ANGPTL4 regulate glutamine metabolism and fatty acid oxidation in nonsmall cell lung cancer cells
Angiopoietin‐like protein (ANGPTL) 4 is a key factor in the regulation of lipid and glucose metabolism in metabolic diseases. ANGPTL4 is highly expressed in various cancers, but the regulation of energy metabolism in tumours remains to be determined. This study explored the role of ANGPTL4 in aerobi...
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| Veröffentlicht in: | Journal of cellular and molecular medicine 2022-04, Vol.26 (7), p.1876-1885 |
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| creator | Xiao, Song Nai‐dong, Wang Jin‐Xiang, Yan Long, Tian Xiu‐Rong, Lu Hong, Gao Jie‐Cheng, Yan Fei, Zhang |
| description | Angiopoietin‐like protein (ANGPTL) 4 is a key factor in the regulation of lipid and glucose metabolism in metabolic diseases. ANGPTL4 is highly expressed in various cancers, but the regulation of energy metabolism in tumours remains to be determined. This study explored the role of ANGPTL4 in aerobic glycolysis, glutamine consumption and fatty acid oxidation in nonsmall cell lung cancer (NSCLC) cells. Two NSCLC cell lines (A549 and H1299) were used to investigate the role of ANGPTL4 in energy metabolism by tracer techniques and with Seahorse XF technology in ANGPTLs4 knockdown cells. RNA microarrays and specific inhibitors were used to identify targets in ANGPTLs4‐overexpressing cells. The results showed that knockdown of ANGPTLs4 could inhibit energy metabolism and proliferation in NSCLC. ANGPTLs4 had no significant effect on glycolysis but affected glutamine consumption and fatty acid oxidation. Knockdown of ANGPTLs4 also significantly inhibited tumour metastasis and energy metabolism in mice and had a weak effect on glycolysis. RNA microarray analysis showed that ANGPTLs4 significantly affected glutaminase (GLS) and carnitine palmitoyl transferase 1 (CPT1). ANGPTLs4‐overexpressing cells were exposed to a glutamine deprivation environment, and cell proliferation and energy metabolism were significantly decreased but still differed from normal NSCLC cells. Treatment of ANGPTLs4‐overexpressing cells with GLS and CPT1 inhibitors simultaneously prevented the regulatory effects on cell proliferation and energy metabolism. ANGPTLs4 could promote glutamine consumption and fatty acid oxidation but not glycolysis or accelerate energy metabolism in NSCLC. |
| doi_str_mv | 10.1111/jcmm.16879 |
| format | Article |
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ANGPTL4 is highly expressed in various cancers, but the regulation of energy metabolism in tumours remains to be determined. This study explored the role of ANGPTL4 in aerobic glycolysis, glutamine consumption and fatty acid oxidation in nonsmall cell lung cancer (NSCLC) cells. Two NSCLC cell lines (A549 and H1299) were used to investigate the role of ANGPTL4 in energy metabolism by tracer techniques and with Seahorse XF technology in ANGPTLs4 knockdown cells. RNA microarrays and specific inhibitors were used to identify targets in ANGPTLs4‐overexpressing cells. The results showed that knockdown of ANGPTLs4 could inhibit energy metabolism and proliferation in NSCLC. ANGPTLs4 had no significant effect on glycolysis but affected glutamine consumption and fatty acid oxidation. Knockdown of ANGPTLs4 also significantly inhibited tumour metastasis and energy metabolism in mice and had a weak effect on glycolysis. RNA microarray analysis showed that ANGPTLs4 significantly affected glutaminase (GLS) and carnitine palmitoyl transferase 1 (CPT1). ANGPTLs4‐overexpressing cells were exposed to a glutamine deprivation environment, and cell proliferation and energy metabolism were significantly decreased but still differed from normal NSCLC cells. Treatment of ANGPTLs4‐overexpressing cells with GLS and CPT1 inhibitors simultaneously prevented the regulatory effects on cell proliferation and energy metabolism. ANGPTLs4 could promote glutamine consumption and fatty acid oxidation but not glycolysis or accelerate energy metabolism in NSCLC.