glycolysis ; Health aspects ; Human Genetics ; Humans ; Internal Medicine ; Lipid Metabolism ; Lipogenesis ; Lung cancer ; Lung Neoplasms - metabolism ; Lung Neoplasms - secondary ; Medicine ; Medicine & Public Health ; Mesenchyme ; Metabolism ; Metastases ; Metastasis ; Mice, Inbred NOD ; Mice, SCID ; Neoplasm Transplantation ; Oncology ; original-article ; Snail Family Transcription Factors ; Transcription Factors - physiology ; Transforming Growth Factor beta1 - physiology ; Transforming growth factor-b1 ; Transforming growth factors</subject><ispartof>Oncogene, 2015-07, Vol.34 (30), p.3908-3916</ispartof><rights>Macmillan Publishers Limited 2015</rights><rights>COPYRIGHT 2015 Nature Publishing Group</rights><rights>Macmillan Publishers Limited 2015.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5681-ae0c7e3c43fdc8772cabc7ae372f53c05b52d64d7d7d192046b5496bef63f68c3</citedby><cites>FETCH-LOGICAL-c5681-ae0c7e3c43fdc8772cabc7ae372f53c05b52d64d7d7d192046b5496bef63f68c3</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/onc.2014.321$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/onc.2014.321$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>230,314,776,780,881,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25284588$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jiang, L</creatorcontrib><creatorcontrib>Xiao, L</creatorcontrib><creatorcontrib>Sugiura, H</creatorcontrib><creatorcontrib>Huang, X</creatorcontrib><creatorcontrib>Ali, A</creatorcontrib><creatorcontrib>Kuro-o, M</creatorcontrib><creatorcontrib>Deberardinis, R J</creatorcontrib><creatorcontrib>Boothman, D A</creatorcontrib><title>Metabolic reprogramming during TGFβ1-induced epithelial-to-mesenchymal transition</title><title>Oncogene</title><addtitle>Oncogene</addtitle><addtitle>Oncogene</addtitle><description>Metastatic progression, including extravasation and micrometastatic outgrowth, is the main cause of cancer patient death. Recent studies suggest that cancer cells reprogram their metabolism to support increased proliferation through increased glycolysis and biosynthetic activities, including lipogenesis pathways. However, metabolic changes during metastatic progression, including alterations in regulatory gene expression, remain undefined. We show that transforming growth factor beta 1 (TGFβ1)-induced epithelial-to-mesenchymal transition (EMT) is accompanied by coordinately reduced enzyme expression required to convert glucose into fatty acids, and concomitant enhanced respiration. Overexpressed Snail1, a transcription factor mediating TGFβ1-induced EMT, was sufficient to suppress carbohydrate-responsive-element-binding protein (ChREBP, a master lipogenic regulator), and fatty acid synthase (FASN), its effector lipogenic gene. Stable FASN knockdown was sufficient to induce EMT, stimulate migration and extravasation
in vitro
. FASN silencing enhanced lung metastasis and death
in vivo
. These data suggest that a metabolic transition that suppresses lipogenesis and favors energy production is an essential component of TGFβ1-induced EMT and metastasis.</description><subject>631/80/84/2176</subject><subject>631/80/86</subject><subject>692/4028/67/2327</subject><subject>692/4028/67/322</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Carbohydrate Metabolism</subject><subject>Cell Biology</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement</subject><subject>Cell proliferation</subject><subject>Development and progression</subject><subject>Enzyme Repression</subject><subject>Epithelial cells</subject><subject>Epithelial-Mesenchymal Transition</subject><subject>Extravasation</subject><subject>Fatty Acid Synthase, Type I - genetics</subject><subject>Fatty Acid Synthase, Type I - metabolism</subject><subject>Fatty acids</subject><subject>Fatty-acid synthase</subject><subject>Female</subject><subject>Gene Expression</subject><subject>Gene Expression Regulation, Enzymologic</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Glycolysis</subject><subject>Health aspects</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Internal