Omega-3 Polyunsaturated Fatty Acids Trigger Cell Cycle Arrest and Induce Apoptosis in Human Neuroblastoma LA-N-1 Cells
Omega-3 (n-3) fatty acids are dietary long-chain fatty acids with an array of health benefits. Previous research has demonstrated the growth-inhibitory effect of n-3 fatty acids on different cancer cell lines in vitro, yet their anti-tumor effects and underlying action mechanisms on human neuroblast...
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| Veröffentlicht in: | Nutrients 2015-08, Vol.7 (8), p.6956-6973 |
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| description | Omega-3 (n-3) fatty acids are dietary long-chain fatty acids with an array of health benefits. Previous research has demonstrated the growth-inhibitory effect of n-3 fatty acids on different cancer cell lines in vitro, yet their anti-tumor effects and underlying action mechanisms on human neuroblastoma LA-N-1 cells have not yet been reported. In this study, we showed that docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) exhibited time- and concentration-dependent anti-proliferative effect on the human neuroblastoma LA-N-1 cells, but had minimal cytotoxicity on the normal or non-tumorigenic cells, as measured by MTT reduction assay. Mechanistic studies indicated that DHA and EPA triggered G0/G1 cell cycle arrest in LA-N-1 cells, as detected by flow cytometry, which was accompanied by a decrease in the expression of CDK2 and cyclin E proteins. Moreover, DHA and EPA could also induce apoptosis in LA-N-1 cells as revealed by an increase in DNA fragmentation, phosphatidylserine externalization and mitochondrial membrane depolarization. Up-regulation of Bax, activated caspase-3 and caspase-9 proteins, and down-regulation of Bcl-XL protein, might account for the occurrence of apoptotic events. Collectively, our results suggest that the growth-inhibitory effect of DHA and EPA on LA-N-1 cells might be mediated, at least in part, via triggering of cell cycle arrest and apoptosis. Therefore, DHA and EPA are potential anti-cancer agents which might be used for the adjuvant therapy or combination therapy with the conventional anti-cancer drugs for the treatment of some forms of human neuroblastoma with minimal toxicity. |
| doi_str_mv | 10.3390/nu7085319 |
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Previous research has demonstrated the growth-inhibitory effect of n-3 fatty acids on different cancer cell lines in vitro, yet their anti-tumor effects and underlying action mechanisms on human neuroblastoma LA-N-1 cells have not yet been reported. In this study, we showed that docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) exhibited time- and concentration-dependent anti-proliferative effect on the human neuroblastoma LA-N-1 cells, but had minimal cytotoxicity on the normal or non-tumorigenic cells, as measured by MTT reduction assay. Mechanistic studies indicated that DHA and EPA triggered G0/G1 cell cycle arrest in LA-N-1 cells, as detected by flow cytometry, which was accompanied by a decrease in the expression of CDK2 and cyclin E proteins. Moreover, DHA and EPA could also induce apoptosis in LA-N-1 cells as revealed by an increase in DNA fragmentation, phosphatidylserine externalization and mitochondrial membrane depolarization. Up-regulation of Bax, activated caspase-3 and caspase-9 proteins, and down-regulation of Bcl-XL protein, might account for the occurrence of apoptotic events. Collectively, our results suggest that the growth-inhibitory effect of DHA and EPA on LA-N-1 cells might be mediated, at least in part, via triggering of cell cycle arrest and apoptosis. Therefore, DHA and EPA are potential anti-cancer agents which might be used for the adjuvant therapy or combination therapy with the conventional anti-cancer drugs for the treatment of some forms of human neuroblastoma with minimal toxicity.