</description><identifier>ISSN: 1582-1838</identifier><identifier>EISSN: 1582-4934</identifier><identifier>DOI: 10.1111/jcmm.16879</identifier><identifier>PMID: 35285130</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>Adenosine triphosphate ; aerobic glycolysis ; Angiogenesis ; Angiopoietin ; ANGPTL4 ; Animals ; Carcinoma, Non-Small-Cell Lung - pathology ; Carnitine ; Cell growth ; Cell Line, Tumor ; Cell proliferation ; Cell Proliferation - genetics ; DNA microarrays ; Energy metabolism ; fatty acid oxidation ; Fatty acids ; Fatty Acids - metabolism ; Glucose ; Glucose metabolism ; Glutaminase ; Glutamine ; Glutamine - metabolism ; Glycolysis ; Hypoxia ; Lipid metabolism ; Lung cancer ; Lung Neoplasms - pathology ; Metabolic disorders ; Metabolism ; Metabolites ; Metastases ; Metastasis ; Mice ; Non-small cell lung carcinoma ; NSCLC ; Original ; Oxidation ; Proteins ; Tumors</subject><ispartof>Journal of cellular and molecular medicine, 2022-04, Vol.26 (7), p.1876-1885</ispartof><rights>2022 The Authors. published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.</rights><rights>2022 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.</rights><rights>2022. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4489-19d7a8483714675aa220218baf7a998119028cb34dabaff401a35d7767d3b9463</citedby><cites>FETCH-LOGICAL-c4489-19d7a8483714675aa220218baf7a998119028cb34dabaff401a35d7767d3b9463</cites><orcidid>0000-0002-4331-9535</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8980907/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8980907/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,1417,11562,27924,27925,45574,45575,46052,46476,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35285130$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Xiao, Song</creatorcontrib><creatorcontrib>Nai‐dong, Wang</creatorcontrib><creatorcontrib>Jin‐Xiang, Yan</creatorcontrib><creatorcontrib>Long, Tian</creatorcontrib><creatorcontrib>Xiu‐Rong, Lu</creatorcontrib><creatorcontrib>Hong, Gao</creatorcontrib><creatorcontrib>Jie‐Cheng, Yan</creatorcontrib><creatorcontrib>Fei, Zhang</creatorcontrib><title>ANGPTL4 regulate glutamine metabolism and fatty acid oxidation in nonsmall cell lung cancer cells</title><title>Journal of cellular and molecular medicine</title><addtitle>J Cell Mol Med</addtitle><description>Angiopoietin‐like protein (ANGPTL) 4 is a key factor in the regulation of lipid and glucose metabolism in metabolic diseases. ANGPTL4 is highly expressed in various cancers, but the regulation of energy metabolism in tumours remains to be determined. This study explored the role of ANGPTL4 in aerobic glycolysis, glutamine consumption and fatty acid oxidation in nonsmall cell lung cancer (NSCLC) cells. Two NSCLC cell lines (A549 and H1299) were used to investigate the role of ANGPTL4 in energy metabolism by tracer techniques and with Seahorse XF technology in ANGPTLs4 knockdown cells. RNA microarrays and specific inhibitors were used to identify targets in ANGPTLs4‐overexpressing cells. The results showed that knockdown of ANGPTLs4 could inhibit energy metabolism and proliferation in NSCLC. ANGPTLs4 had no significant effect on glycolysis but affected glutamine consumption and fatty acid oxidation. Knockdown of ANGPTLs4 also significantly inhibited tumour metastasis and energy metabolism in mice and had a weak effect on glycolysis. RNA microarray analysis showed that ANGPTLs4 significantly affected glutaminase (GLS) and carnitine palmitoyl transferase 1 (CPT1). ANGPTLs4‐overexpressing cells were exposed to a glutamine deprivation environment, and cell proliferation and energy metabolism were significantly decreased but still differed from normal NSCLC cells. Treatment of ANGPTLs4‐overexpressing cells with GLS and CPT1 inhibitors simultaneously prevented the regulatory effects on cell proliferation and energy metabolism. ANGPTLs4 could promote glutamine consumption and fatty acid oxidation but not glycolysis or accelerate energy metabolism in NSCLC.