CPT1A-mediated fatty acid oxidation promotes colorectal cancer cell metastasis by inhibiting anoikis
Anoikis is a critical obstacle to cancer metastasis. Colorectal cancer (CRC) exhibits a high rate of metastasis, leading to death, and the mechanisms involved in anoikis resistance are still unclear. We identified that the fatty acid oxidation (FAO) pathway was activated in detached CRC cells. Multi...
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| Veröffentlicht in: | Oncogene 2018-11, Vol.37 (46), p.6025-6040 |
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| creator | Wang, Ying-nan Zeng, Zhao-lei Lu, Jiahuan Wang, Yun Liu, Ze-xian He, Ming-ming Zhao, Qi Wang, Zi-xian Li, Ting Lu, Yun-xin Wu, Qi-nian Yu, Kai Wang, Feng Pu, Heng-Ying Li, Bo Jia, Wei-hua shi, Ming Xie, Dan Kang, Tie-bang Huang, Peng Ju, Huai-qiang Xu, Rui-hua |
| description | Anoikis is a critical obstacle to cancer metastasis. Colorectal cancer (CRC) exhibits a high rate of metastasis, leading to death, and the mechanisms involved in anoikis resistance are still unclear. We identified that the fatty acid oxidation (FAO) pathway was activated in detached CRC cells. Multiple genes in the FAO pathway, specifically the rate-limiting enzyme CPT1A, were upregulated in CRC cells grown in suspension. Reactive oxygen species elimination mediated by CPT1A in CRC cells was vital to anoikis resistance. In vivo experiments showed that CPT1A-suppressed CRC cells colonized the lung at a much lower rate than normal CRC cells, suggesting that CPT1A-mediated FAO activation increased metastatic capacity. In clinical tissue specimens from CRC patients, elevated expression of CPT1A was observed in metastatic sites compared with primary sites. Our results demonstrate that CPT1A-mediated FAO activation induces CRC cells to resist anoikis, suggesting that CPT1A is an attractive target for treating metastatic CRC. |
| doi_str_mv | 10.1038/s41388-018-0384-z |
| format | Article |
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Colorectal cancer (CRC) exhibits a high rate of metastasis, leading to death, and the mechanisms involved in anoikis resistance are still unclear. We identified that the fatty acid oxidation (FAO) pathway was activated in detached CRC cells. Multiple genes in the FAO pathway, specifically the rate-limiting enzyme CPT1A, were upregulated in CRC cells grown in suspension. Reactive oxygen species elimination mediated by CPT1A in CRC cells was vital to anoikis resistance. In vivo experiments showed that CPT1A-suppressed CRC cells colonized the lung at a much lower rate than normal CRC cells, suggesting that CPT1A-mediated FAO activation increased metastatic capacity. In clinical tissue specimens from CRC patients, elevated expression of CPT1A was observed in metastatic sites compared with primary sites. Our results demonstrate that CPT1A-mediated FAO activation induces CRC cells to resist anoikis, suggesting that CPT1A is an attractive target for treating metastatic CRC.</description><identifier>ISSN: 0950-9232</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/s41388-018-0384-z</identifier><identifier>PMID: 29995871</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/1 ; 13/109 ; 13/31 ; 13/51 ; 14/34 ; 14/5 ; 38/61 ; 38/77 ; 45/90 ; 631/67/1504/1885 ; 631/80/84 ; 64/60 ; Animals ; Anoikis ; Anoikis - physiology ; Apoptosis ; Caco-2 Cells ; Cancer metastasis ; Care and treatment ; Carnitine O-Palmitoyltransferase - metabolism ; Cell Biology ; Cell Line, Tumor ; Colorectal cancer ; Colorectal carcinoma ; Colorectal Neoplasms - genetics ; Colorectal Neoplasms - metabolism ; Colorectal Neoplasms - pathology ; Complications and side effects ; Enzymes ; Fatty acids ; Fatty Acids - metabolism ; Gene Expression Regulation, Neoplastic - physiology ; Genes ; Genetic aspects ; HCT116 Cells ; Health aspects ; HT29 Cells ; Human Genetics ; Humans ; Internal Medicine ; Lipid Metabolism - physiology ; Male ; Medical schools ; Medicine ; Medicine & Public Health ; Metastases ; Metastasis ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Neoplasm Metastasis - pathology ; Oncology ; Oxidation ; Oxidation-Reduction ; Oxidation-reduction reactions ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Risk factors ; Transferases</subject><ispartof>Oncogene, 2018-11, Vol.37 (46), p.6025-6040</ispartof><rights>Macmillan Publishers Limited, part of Springer Nature 2018</rights><rights>COPYRIGHT 2018 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Nov 