DHA- and EPA-Enriched Phosphatidylcholine Suppress Human Lung Carcinoma 95D Cells Metastasis via Activating the Peroxisome Proliferator-Activated Receptor γ
The antineoplastic effects of docosahexaenoic acid-containing phosphatidylcholine (DHA-PC) and eicosapentaenoic acid-containing phosphatidylcholine (EPA-PC) were explored, and their underlying mechanisms in the human lung carcinoma 95D cells (95D cells) were investigated. After treatment of 95D cell...
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| Veröffentlicht in: | Nutrients 2022-11, Vol.14 (21), p.4675 |
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| creator | Yin, Haowen Liu, Yuanyuan Yue, Hao Tian, Yingying Dong, Ping Xue, Changhu Zhao, Yun-Tao Zhao, Zifang Wang, Jingfeng |
| description | The antineoplastic effects of docosahexaenoic acid-containing phosphatidylcholine (DHA-PC) and eicosapentaenoic acid-containing phosphatidylcholine (EPA-PC) were explored, and their underlying mechanisms in the human lung carcinoma 95D cells (95D cells) were investigated. After treatment of 95D cells with DHA-PC or EPA-PC, cell biological behaviors such as growth, adhesion, migration, and invasion were studied. Immunofluorescence and western blotting were carried out to assess underlying molecular mechanisms. Results showed that 95D cells proliferation and adherence in the DHA-PC or EPA-PC group were drastically inhibited than the control group. DHA-PC and EPA-PC suppressed the migration and invasion of 95D cells by disrupting intracellular F-actin, which drives cell movement. The protein expression of PPARγ was induced versus the control group. Furthermore, critical factors related to invasion, including matrix metallopeptidase 9 (MMP9), heparanase (Hpa), and vascular endothelial growth factor (VEGF), were drastically downregulated through the PPARγ/NF-κB signaling pathway. C-X-C chemokine receptor type 4 (CXCR4) and cofilin were significantly suppressed via DHA-PC and EPA-PC through the PPARγ/phosphatase and tensin homolog (PTEN)/serine-threonine protein kinase (AKT) signaling pathway. DHA-PC and EPA-PC reversed the PPARγ antagonist GW9662-induced reduction of 95D cells in migration and invasion capacity, suggesting that PPARγ was directly involved in the anti-metastasis efficacy of DHA-PC and EPA-PC. In conclusion, DHA-PC and EPA-PC have great potential for cancer therapy, and the antineoplastic effects involve the activation of PPARγ. EPA-PC showed more pronounced antineoplastic effects than DHA-PC, possibly due to the more robust activation of PPARγ by EPA-PC. |
| doi_str_mv | 10.3390/nu14214675 |
| format | Article |
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After treatment of 95D cells with DHA-PC or EPA-PC, cell biological behaviors such as growth, adhesion, migration, and invasion were studied. Immunofluorescence and western blotting were carried out to assess underlying molecular mechanisms. Results showed that 95D cells proliferation and adherence in the DHA-PC or EPA-PC group were drastically inhibited than the control group. DHA-PC and EPA-PC suppressed the migration and invasion of 95D cells by disrupting intracellular F-actin, which drives cell movement. The protein expression of PPARγ was induced versus the control group. Furthermore, critical factors related to invasion, including matrix metallopeptidase 9 (MMP9), heparanase (Hpa), and vascular endothelial growth factor (VEGF), were drastically downregulated through the PPARγ/NF-κB signaling pathway. C-X-C chemokine receptor type 4 (CXCR4) and cofilin were significantly