</description><identifier>ISSN: 2072-6643</identifier><identifier>EISSN: 2072-6643</identifier><identifier>DOI: 10.3390/nu7085319</identifier><identifier>PMID: 26295255</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>adjuvants ; Antibiotics ; antineoplastic activity ; antineoplastic agents ; Antineoplastic Agents - pharmacology ; Apoptosis ; Apoptosis - drug effects ; bcl-2-Associated X Protein - genetics ; bcl-2-Associated X Protein - metabolism ; bcl-X Protein - genetics ; bcl-X Protein - metabolism ; Cancer therapies ; Carbon ; Caspase 3 - genetics ; Caspase 3 - metabolism ; Caspase 9 - genetics ; Caspase 9 - metabolism ; caspase-3 ; caspase-9 ; Cell cycle ; cell cycle checkpoints ; Cell Cycle Checkpoints - drug effects ; Cell Line, Tumor ; cell lines ; Chemotherapy ; cyclin-dependent kinase ; cyclins ; Cytotoxicity ; DNA fragmentation ; DNA Fragmentation - drug effects ; docosahexaenoic acid ; Docosahexaenoic Acids - pharmacology ; Down-Regulation ; eicosapentaenoic acid ; Eicosapentaenoic Acid - pharmacology ; Fatty acids ; flow cytometry ; HEK293 Cells ; Humans ; Melanoma ; Metastasis ; mitochondrial membrane ; neoplasm cells ; Neuroblastoma ; Neuroblastoma - pathology ; omega-3 fatty acids ; phosphatidylserines ; Radiation therapy ; therapeutics ; Up-Regulation</subject><ispartof>Nutrients, 2015-08, Vol.7 (8), p.6956-6973</ispartof><rights>Copyright MDPI AG 2015</rights><rights>2015 by the authors; licensee MDPI, Basel, Switzerland. 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c469t-5a7b9b55b4f0e82fde6e671124a4634327829e7459cbfb0060de5ce6b8338d503</citedby><cites>FETCH-LOGICAL-c469t-5a7b9b55b4f0e82fde6e671124a4634327829e7459cbfb0060de5ce6b8338d503</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4555158/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4555158/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27903,27904,53769,53771</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26295255$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>So, Wai Wing</creatorcontrib><creatorcontrib>Liu, Wai Nam</creatorcontrib><creatorcontrib>Leung, Kwok Nam</creatorcontrib><title>Omega-3 Polyunsaturated Fatty Acids Trigger Cell Cycle Arrest and Induce Apoptosis in Human Neuroblastoma LA-N-1 Cells</title><title>Nutrients</title><addtitle>Nutrients</addtitle><description>Omega-3 (n-3) fatty acids are dietary long-chain fatty acids with an array of health benefits. Previous research has demonstrated the growth-inhibitory effect of n-3 fatty acids on different cancer cell lines in vitro, yet their anti-tumor effects and underlying action mechanisms on human neuroblastoma LA-N-1 cells have not yet been reported. In this study, we showed that docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) exhibited time- and concentration-dependent anti-proliferative effect on the human neuroblastoma LA-N-1 cells, but had minimal cytotoxicity on the normal or non-tumorigenic cells, as measured by MTT reduction assay. Mechanistic studies indicated that DHA and EPA triggered G0/G1 cell cycle arrest in LA-N-1 cells, as detected by flow cytometry, which was accompanied by a decrease in the expression of CDK2 and cyclin E proteins. Moreover, DHA and EPA could also induce apoptosis in LA-N-1 cells as revealed by an increase in DNA fragmentation, phosphatidylserine externalization and mitochondrial membrane depolarization. Up-regulation of Bax, activated caspase-3 and caspase-9 proteins, and down-regulation of Bcl-XL protein, might account for the occurrence of apoptotic events. Collectively, our results suggest that the growth-inhibitory effect of DHA and EPA on LA-N-1 cells might be mediated, at least in part, via triggering of cell cycle arrest and apoptosis. Therefore, DHA and EPA are potential anti-cancer agents which might be used for the adjuvant therapy or combination therapy with the conventional anti-cancer drugs for the treatment of some forms of human neuroblastoma with minimal toxicity.