2018</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c439t-34b5870613c0ea416064b731dc0c7f35ecc024927be9945e5076013649605de53</citedby><cites>FETCH-LOGICAL-c439t-34b5870613c0ea416064b731dc0c7f35ecc024927be9945e5076013649605de53</cites><orcidid>0000-0003-4420-5625 ; 0000-0001-9698-0610 ; 0000-0002-4051-4474 ; 0000-0002-8683-6145</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/s41388-018-0384-z$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/s41388-018-0384-z$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29995871$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Ying-nan</creatorcontrib><creatorcontrib>Zeng, Zhao-lei</creatorcontrib><creatorcontrib>Lu, Jiahuan</creatorcontrib><creatorcontrib>Wang, Yun</creatorcontrib><creatorcontrib>Liu, Ze-xian</creatorcontrib><creatorcontrib>He, Ming-ming</creatorcontrib><creatorcontrib>Zhao, Qi</creatorcontrib><creatorcontrib>Wang, Zi-xian</creatorcontrib><creatorcontrib>Li, Ting</creatorcontrib><creatorcontrib>Lu, Yun-xin</creatorcontrib><creatorcontrib>Wu, Qi-nian</creatorcontrib><creatorcontrib>Yu, Kai</creatorcontrib><creatorcontrib>Wang, Feng</creatorcontrib><creatorcontrib>Pu, Heng-Ying</creatorcontrib><creatorcontrib>Li, Bo</creatorcontrib><creatorcontrib>Jia, Wei-hua</creatorcontrib><creatorcontrib>shi, Ming</creatorcontrib><creatorcontrib>Xie, Dan</creatorcontrib><creatorcontrib>Kang, Tie-bang</creatorcontrib><creatorcontrib>Huang, Peng</creatorcontrib><creatorcontrib>Ju, Huai-qiang</creatorcontrib><creatorcontrib>Xu, Rui-hua</creatorcontrib><title>CPT1A-mediated fatty acid oxidation promotes colorectal cancer cell metastasis by inhibiting anoikis</title><title>Oncogene</title><addtitle>Oncogene</addtitle><addtitle>Oncogene</addtitle><description>Anoikis is a critical obstacle to cancer metastasis. Colorectal cancer (CRC) exhibits a high rate of metastasis, leading to death, and the mechanisms involved in anoikis resistance are still unclear. We identified that the fatty acid oxidation (FAO) pathway was activated in detached CRC cells. Multiple genes in the FAO pathway, specifically the rate-limiting enzyme CPT1A, were upregulated in CRC cells grown in suspension. Reactive oxygen species elimination mediated by CPT1A in CRC cells was vital to anoikis resistance. In vivo experiments showed that CPT1A-suppressed CRC cells colonized the lung at a much lower rate than normal CRC cells, suggesting that CPT1A-mediated FAO activation increased metastatic capacity. In clinical tissue specimens from CRC patients, elevated expression of CPT1A was observed in metastatic sites compared with primary sites. Our results demonstrate that CPT1A-mediated FAO activation induces CRC cells to resist anoikis, suggesting that CPT1A is an attractive target for treating metastatic CRC.</description><subject>13/1</subject><subject>13/109</subject><subject>13/31</subject><subject>13/51</subject><subject>14/34</subject><subject>14/5</subject><subject>38/61</subject><subject>38/77</subject><subject>45/90</subject><subject>631/67/1504/1885</subject><subject>631/80/84</subject><subject>64/60</subject><subject>Animals</subject><subject>Anoikis</subject><subject>Anoikis - physiology</subject><subject>Apoptosis</subject><subject>Caco-2 Cells</subject><subject>Cancer metastasis</subject><subject>Care and treatment</subject><subject>Carnitine O-Palmitoyltransferase - metabolism</subject><subject>Cell Biology</subject><subject>Cell Line, Tumor</subject><subject>Colorectal cancer</subject><subject>Colorectal carcinoma</subject><subject>Colorectal Neoplasms - genetics</subject><subject>Colorectal Neoplasms - metabolism</subject><subject>Colorectal Neoplasms - pathology</subject><subject>Complications and side effects</subject><subject>Enzymes</subject><subject>Fatty acids</subject><subject>Fatty Acids - metabolism</subject><subject>Gene Expression Regulation, Neoplastic - physiology</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>HCT116 Cells</subject><subject>Health aspects</subject><subject>HT29 Cells</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Internal Medicine</subject><subject>Lipid Metabolism - physiology</subject><subject>Male</subject><subject>Medical schools</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Nude</subject><subject>Neoplasm Metastasis - pathology</subject><subject>Oncology</subject><subject>Oxidation</subject><subject>Oxidation-Reduction</subject><subject>Oxidation-reduction reactions</subject><subject>Reactive oxygen species</subject><subject>Reactive Oxygen Species - 