Sodium selenite inhibits leukemia HL-60 cell proliferation and induces cell apoptosis by enhancing the phosphorylation of JNK1 and increasing the expression of p21 and p27
Selenium is an essential trace element and has shown chemopreventive or therapeutic activities on human solid cancers; however, whether it has anticancer effects on leukemia has not yet been elucidated. The present study was designed to determine the role of selenium on HL-60 human promyelocytic leu...
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| Veröffentlicht in: | International journal of molecular medicine 2014-10, Vol.34 (4), p.1175-1179 |
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| creator | WU, SUN BAO, YONGHUA MA, DONG ZI, YOUMEI YANG, CUI YANG, MAN XING, MENGTAO YANG, WANCAI |
| description | Selenium is an essential trace element and has shown chemopreventive or therapeutic activities on human solid cancers; however, whether it has anticancer effects on leukemia has not yet been elucidated. The present study was designed to determine the role of selenium on HL-60 human promyelocytic leukemia cells. We found that 100 nM of sodium selenite (Se) had no significant effects on cell proliferation, apoptosis and the cell cycle; however, a higher concentration of 250 nM of Se significantly inhibited cell proliferation, promoted apoptosis and induced cell cycle arrest at the S phase after 48 h of treatment (P |
| doi_str_mv | 10.3892/ijmm.2014.1854 |
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The present study was designed to determine the role of selenium on HL-60 human promyelocytic leukemia cells. We found that 100 nM of sodium selenite (Se) had no significant effects on cell proliferation, apoptosis and the cell cycle; however, a higher concentration of 250 nM of Se significantly inhibited cell proliferation, promoted apoptosis and induced cell cycle arrest at the S phase after 48 h of treatment (P<0.05), thus demonstrating the anticancer activities of selenium in leukemia. However, the decrease in c-Jun NH2-terminal kinase 1 (JNK1) expression by targeting JNK1 using small interfering RNA attenuated the inhibitory effects of Se on cell proliferation and the induction of apoptosis. Mechanistic studies showed that the anticancer activities of Se were associated with the enhanced phosphorylation of JNK1 and the increased expression of the cell cycle regulators, p21 and p27, as well as the downregulation of cyclin D1. Our data provide further evidence that the appropriate concentration of selenium has therapeutic potential in leukemia.</description><identifier>ISSN: 1107-3756</identifier><identifier>EISSN: 1791-244X</identifier><identifier>DOI: 10.3892/ijmm.2014.1854</identifier><identifier>PMID: 25198010</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>Apoptosis ; Apoptosis - drug effects ; Biotechnology ; c-Jun NH2- terminal kinase 1 ; Cancer therapies ; Care and treatment ; Cell cycle ; Cell Cycle - drug effects ; Cell growth ; Cell proliferation ; Cell Proliferation - drug effects ; Clinical trials ; Colorectal cancer ; Cyclin-Dependent Kinase Inhibitor p21 - metabolism ; Cyclin-Dependent Kinase Inhibitor p27 - metabolism ; Cyclin-dependent kinases ; Disease prevention ; Genetic aspects ; HL-60 Cells ; Humans ; JNK Mitogen-Activated Protein Kinases - metabolism ; Kinases ; Leukemia ; Models, Biological ; p21 ; p27 ; Phosphorylation ; Phosphorylation - drug effects ; proliferation ; Properties ; Proteins ; Roles ; Selenium ; Selenium compounds ; Sodium Selenite - pharmacology ; Studies ; Testing ; Tumor suppressor genes</subject><ispartof>International journal of molecular medicine, 2014-10, Vol.34 (4), p.1175-1179</ispartof><rights>Copyright © 2014, Spandidos Publications</rights><rights>COPYRIGHT 2014 