suppressed via DHA-PC and EPA-PC through the PPARγ/phosphatase and tensin homolog (PTEN)/serine-threonine protein kinase (AKT) signaling pathway. DHA-PC and EPA-PC reversed the PPARγ antagonist GW9662-induced reduction of 95D cells in migration and invasion capacity, suggesting that PPARγ was directly involved in the anti-metastasis efficacy of DHA-PC and EPA-PC. In conclusion, DHA-PC and EPA-PC have great potential for cancer therapy, and the antineoplastic effects involve the activation of PPARγ. EPA-PC showed more pronounced antineoplastic effects than DHA-PC, possibly due to the more robust activation of PPARγ by EPA-PC.</description><identifier>ISSN: 2072-6643</identifier><identifier>EISSN: 2072-6643</identifier><identifier>DOI: 10.3390/nu14214675</identifier><identifier>PMID: 36364935</identifier><language>eng</language><publisher>Basel: MDPI AG</publisher><subject>Actin ; AKT protein ; Angiogenesis ; Antibodies ; Cancer ; Carcinoma ; Care and treatment ; Cell adhesion & migration ; Cell culture ; Cell cycle ; Cell growth ; Cell proliferation ; Chemokine receptors ; Cofilin ; Comparative analysis ; CXCR4 protein ; Dietary supplements ; Docosahexaenoic acid ; Eicosapentaenoic acid ; Fatty acids ; Gelatinase B ; Growth factors ; Health aspects ; Immunofluorescence ; Kinases ; Lecithin ; Lipids ; Lung cancer ; Lung carcinoma ; Lungs ; Matrix metalloproteinases ; Metalloproteinase ; Metastases ; Metastasis ; Molecular modelling ; Muscle proteins ; NF-κB protein ; Omega-3 fatty acids ; Peroxisome proliferator-activated receptors ; Phosphatases ; Phosphatidylcholine ; Phospholipids ; Physiological aspects ; Prevention ; Protein kinase ; Proteins ; PTEN protein ; Signal transduction ; Tensin ; Unsaturated fatty acids ; Vascular endothelial growth factor ; Western blotting</subject><ispartof>Nutrients, 2022-11, Vol.14 (21), p.4675</ispartof><rights>COPYRIGHT 2022 MDPI AG</rights><rights>2022 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2022 by the authors. 2022</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c450t-6d09aed75b6d8506e7fa147f941f9afca160a9b504d9172fc30b305f6f77fa573</citedby><cites>FETCH-LOGICAL-c450t-6d09aed75b6d8506e7fa147f941f9afca160a9b504d9172fc30b305f6f77fa573</cites><orcidid>0000-0002-7236-7448</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/PMC9654432/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9654432/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids></links><search><creatorcontrib>Yin, Haowen</creatorcontrib><creatorcontrib>Liu, Yuanyuan</creatorcontrib><creatorcontrib>Yue, Hao</creatorcontrib><creatorcontrib>Tian, Yingying</creatorcontrib><creatorcontrib>Dong, Ping</creatorcontrib><creatorcontrib>Xue, Changhu</creatorcontrib><creatorcontrib>Zhao, Yun-Tao</creatorcontrib><creatorcontrib>Zhao, Zifang</creatorcontrib><creatorcontrib>Wang, Jingfeng</creatorcontrib><title>DHA- and EPA-Enriched Phosphatidylcholine Suppress Human Lung Carcinoma 95D Cells Metastasis via Activating the Peroxisome Proliferator-Activated Receptor γ</title><title>Nutrients</title><description>The antineoplastic effects of docosahexaenoic acid-containing phosphatidylcholine (DHA-PC) and eicosapentaenoic acid-containing phosphatidylcholine (EPA-PC) were explored, and their underlying mechanisms in the human lung carcinoma 95D cells (95D cells) were investigated. After treatment of 95D cells with DHA-PC or EPA-PC, cell biological behaviors such as growth, adhesion, migration, and invasion were studied. Immunofluorescence and western blotting were carried out to assess underlying