</description><subject>Adenosine triphosphate</subject><subject>aerobic glycolysis</subject><subject>Angiogenesis</subject><subject>Angiopoietin</subject><subject>ANGPTL4</subject><subject>Animals</subject><subject>Carcinoma, Non-Small-Cell Lung - pathology</subject><subject>Carnitine</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell proliferation</subject><subject>Cell Proliferation - genetics</subject><subject>DNA microarrays</subject><subject>Energy metabolism</subject><subject>fatty acid oxidation</subject><subject>Fatty acids</subject><subject>Fatty Acids - metabolism</subject><subject>Glucose</subject><subject>Glucose metabolism</subject><subject>Glutaminase</subject><subject>Glutamine</subject><subject>Glutamine - metabolism</subject><subject>Glycolysis</subject><subject>Hypoxia</subject><subject>Lipid metabolism</subject><subject>Lung cancer</subject><subject>Lung Neoplasms - pathology</subject><subject>Metabolic disorders</subject><subject>Metabolism</subject><subject>Metabolites</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>Mice</subject><subject>Non-small cell lung carcinoma</subject><subject>NSCLC</subject><subject>Original</subject><subject>Oxidation</subject><subject>Proteins</subject><subject>Tumors</subject><issn>1582-1838</issn><issn>1582-4934</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>WIN</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kc9rFDEUx4NYbK1e_AMk4EWErckkkx8XoSy1WrbqoZ7Dm0xmzZJJajJj3f_ebHct6sEcksfLhw_v8UXoBSVntJ63GzuOZ1QoqR-hE9qqZsE1448PNVVMHaOnpWwIYYIy_QQds7ZRLWXkBMH5p8svNyuOs1vPASaH12GeYPTR4dFN0KXgy4gh9niAadpisL7H6afvYfIpYh9xTLGMEAK2rl5hjmtsIVqX7xvlGToaIBT3_PCeoq_vL26WHxarz5cfl-erheVc6QXVvQTFFZOUC9kCNA1pqOpgkKC1olSTRtmO8R5qb-CEAmt7KYXsWae5YKfo3d57O3ej662LU4ZgbrMfIW9NAm_-_on-m1mnH0ZpRTSRVfD6IMjp--zKZEZfditAdGkuphFMaU6EVhV99Q-6SXOOdb1KcaGUUJpW6s2esjmVkt3wMAwlZpec2SVn7pOr8Ms_x39Af0dVAboH7nxw2_-ozNXy-nov_QW-_aPJ</recordid><startdate>202204</startdate><enddate>202204</enddate><creator>Xiao, Song</creator><creator>Nai‐dong, Wang</creator><creator>Jin‐Xiang, Yan</creator><creator>Long, Tian</creator><creator>Xiu‐Rong, Lu</creator><creator>Hong, Gao</creator><creator>Jie‐Cheng, Yan</creator><creator>Fei, Zhang</creator><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</scope><scope>WIN</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>3V.</scope><scope>7QP</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</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>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PIMPY</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><orcidid>https://orcid.org/0000-0002-4331-9535</orcidid></search><sort><creationdate>202204</creationdate><title>ANGPTL4 regulate glutamine metabolism and fatty acid oxidation in nonsmall cell lung cancer cells</title><author>Xiao, Song ; Nai‐dong, Wang ; Jin‐Xiang, Yan ; Long, Tian ; Xiu‐Rong, Lu ; Hong, Gao ; Jie‐Cheng, Yan ; Fei, Zhang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4489-19d7a8483714675aa220218baf7a998119028cb34dabaff401a35d7767d3b9463</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Adenosine triphosphate</topic><topic>aerobic glycolysis</topic><topic>Angiogenesis</topic><topic>Angiopoietin</topic><topic>ANGPTL4</topic><topic>Animals</topic><topic>Carcinoma, Non-Small-Cell Lung - pathology</topic><topic>Carnitine</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell proliferation</topic><topic>Cell Proliferation - genetics</topic><topic>DNA microarrays</topic><topic>Energy metabolism</topic><topic>fatty acid oxidation</topic><topic>Fatty acids</topic><topic>Fatty Acids - metabolism</topic><topic>Glucose</topic><topic>Glucose metabolism</topic><topic>Glutaminase</topic><topic>Glutamine</topic><topic>Glutamine - metabolism</topic><topic>Glycolysis</topic><topic>Hypoxia</topic><topic>Lipid metabolism</topic><topic>Lung cancer</topic><topic>Lung Neoplasms - pathology</topic><topic>Metabolic disorders</topic><topic>Metabolism</topic><topic>Metabolites</topic><topic>Metastases</topic><topic>Metastasis</topic><topic>Mice</topic><topic>Non-small cell lung