</description><subject>adjuvants</subject><subject>Antibiotics</subject><subject>antineoplastic activity</subject><subject>antineoplastic agents</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>bcl-2-Associated X Protein - genetics</subject><subject>bcl-2-Associated X Protein - metabolism</subject><subject>bcl-X Protein - genetics</subject><subject>bcl-X Protein - metabolism</subject><subject>Cancer therapies</subject><subject>Carbon</subject><subject>Caspase 3 - genetics</subject><subject>Caspase 3 - metabolism</subject><subject>Caspase 9 - genetics</subject><subject>Caspase 9 - metabolism</subject><subject>caspase-3</subject><subject>caspase-9</subject><subject>Cell cycle</subject><subject>cell cycle checkpoints</subject><subject>Cell Cycle Checkpoints - drug effects</subject><subject>Cell Line, Tumor</subject><subject>cell lines</subject><subject>Chemotherapy</subject><subject>cyclin-dependent kinase</subject><subject>cyclins</subject><subject>Cytotoxicity</subject><subject>DNA fragmentation</subject><subject>DNA Fragmentation - drug effects</subject><subject>docosahexaenoic acid</subject><subject>Docosahexaenoic Acids - pharmacology</subject><subject>Down-Regulation</subject><subject>eicosapentaenoic acid</subject><subject>Eicosapentaenoic Acid - pharmacology</subject><subject>Fatty acids</subject><subject>flow cytometry</subject><subject>HEK293 Cells</subject><subject>Humans</subject><subject>Melanoma</subject><subject>Metastasis</subject><subject>mitochondrial membrane</subject><subject>neoplasm cells</subject><subject>Neuroblastoma</subject><subject>Neuroblastoma - pathology</subject><subject>omega-3 fatty acids</subject><subject>phosphatidylserines</subject><subject>Radiation therapy</subject><subject>therapeutics</subject><subject>Up-Regulation</subject><issn>2072-6643</issn><issn>2072-6643</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqNkstrFTEYxYMottQu_Ack4EYXo3k_NsLlYh9waV3UdchkMtcpM8k1j8L9701te6lu9NvkI_lxyDkcAN5i9IlSjT6HKpHiFOsX4JggSTohGH35bD8CpznfovuRSAr6GhwRQTQnnB-Du-vFb21H4bc472vIttRkix_gmS1lD1duGjK8SdN26xNc-3mG672bPVyl5HOBNgzwMgzVtZtd3JWYpwynAC_qYgO88jXFfra5xMXCzaq76vBvkfwGvBrtnP3p43kCvp99vVlfdJvr88v1atM5JnTpuJW97jnv2Yi8IuPghRcSY8IsE5RRIhXRXjKuXT_2CAk0eO686BWlauCInoAvD7q72i9-cD6UZGezS9Ni095EO5k_X8L0w2zjnWGcc8xVE_jwKJDiz9osm2XKrlmwwceaDSFKqPYJTf6JYikUV5Ih9B8oElxKRHVD3_-F3saaQgutUUQTLBWmjfr4QLkUc05-PFjEyNzXxBxq0th3zzM5kE-loL8AtUS2CA</recordid><startdate>20150818</startdate><enddate>20150818</enddate><creator>So, Wai Wing</creator><creator>Liu, Wai Nam</creator><creator>Leung, Kwok Nam</creator><general>MDPI AG</general><general>MDPI</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>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>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7S9</scope><scope>L.6</scope><scope>5PM</scope></search><sort><creationdate>20150818</creationdate><title>Omega-3 Polyunsaturated Fatty Acids Trigger Cell Cycle Arrest and Induce Apoptosis in Human Neuroblastoma LA-N-1 Cells</title><author>So, Wai Wing ; Liu, Wai Nam ; Leung, Kwok Nam</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c469t-5a7b9b55b4f0e82fde6e671124a4634327829e7459cbfb0060de5ce6b8338d503</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>adjuvants</topic><topic>Antibiotics</topic><topic>antineoplastic activity</topic><topic>antineoplastic agents</topic><topic>Antineoplastic Agents - pharmacology</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>bcl-2-Associated X Protein - genetics</topic><topic>bcl-2-Associated X Protein - metabolism</topic><topic>bcl-X Protein - genetics</topic><topic>bcl-X Protein - metabolism</topic><topic>Cancer therapies</topic><topic>Carbon</topic><topic>Caspase 3 - genetics</topic><topic>Caspase 3 - metabolism</topic><topic>Caspase 9 - genetics</topic><topic>Caspase 9 - metabolism</topic><topic>caspase-3</topic><topic>caspase-9</topic><topic>Cell cycle</topic><topic>cell cycle checkpoints</topic><topic>Cell Cycle Checkpoints - drug effects</topic><topic>Cell Line, Tumor</topic><topic>cell lines</topic><topic>Chemotherapy</topic><topic>cyclin-dependent kinase</topic><topic>cyclins</topic><topic>Cytotoxicity</topic><topic>DNA fragmentation</topic><topic>DNA Fragmentation - drug effects</topic><topic>docosahexaenoic acid</topic><topic>Docosahexaenoic Acids - pharmacology</topic><topic>Down-Regulation</topic><topic>eicosapentaenoic acid</topic><topic>Eicosapentaenoic Acid - pharmacology</topic><topic>Fatty acids</topic><topic>flow cytometry</topic><topic>HEK293 Cells</topic><topic>Humans</topic><topic>Melanoma</topic><topic>Metastasis</topic><topic>mitochondrial