molecular mechanisms. Results showed that 95D cells proliferation and adherence in the DHA-PC or EPA-PC group were drastically inhibited than the control group. DHA-PC and EPA-PC suppressed the migration and invasion of 95D cells by disrupting intracellular F-actin, which drives cell movement. The protein expression of PPARγ was induced versus the control group. Furthermore, critical factors related to invasion, including matrix metallopeptidase 9 (MMP9), heparanase (Hpa), and vascular endothelial growth factor (VEGF), were drastically downregulated through the PPARγ/NF-κB signaling pathway. C-X-C chemokine receptor type 4 (CXCR4) and cofilin were significantly suppressed via DHA-PC and EPA-PC through the PPARγ/phosphatase and tensin homolog (PTEN)/serine-threonine protein kinase (AKT) signaling pathway. DHA-PC and EPA-PC reversed the PPARγ antagonist GW9662-induced reduction of 95D cells in migration and invasion capacity, suggesting that PPARγ was directly involved in the anti-metastasis efficacy of DHA-PC and EPA-PC. In conclusion, DHA-PC and EPA-PC have great potential for cancer therapy, and the antineoplastic effects involve the activation of PPARγ. EPA-PC showed more pronounced antineoplastic effects than DHA-PC, possibly due to the more robust activation of PPARγ by EPA-PC.</description><subject>Actin</subject><subject>AKT protein</subject><subject>Angiogenesis</subject><subject>Antibodies</subject><subject>Cancer</subject><subject>Carcinoma</subject><subject>Care and treatment</subject><subject>Cell adhesion & migration</subject><subject>Cell culture</subject><subject>Cell cycle</subject><subject>Cell growth</subject><subject>Cell proliferation</subject><subject>Chemokine receptors</subject><subject>Cofilin</subject><subject>Comparative analysis</subject><subject>CXCR4 protein</subject><subject>Dietary supplements</subject><subject>Docosahexaenoic acid</subject><subject>Eicosapentaenoic acid</subject><subject>Fatty acids</subject><subject>Gelatinase B</subject><subject>Growth factors</subject><subject>Health aspects</subject><subject>Immunofluorescence</subject><subject>Kinases</subject><subject>Lecithin</subject><subject>Lipids</subject><subject>Lung cancer</subject><subject>Lung carcinoma</subject><subject>Lungs</subject><subject>Matrix metalloproteinases</subject><subject>Metalloproteinase</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>Molecular modelling</subject><subject>Muscle proteins</subject><subject>NF-κB protein</subject><subject>Omega-3 fatty acids</subject><subject>Peroxisome proliferator-activated receptors</subject><subject>Phosphatases</subject><subject>Phosphatidylcholine</subject><subject>Phospholipids</subject><subject>Physiological aspects</subject><subject>Prevention</subject><subject>Protein kinase</subject><subject>Proteins</subject><subject>PTEN protein</subject><subject>Signal transduction</subject><subject>Tensin</subject><subject>Unsaturated fatty acids</subject><subject>Vascular endothelial growth factor</subject><subject>Western blotting</subject><issn>2072-6643</issn><issn>2072-6643</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>BENPR</sourceid><recordid>eNptkl1q3DAQx01pacI2Lz2BoC-l4FS2vtYvBbPZdgNbuvTjWWjl0VrBllzJXprD9BS9R88UmSxNUyoJNIx-8x_NMFn2ssCXhFT4rZsKWhaUC_YkOy-xKHPOKXn6l32WXcR4g-clsODkeXZGOOG0Iuw8-3m1qXOkXIPWuzpfu2B1Cw3atT4OrRptc9vp1nfWAfoyDUOAGNFm6pVD28kd0EoFbZ3vFarYFVpB10X0EUYV07ERHa1CtR7tMSklemwB7SD4Hzb6PpkhCRsIavQhP2Ep92fQMCQX-v3rRfbMqC7CxeleZN_er7-uNvn204frVb3NNWV4zHmDKwWNYHveLBnmIIwqqDAVLUyljFYFx6raM0ybqhCl0QTvCWaGG5FIJsgie3evO0z7HhoNbgyqk0OwvQq30isrH78428qDP8qKM0pJmQRenwSC_z5BHGVvo07tUA78FGUpCFsKOrd_kb36B73xU3CpvJmivCoZXT5QB9WBtM74lFfPorIWlJOSFeX878v_UGk30FvtHRib_I8C3twH6OBjDGD-1FhgOc-TfJgncgcucbzS</recordid><startdate>20221101</startdate><enddate>20221101</enddate><creator>Yin, Haowen</creator><creator>Liu, Yuanyuan</creator><creator>Yue, Hao</creator><creator>Tian, Yingying</creator><creator>Dong, Ping</creator><creator>Xue, Changhu</creator><creator>Zhao, Yun-Tao</creator><creator>Zhao, Zifang</creator><creator>Wang, Jingfeng</creator><general>MDPI