carcinoma</topic><topic>NSCLC</topic><topic>Original</topic><topic>Oxidation</topic><topic>Proteins</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Xiao, Song</creatorcontrib><creatorcontrib>Nai‐dong, Wang</creatorcontrib><creatorcontrib>Jin‐Xiang, Yan</creatorcontrib><creatorcontrib>Long, Tian</creatorcontrib><creatorcontrib>Xiu‐Rong, Lu</creatorcontrib><creatorcontrib>Hong, Gao</creatorcontrib><creatorcontrib>Jie‐Cheng, Yan</creatorcontrib><creatorcontrib>Fei, Zhang</creatorcontrib><collection>Wiley-Blackwell Open Access Titles</collection><collection>Wiley Free Content</collection><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>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</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>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>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>Science Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Publicly Available Content Database</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>Journal of cellular and molecular medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Xiao, Song</au><au>Nai‐dong, Wang</au><au>Jin‐Xiang, Yan</au><au>Long, Tian</au><au>Xiu‐Rong, Lu</au><au>Hong, Gao</au><au>Jie‐Cheng, Yan</au><au>Fei, Zhang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>ANGPTL4 regulate glutamine metabolism and fatty acid oxidation in nonsmall cell lung cancer cells</atitle><jtitle>Journal of cellular and molecular medicine</jtitle><addtitle>J Cell Mol Med</addtitle><date>2022-04</date><risdate>2022</risdate><volume>26</volume><issue>7</issue><spage>1876</spage><epage>1885</epage><pages>1876-1885</pages><issn>1582-1838</issn><eissn>1582-4934</eissn><abstract>Angiopoietin‐like protein (ANGPTL) 4 is a key factor in the regulation of lipid and glucose metabolism in metabolic diseases. ANGPTL4 is highly expressed in various cancers, but the regulation of energy metabolism in tumours remains to be determined. This study explored the role of ANGPTL4 in aerobic glycolysis, glutamine consumption and fatty acid oxidation in nonsmall cell lung cancer (NSCLC) cells. Two NSCLC cell lines (A549 and H1299) were used to investigate the role of ANGPTL4 in energy metabolism by tracer techniques and with Seahorse XF technology in ANGPTLs4 knockdown cells. RNA microarrays and specific inhibitors were used to identify targets in ANGPTLs4‐overexpressing cells. The results showed that knockdown of ANGPTLs4 could inhibit energy metabolism and proliferation in NSCLC. ANGPTLs4 had no significant effect on glycolysis but affected glutamine consumption and fatty acid oxidation. Knockdown of ANGPTLs4 also significantly inhibited tumour metastasis and energy metabolism in mice and had a weak effect on glycolysis. RNA microarray analysis showed that ANGPTLs4 significantly affected glutaminase (GLS) and carnitine palmitoyl transferase 1 (CPT1). ANGPTLs4‐overexpressing cells were exposed to a glutamine deprivation environment, and cell proliferation and energy metabolism were significantly decreased but still differed from normal NSCLC cells. Treatment of ANGPTLs4‐overexpressing cells with GLS and CPT1 inhibitors simultaneously prevented the regulatory effects on cell proliferation and energy metabolism. ANGPTLs4 could promote glutamine consumption and fatty acid oxidation but not glycolysis or accelerate energy metabolism in NSCLC.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>35285130</pmid><doi>10.1111/jcmm.16879</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0002-4331-9535</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Adenosine triphosphate aerobic glycolysis Angiogenesis Angiopoietin ANGPTL4 Animals Carcinoma, Non-Small-Cell Lung - pathology Carnitine Cell growth Cell Line, Tumor Cell proliferation Cell Proliferation - genetics DNA microarrays Energy metabolism fatty acid oxidation Fatty acids Fatty Acids - metabolism Glucose Glucose metabolism Glutaminase Glutamine Glutamine - metabolism Glycolysis Hypoxia Lipid metabolism Lung cancer Lung Neoplasms - pathology Metabolic disorders Metabolism Metabolites Metastases Metastasis Mice Non-small cell lung carcinoma NSCLC Original Oxidation Proteins Tumors |
| title | ANGPTL4 regulate glutamine metabolism and fatty acid oxidation in nonsmall cell lung cancer cells |
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