Medicine</subject><subject>Lipid Metabolism</subject><subject>Lipogenesis</subject><subject>Lung cancer</subject><subject>Lung Neoplasms - metabolism</subject><subject>Lung Neoplasms - secondary</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Mesenchyme</subject><subject>Metabolism</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>Mice, Inbred NOD</subject><subject>Mice, SCID</subject><subject>Neoplasm Transplantation</subject><subject>Oncology</subject><subject>original-article</subject><subject>Snail Family Transcription Factors</subject><subject>Transcription Factors - physiology</subject><subject>Transforming Growth Factor beta1 - physiology</subject><subject>Transforming growth factor-b1</subject><subject>Transforming growth factors</subject><issn>0950-9232</issn><issn>1476-5594</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNptks9u1DAQxi0EokvLjTNaiQsHsvh_7AtSVdGC1KoSas-W40x2XSV2sBOkvhYPwjPhsKWlqJrDSJ7ffPY3HoTeELwhmKmPMbgNxYRvGCXP0IrwWlZCaP4crbAWuNKU0QP0KucbjHGtMX2JDqigigulVujbBUy2ib136wRjittkh8GH7bqd05Kuzk5__SSVD-3soF3D6Kcd9N721RSrATIEt7sdbL-ekg3ZTz6GI_Sis32G13f5EF2ffr46-VKdX559PTk-r5yQilQWsKuBOc661qm6ps42rrbAatoJ5rBoBG0lb-sSRFPMZSO4lg10knVSOXaIPu11x7kZoHUQyht6MyY_2HRrovXmcSX4ndnGH4YzVRNKisD7O4EUv8-QJzP47KDvbYA4Z0OkVlpiRVlB3_2H3sQ5hWLPlCqRhAkmH6it7cH40MVyr1tEzTGnvExd64XaPEGVaGHwLgbofDl_1PBh3-BSzDlBd--RYLPsgCk7YJYdMOyPrbf_zuUe_vvpBaj2QB6XP4b0YOZJwd883Lxn</recordid><startdate>20150723</startdate><enddate>20150723</enddate><creator>Jiang, L</creator><creator>Xiao, L</creator><creator>Sugiura, H</creator><creator>Huang, X</creator><creator>Ali, A</creator><creator>Kuro-o, M</creator><creator>Deberardinis, R J</creator><creator>Boothman, D A</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</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>3V.</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20150723</creationdate><title>Metabolic reprogramming during TGFβ1-induced epithelial-to-mesenchymal transition</title><author>Jiang, L ; Xiao, L ; Sugiura, H ; Huang, X ; Ali, A ; Kuro-o, M ; Deberardinis, R J ; Boothman, D A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5681-ae0c7e3c43fdc8772cabc7ae372f53c05b52d64d7d7d192046b5496bef63f68c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>631/80/84/2176</topic><topic>631/80/86</topic><topic>692/4028/67/2327</topic><topic>692/4028/67/322</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Carbohydrate Metabolism</topic><topic>Cell Biology</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement</topic><topic>Cell proliferation</topic><topic>Development and progression</topic><topic>Enzyme Repression</topic><topic>Epithelial cells</topic><topic>Epithelial-Mesenchymal Transition</topic><topic>Extravasation</topic><topic>Fatty Acid Synthase, Type I - genetics</topic><topic>Fatty Acid Synthase, Type I - metabolism</topic><topic>Fatty acids</topic><topic>Fatty-acid synthase</topic><topic>Female</topic><topic>Gene Expression</topic><topic>Gene Expression Regulation, Enzymologic</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Glycolysis</topic><topic>Health aspects</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>Internal Medicine</topic><topic>Lipid Metabolism</topic><topic>Lipogenesis</topic><topic>Lung cancer</topic><topic>Lung Neoplasms - metabolism</topic><topic>Lung Neoplasms - secondary</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Mesenchyme</topic><topic>Metabolism</topic><topic>Metastases</topic><topic>Metastasis</topic><topic>Mice, Inbred NOD</topic><topic>Mice, SCID</topic><topic>Neoplasm Transplantation</topic><topic>Oncology</topic><topic>original-article</topic><topic>Snail Family Transcription Factors</topic><topic>Transcription Factors - physiology</topic><topic>Transforming Growth Factor beta1 - physiology</topic><topic>Transforming growth factor-b1</topic><topic>Transforming growth factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jiang, L</creatorcontrib><creatorcontrib>Xiao, L</creatorcontrib><creatorcontrib>Sugiura, H</creatorcontrib><creatorcontrib>Huang, X</creatorcontrib><creatorcontrib>Ali, A</creatorcontrib><creatorcontrib>Kuro-o, M</creatorcontrib><creatorcontrib>Deberardinis, R