AG</general><general>MDPI</general><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7TS</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-7236-7448</orcidid></search><sort><creationdate>20221101</creationdate><title>DHA- and EPA-Enriched Phosphatidylcholine Suppress Human Lung Carcinoma 95D Cells Metastasis via Activating the Peroxisome Proliferator-Activated Receptor γ</title><author>Yin, Haowen ; Liu, Yuanyuan ; Yue, Hao ; Tian, Yingying ; Dong, Ping ; Xue, Changhu ; Zhao, Yun-Tao ; Zhao, Zifang ; Wang, Jingfeng</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c450t-6d09aed75b6d8506e7fa147f941f9afca160a9b504d9172fc30b305f6f77fa573</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Actin</topic><topic>AKT protein</topic><topic>Angiogenesis</topic><topic>Antibodies</topic><topic>Cancer</topic><topic>Carcinoma</topic><topic>Care and treatment</topic><topic>Cell adhesion & migration</topic><topic>Cell culture</topic><topic>Cell cycle</topic><topic>Cell growth</topic><topic>Cell proliferation</topic><topic>Chemokine receptors</topic><topic>Cofilin</topic><topic>Comparative analysis</topic><topic>CXCR4 protein</topic><topic>Dietary supplements</topic><topic>Docosahexaenoic acid</topic><topic>Eicosapentaenoic acid</topic><topic>Fatty acids</topic><topic>Gelatinase B</topic><topic>Growth factors</topic><topic>Health aspects</topic><topic>Immunofluorescence</topic><topic>Kinases</topic><topic>Lecithin</topic><topic>Lipids</topic><topic>Lung cancer</topic><topic>Lung carcinoma</topic><topic>Lungs</topic><topic>Matrix metalloproteinases</topic><topic>Metalloproteinase</topic><topic>Metastases</topic><topic>Metastasis</topic><topic>Molecular modelling</topic><topic>Muscle proteins</topic><topic>NF-κB protein</topic><topic>Omega-3 fatty acids</topic><topic>Peroxisome proliferator-activated receptors</topic><topic>Phosphatases</topic><topic>Phosphatidylcholine</topic><topic>Phospholipids</topic><topic>Physiological aspects</topic><topic>Prevention</topic><topic>Protein kinase</topic><topic>Proteins</topic><topic>PTEN protein</topic><topic>Signal transduction</topic><topic>Tensin</topic><topic>Unsaturated fatty acids</topic><topic>Vascular endothelial growth factor</topic><topic>Western blotting</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yin, Haowen</creatorcontrib><creatorcontrib>Liu, Yuanyuan</creatorcontrib><creatorcontrib>Yue, Hao</creatorcontrib><creatorcontrib>Tian, Yingying</creatorcontrib><creatorcontrib>Dong, Ping</creatorcontrib><creatorcontrib>Xue, Changhu</creatorcontrib><creatorcontrib>Zhao, Yun-Tao</creatorcontrib><creatorcontrib>Zhao, Zifang</creatorcontrib><creatorcontrib>Wang, Jingfeng</creatorcontrib><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Physical Education Index</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</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>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Nutrients</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yin, Haowen</au><au>Liu, Yuanyuan</au><au>Yue, Hao</au><au>Tian, Yingying</au><au>Dong, Ping</au><au>Xue, Changhu</au><au>Zhao, Yun-Tao</au><au>Zhao, Zifang</au><au>Wang, Jingfeng</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>DHA- and