membrane</topic><topic>neoplasm cells</topic><topic>Neuroblastoma</topic><topic>Neuroblastoma - pathology</topic><topic>omega-3 fatty acids</topic><topic>phosphatidylserines</topic><topic>Radiation therapy</topic><topic>therapeutics</topic><topic>Up-Regulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>So, Wai Wing</creatorcontrib><creatorcontrib>Liu, Wai Nam</creatorcontrib><creatorcontrib>Leung, Kwok Nam</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>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>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>AGRICOLA</collection><collection>AGRICOLA - 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>So, Wai Wing</au><au>Liu, Wai Nam</au><au>Leung, Kwok Nam</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Omega-3 Polyunsaturated Fatty Acids Trigger Cell Cycle Arrest and Induce Apoptosis in Human Neuroblastoma LA-N-1 Cells</atitle><jtitle>Nutrients</jtitle><addtitle>Nutrients</addtitle><date>2015-08-18</date><risdate>2015</risdate><volume>7</volume><issue>8</issue><spage>6956</spage><epage>6973</epage><pages>6956-6973</pages><issn>2072-6643</issn><eissn>2072-6643</eissn><abstract>Omega-3 (n-3) fatty acids are dietary long-chain fatty acids with an array of health benefits. Previous research has demonstrated the growth-inhibitory effect of n-3 fatty acids on different cancer cell lines in vitro, yet their anti-tumor effects and underlying action mechanisms on human neuroblastoma LA-N-1 cells have not yet been reported. In this study, we showed that docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) exhibited time- and concentration-dependent anti-proliferative effect on the human neuroblastoma LA-N-1 cells, but had minimal cytotoxicity on the normal or non-tumorigenic cells, as measured by MTT reduction assay. Mechanistic studies indicated that DHA and EPA triggered G0/G1 cell cycle arrest in LA-N-1 cells, as detected by flow cytometry, which was accompanied by a decrease in the expression of CDK2 and cyclin E proteins. Moreover, DHA and EPA could also induce apoptosis in LA-N-1 cells as revealed by an increase in DNA fragmentation, phosphatidylserine externalization and mitochondrial membrane depolarization. Up-regulation of Bax, activated caspase-3 and caspase-9 proteins, and down-regulation of Bcl-XL protein, might account for the occurrence of apoptotic events. Collectively, our results suggest that the growth-inhibitory effect of DHA and EPA on LA-N-1 cells might be mediated, at least in part, via triggering of cell cycle arrest and apoptosis. Therefore, DHA and EPA are potential anti-cancer agents which might be used for the adjuvant therapy or combination therapy with the conventional anti-cancer drugs for the treatment of some forms of human neuroblastoma with minimal toxicity.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>26295255</pmid><doi>10.3390/nu7085319</doi><tpages>18</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | adjuvants Antibiotics antineoplastic activity antineoplastic agents Antineoplastic Agents - pharmacology Apoptosis Apoptosis - drug effects bcl-2-Associated X Protein - genetics bcl-2-Associated X Protein - metabolism bcl-X Protein - genetics bcl-X Protein - metabolism Cancer therapies Carbon Caspase 3 - genetics Caspase 3 - metabolism Caspase 9 - genetics Caspase 9 - metabolism caspase-3 caspase-9 Cell cycle cell cycle checkpoints Cell Cycle Checkpoints - drug effects Cell Line, Tumor cell lines Chemotherapy cyclin-dependent kinase cyclins Cytotoxicity DNA fragmentation DNA Fragmentation - drug effects docosahexaenoic acid Docosahexaenoic Acids - pharmacology Down-Regulation eicosapentaenoic acid Eicosapentaenoic Acid - pharmacology Fatty acids flow cytometry HEK293 Cells Humans Melanoma Metastasis mitochondrial membrane neoplasm cells Neuroblastoma Neuroblastoma - pathology omega-3 fatty acids phosphatidylserines Radiation therapy therapeutics Up-Regulation |
| title | Omega-3 Polyunsaturated Fatty Acids Trigger Cell Cycle Arrest and Induce Apoptosis in Human Neuroblastoma LA-N-1 Cells |
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