J</creatorcontrib><creatorcontrib>Boothman, D A</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>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</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>Research Library (Alumni Edition)</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>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</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>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Oncogene</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jiang, L</au><au>Xiao, L</au><au>Sugiura, H</au><au>Huang, X</au><au>Ali, A</au><au>Kuro-o, M</au><au>Deberardinis, R J</au><au>Boothman, D A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Metabolic reprogramming during TGFβ1-induced epithelial-to-mesenchymal transition</atitle><jtitle>Oncogene</jtitle><stitle>Oncogene</stitle><addtitle>Oncogene</addtitle><date>2015-07-23</date><risdate>2015</risdate><volume>34</volume><issue>30</issue><spage>3908</spage><epage>3916</epage><pages>3908-3916</pages><issn>0950-9232</issn><eissn>1476-5594</eissn><abstract>Metastatic progression, including extravasation and micrometastatic outgrowth, is the main cause of cancer patient death. Recent studies suggest that cancer cells reprogram their metabolism to support increased proliferation through increased glycolysis and biosynthetic activities, including lipogenesis pathways. However, metabolic changes during metastatic progression, including alterations in regulatory gene expression, remain undefined. We show that transforming growth factor beta 1 (TGFβ1)-induced epithelial-to-mesenchymal transition (EMT) is accompanied by coordinately reduced enzyme expression required to convert glucose into fatty acids, and concomitant enhanced respiration. Overexpressed Snail1, a transcription factor mediating TGFβ1-induced EMT, was sufficient to suppress carbohydrate-responsive-element-binding protein (ChREBP, a master lipogenic regulator), and fatty acid synthase (FASN), its effector lipogenic gene. Stable FASN knockdown was sufficient to induce EMT, stimulate migration and extravasation
in vitro
. FASN silencing enhanced lung metastasis and death
in vivo
. These data suggest that a metabolic transition that suppresses lipogenesis and favors energy production is an essential component of TGFβ1-induced EMT and metastasis.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>25284588</pmid><doi>10.1038/onc.2014.321</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Oncogene, 2015-07, Vol.34 (30), p.3908-3916 |
| issn | 0950-9232 1476-5594 |
| language | eng |
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| source | MEDLINE; SpringerLink Journals; Nature Journals Online; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals |
| subjects | 631/80/84/2176 631/80/86 692/4028/67/2327 692/4028/67/322 Animals Apoptosis Carbohydrate Metabolism Cell Biology Cell Line, Tumor Cell Movement Cell proliferation Development and progression Enzyme Repression Epithelial cells Epithelial-Mesenchymal Transition Extravasation Fatty Acid Synthase, Type I - genetics Fatty Acid Synthase, Type I - metabolism Fatty acids Fatty-acid synthase Female Gene Expression Gene Expression Regulation, Enzymologic Gene Expression Regulation, Neoplastic Glycolysis Health aspects Human Genetics Humans Internal Medicine Lipid Metabolism Lipogenesis Lung cancer Lung Neoplasms - metabolism Lung Neoplasms - secondary Medicine Medicine & Public Health Mesenchyme Metabolism Metastases Metastasis Mice, Inbred NOD Mice, SCID Neoplasm Transplantation Oncology original-article Snail Family Transcription Factors Transcription Factors - physiology Transforming Growth Factor beta1 - physiology Transforming growth factor-b1 Transforming growth factors |
| title | Metabolic reprogramming during TGFβ1-induced epithelial-to-mesenchymal transition |
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