EPA-Enriched Phosphatidylcholine Suppress Human Lung Carcinoma 95D Cells Metastasis via Activating the Peroxisome Proliferator-Activated Receptor γ</atitle><jtitle>Nutrients</jtitle><date>2022-11-01</date><risdate>2022</risdate><volume>14</volume><issue>21</issue><spage>4675</spage><pages>4675-</pages><issn>2072-6643</issn><eissn>2072-6643</eissn><abstract>The antineoplastic effects of docosahexaenoic acid-containing phosphatidylcholine (DHA-PC) and eicosapentaenoic acid-containing phosphatidylcholine (EPA-PC) were explored, and their underlying mechanisms in the human lung carcinoma 95D cells (95D cells) were investigated. After treatment of 95D cells with DHA-PC or EPA-PC, cell biological behaviors such as growth, adhesion, migration, and invasion were studied. Immunofluorescence and western blotting were carried out to assess underlying molecular mechanisms. Results showed that 95D cells proliferation and adherence in the DHA-PC or EPA-PC group were drastically inhibited than the control group. DHA-PC and EPA-PC suppressed the migration and invasion of 95D cells by disrupting intracellular F-actin, which drives cell movement. The protein expression of PPARγ was induced versus the control group. Furthermore, critical factors related to invasion, including matrix metallopeptidase 9 (MMP9), heparanase (Hpa), and vascular endothelial growth factor (VEGF), were drastically downregulated through the PPARγ/NF-κB signaling pathway. C-X-C chemokine receptor type 4 (CXCR4) and cofilin were significantly suppressed via DHA-PC and EPA-PC through the PPARγ/phosphatase and tensin homolog (PTEN)/serine-threonine protein kinase (AKT) signaling pathway. DHA-PC and EPA-PC reversed the PPARγ antagonist GW9662-induced reduction of 95D cells in migration and invasion capacity, suggesting that PPARγ was directly involved in the anti-metastasis efficacy of DHA-PC and EPA-PC. In conclusion, DHA-PC and EPA-PC have great potential for cancer therapy, and the antineoplastic effects involve the activation of PPARγ. EPA-PC showed more pronounced antineoplastic effects than DHA-PC, possibly due to the more robust activation of PPARγ by EPA-PC.</abstract><cop>Basel</cop><pub>MDPI AG</pub><pmid>36364935</pmid><doi>10.3390/nu14214675</doi><orcidid>https://orcid.org/0000-0002-7236-7448</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Actin AKT protein Angiogenesis Antibodies Cancer Carcinoma Care and treatment Cell adhesion & migration Cell culture Cell cycle Cell growth Cell proliferation Chemokine receptors Cofilin Comparative analysis CXCR4 protein Dietary supplements Docosahexaenoic acid Eicosapentaenoic acid Fatty acids Gelatinase B Growth factors Health aspects Immunofluorescence Kinases Lecithin Lipids Lung cancer Lung carcinoma Lungs Matrix metalloproteinases Metalloproteinase Metastases Metastasis Molecular modelling Muscle proteins NF-κB protein Omega-3 fatty acids Peroxisome proliferator-activated receptors Phosphatases Phosphatidylcholine Phospholipids Physiological aspects Prevention Protein kinase Proteins PTEN protein Signal transduction Tensin Unsaturated fatty acids Vascular endothelial growth factor Western blotting |
| title | DHA- and EPA-Enriched Phosphatidylcholine Suppress Human Lung Carcinoma 95D Cells Metastasis via Activating the Peroxisome Proliferator-Activated Receptor γ |
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