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Academic</collection><jtitle>Oncogene</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Ying-nan</au><au>Zeng, Zhao-lei</au><au>Lu, Jiahuan</au><au>Wang, Yun</au><au>Liu, Ze-xian</au><au>He, Ming-ming</au><au>Zhao, Qi</au><au>Wang, Zi-xian</au><au>Li, Ting</au><au>Lu, Yun-xin</au><au>Wu, Qi-nian</au><au>Yu, Kai</au><au>Wang, Feng</au><au>Pu, Heng-Ying</au><au>Li, Bo</au><au>Jia, Wei-hua</au><au>shi, Ming</au><au>Xie, Dan</au><au>Kang, Tie-bang</au><au>Huang, Peng</au><au>Ju, Huai-qiang</au><au>Xu, Rui-hua</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CPT1A-mediated fatty acid oxidation promotes colorectal cancer cell metastasis by inhibiting anoikis</atitle><jtitle>Oncogene</jtitle><stitle>Oncogene</stitle><addtitle>Oncogene</addtitle><date>2018-11</date><risdate>2018</risdate><volume>37</volume><issue>46</issue><spage>6025</spage><epage>6040</epage><pages>6025-6040</pages><issn>0950-9232</issn><eissn>1476-5594</eissn><abstract>Anoikis is a critical obstacle to cancer metastasis. Colorectal cancer (CRC) exhibits a high rate of metastasis, leading to death, and the mechanisms involved in anoikis resistance are still unclear. We identified that the fatty acid oxidation (FAO) pathway was activated in detached CRC cells. Multiple genes in the FAO pathway, specifically the rate-limiting enzyme CPT1A, were upregulated in CRC cells grown in suspension. Reactive oxygen species elimination mediated by CPT1A in CRC cells was vital to anoikis resistance. In vivo experiments showed that CPT1A-suppressed CRC cells colonized the lung at a much lower rate than normal CRC cells, suggesting that CPT1A-mediated FAO activation increased metastatic capacity. In clinical tissue specimens from CRC patients, elevated expression of CPT1A was observed in metastatic sites compared with primary sites. Our results demonstrate that CPT1A-mediated FAO activation induces CRC cells to resist anoikis, suggesting that CPT1A is an attractive target for treating metastatic CRC.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>29995871</pmid><doi>10.1038/s41388-018-0384-z</doi><tpages>16</tpages><orcidid>https://orcid.org/0000-0003-4420-5625</orcidid><orcidid>https://orcid.org/0000-0001-9698-0610</orcidid><orcidid>https://orcid.org/0000-0002-4051-4474</orcidid><orcidid>https://orcid.org/0000-0002-8683-6145</orcidid></addata></record> |
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| identifier | ISSN: 0950-9232 |
| ispartof | Oncogene, 2018-11, Vol.37 (46), p.6025-6040 |
| issn | 0950-9232 1476-5594 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_2068912131 |
| source | MEDLINE; Springer Nature - Complete Springer Journals; Nature Journals Online |
| subjects | 13/1 13/109 13/31 13/51 14/34 14/5 38/61 38/77 45/90 631/67/1504/1885 631/80/84 64/60 Animals Anoikis Anoikis - physiology Apoptosis Caco-2 Cells Cancer metastasis Care and treatment Carnitine O-Palmitoyltransferase - metabolism Cell Biology Cell Line, Tumor Colorectal cancer Colorectal carcinoma Colorectal Neoplasms - genetics Colorectal Neoplasms - metabolism Colorectal Neoplasms - pathology Complications and side effects Enzymes Fatty acids Fatty Acids - metabolism Gene Expression Regulation, Neoplastic - physiology Genes Genetic aspects HCT116 Cells Health aspects HT29 Cells Human Genetics Humans Internal Medicine Lipid Metabolism - physiology Male Medical schools Medicine Medicine & Public Health Metastases Metastasis Mice Mice, Inbred BALB C Mice, Nude Neoplasm Metastasis - pathology Oncology Oxidation Oxidation-Reduction Oxidation-reduction reactions Reactive oxygen species Reactive Oxygen Species - metabolism Risk factors Transferases |
| title | CPT1A-mediated fatty acid oxidation promotes colorectal cancer cell metastasis by inhibiting anoikis |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-30T08%3A16%3A38IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_proqu&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=CPT1A-mediated%20fatty%20acid%20oxidation%20promotes%20colorectal%20cancer%20cell%20metastasis%20by%20inhibiting%20anoikis&rft.jtitle=Oncogene&rft.au=Wang,%20Ying-nan&rft.date=2018-11&rft.volume=37&rft.issue=46&rft.spage=6025&rft.epage=6040&rft.pages=6025-6040&rft.issn=0950-9232&rft.eissn=1476-5594&rft_id=info:doi/10.1038/s41388-018-0384-z&rft_dat=%3Cgale_proqu%3EA573155539%3C/gale_proqu%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2133834139&rft_id=info:pmid/29995871&rft_galeid=A573155539&rfr_iscdi=true |