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2014</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c463t-340c287782ae69e81b2c17621d15d5b5e1c0137dc30d97ebf8af24df6e800d393</citedby><cites>FETCH-LOGICAL-c463t-340c287782ae69e81b2c17621d15d5b5e1c0137dc30d97ebf8af24df6e800d393</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785,5573,27929,27930</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25198010$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>WU, SUN</creatorcontrib><creatorcontrib>BAO, YONGHUA</creatorcontrib><creatorcontrib>MA, DONG</creatorcontrib><creatorcontrib>ZI, YOUMEI</creatorcontrib><creatorcontrib>YANG, CUI</creatorcontrib><creatorcontrib>YANG, MAN</creatorcontrib><creatorcontrib>XING, MENGTAO</creatorcontrib><creatorcontrib>YANG, WANCAI</creatorcontrib><title>Sodium selenite inhibits leukemia HL-60 cell proliferation and induces cell apoptosis by enhancing the phosphorylation of JNK1 and increasing the expression of p21 and p27</title><title>International journal of molecular medicine</title><addtitle>Int J Mol Med</addtitle><description>Selenium is an essential trace element and has shown chemopreventive or therapeutic activities on human solid cancers; however, whether it has anticancer effects on leukemia has not yet been elucidated. The present study was designed to determine the role of selenium on HL-60 human promyelocytic leukemia cells. We found that 100 nM of sodium selenite (Se) had no significant effects on cell proliferation, apoptosis and the cell cycle; however, a higher concentration of 250 nM of Se significantly inhibited cell proliferation, promoted apoptosis and induced cell cycle arrest at the S phase after 48 h of treatment (P<0.05), thus demonstrating the anticancer activities of selenium in leukemia. However, the decrease in c-Jun NH2-terminal kinase 1 (JNK1) expression by targeting JNK1 using small interfering RNA attenuated the inhibitory effects of Se on cell proliferation and the induction of apoptosis. Mechanistic studies showed that the anticancer activities of Se were associated with the enhanced phosphorylation of JNK1 and the increased expression of the cell cycle regulators, p21 and p27, as well as the downregulation of cyclin D1. Our data provide further evidence that the appropriate concentration of selenium has therapeutic potential in leukemia.</description><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Biotechnology</subject><subject>c-Jun NH2- terminal kinase 1</subject><subject>Cancer therapies</subject><subject>Care and treatment</subject><subject>Cell cycle</subject><subject>Cell Cycle - drug effects</subject><subject>Cell growth</subject><subject>Cell proliferation</subject><subject>Cell Proliferation - drug effects</subject><subject>Clinical trials</subject><subject>Colorectal cancer</subject><subject>Cyclin-Dependent Kinase Inhibitor p21 - metabolism</subject><subject>Cyclin-Dependent Kinase Inhibitor p27 - metabolism</subject><subject>Cyclin-dependent kinases</subject><subject>Disease prevention</subject><subject>Genetic aspects</subject><subject>HL-60 Cells</subject><subject>Humans</subject><subject>JNK Mitogen-Activated Protein Kinases - metabolism</subject><subject>Kinases</subject><subject>Leukemia</subject><subject>Models, Biological</subject><subject>p21</subject><subject>p27</subject><subject>Phosphorylation</subject><subject>Phosphorylation - drug effects</subject><subject>proliferation</subject><subject>Properties</subject><subject>Proteins</subject><subject>Roles</subject><subject>Selenium</subject><subject>Selenium compounds</subject><subject>Sodium Selenite - pharmacology</subject><subject>Studies</subject><subject>Testing</subject><subject>Tumor suppressor genes</subject><issn>1107-3756</issn><issn>1791-244X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNptkUtv1DAUhSMEog_YskSW2HSTwa_EzrKqgAKjdgFI7CzHvul4SOxgJ1LnN_En6yjTsqksy1f2d47te4riHcEbJhv60e2HYUMx4RsiK_6iOCWiISXl_PfLXBMsSiaq-qQ4S2mPMa14I18XJ7QijcQEnxb_fgTr5gEl6MG7CZDzO9e6KaEe5j8wOI2ut2WNkYG-R2MMvesg6skFj7S3GbezgbQe6zGMU0guofaAwO-0N87foWkHaNyFlGc89Ks2dOjbzXdy9DARdHpE4X6MkNKRGukKjVS8KV51uk_w9rieF78-f_p5dV1ub798vbrclobXbCoZx4ZKISTVUDcgSUsNETUlllS2aisgBhMmrGHYNgLaTuqOctvVIDG2rGHnxYfVN3_37wxpUvswR5-vVKRhlPGGCf6futM9KOe7MEVtBpeMumSSV5xTwTK1eYbKw-bemuChc3n_OYGJIaUInRqjG3Q8KILVErlaIldL5GqJPAveH187twPYJ_wx4wxcrEAacyOdDemJWaxyv0rMS0JExR4A2CS1EA</recordid><startdate>20141001</startdate><enddate>20141001</enddate><creator>WU, SUN</creator><creator>BAO, YONGHUA</creator><creator>MA, DONG</creator><creator>ZI, YOUMEI</creator><creator>YANG, CUI</creator><creator>YANG, MAN</creator><creator>XING, MENGTAO</creator><creator>YANG, WANCAI</creator><general>D.A. 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drug effects</topic><topic>Biotechnology</topic><topic>c-Jun NH2- terminal kinase 1</topic><topic>Cancer therapies</topic><topic>Care and treatment</topic><topic>Cell cycle</topic><topic>Cell Cycle - drug effects</topic><topic>Cell growth</topic><topic>Cell proliferation</topic><topic>Cell Proliferation - drug effects</topic><topic>Clinical trials</topic><topic>Colorectal cancer</topic><topic>Cyclin-Dependent Kinase Inhibitor p21 - metabolism</topic><topic>Cyclin-Dependent Kinase Inhibitor p27 - metabolism</topic><topic>Cyclin-dependent kinases</topic><topic>Disease prevention</topic><topic>Genetic aspects</topic><topic>HL-60 Cells</topic><topic>Humans</topic><topic>JNK Mitogen-Activated Protein Kinases - metabolism</topic><topic>Kinases</topic><topic>Leukemia</topic><topic>Models, Biological</topic><topic>p21</topic><topic>p27</topic><topic>Phosphorylation</topic><topic>Phosphorylation - drug effects</topic><topic>proliferation</topic><topic>Properties</topic><topic>Proteins</topic><topic>Roles</topic><topic>Selenium</topic><topic>Selenium compounds</topic><topic>Sodium Selenite - 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The present study was designed to determine the role of selenium on HL-60 human promyelocytic leukemia cells. We found that 100 nM of sodium selenite (Se) had no significant effects on cell proliferation, apoptosis and the cell cycle; however, a higher concentration of 250 nM of Se significantly inhibited cell proliferation, promoted apoptosis and induced cell cycle arrest at the S phase after 48 h of treatment (P<0.05), thus demonstrating the anticancer activities of selenium in leukemia. However, the decrease in c-Jun NH2-terminal kinase 1 (JNK1) expression by targeting JNK1 using small interfering RNA attenuated the inhibitory effects of Se on cell proliferation and the induction of apoptosis. Mechanistic studies showed that the anticancer activities of Se were associated with the enhanced phosphorylation of JNK1 and the increased expression of the cell cycle regulators, p21 and p27, as well as the downregulation of cyclin D1. Our data provide further evidence that the appropriate concentration of selenium has therapeutic potential in leukemia.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>25198010</pmid><doi>10.3892/ijmm.2014.1854</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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| source | Spandidos Publications Journals; MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Apoptosis Apoptosis - drug effects Biotechnology c-Jun NH2- terminal kinase 1 Cancer therapies Care and treatment Cell cycle Cell Cycle - drug effects Cell growth Cell proliferation Cell Proliferation - drug effects Clinical trials Colorectal cancer Cyclin-Dependent Kinase Inhibitor p21 - metabolism Cyclin-Dependent Kinase Inhibitor p27 - metabolism Cyclin-dependent kinases Disease prevention Genetic aspects HL-60 Cells Humans JNK Mitogen-Activated Protein Kinases - metabolism Kinases Leukemia Models, Biological p21 p27 Phosphorylation Phosphorylation - drug effects proliferation Properties Proteins Roles Selenium Selenium compounds Sodium Selenite - pharmacology Studies Testing Tumor suppressor genes |
| title | Sodium selenite inhibits leukemia HL-60 cell proliferation and induces cell apoptosis by enhancing the phosphorylation of JNK1 and increasing the expression of p21 and p27 |
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