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Antileukemic activity of an arsenomolybdate in the human HL-60 and U937 leukemia cells
The antileukemic activity, mechanisms and serum albumin interactions of an arsenomolybdate, K2Na[AsMo6O21(O2CCH2NH3)3]·6H2O (1), was evaluated in the human leukemia HL-60 and U937 cells. The results indicated that 1 could inhibit the proliferation of both leukemia cell lines in a dose-dependent mann...
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| Published in: | Journal of inorganic biochemistry 2017-03, Vol.168, p.67-75 |
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| container_title | Journal of inorganic biochemistry |
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| creator | Li, Chunyan Cao, Hongqian Sun, Jiaheng Tian, Rui Li, Dongbei Qi, Yanfei Yang, Wei Li, Juan |
| description | The antileukemic activity, mechanisms and serum albumin interactions of an arsenomolybdate, K2Na[AsMo6O21(O2CCH2NH3)3]·6H2O (1), was evaluated in the human leukemia HL-60 and U937 cells. The results indicated that 1 could inhibit the proliferation of both leukemia cell lines in a dose-dependent manner with the 50% lethal concentration (IC50) value of 8.61μM for HL-60 and 14.50μM for U937 at 24h, compare to the positive controls, all-trans retinoic acid (ATRA) with IC50 value of 20.76μM and 14.85μM,and As2O3 with IC50 value of 6.40μM and 8.75μM at 24h, respectively (P |
| doi_str_mv | 10.1016/j.jinorgbio.2016.12.002 |
| format | article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1859755460</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0162013416304950</els_id><sourcerecordid>1859755460</sourcerecordid><originalsourceid>FETCH-LOGICAL-c408t-2008d5d1ecdf970e05e2f6c4c54edb00412831acabd17aaeb0d8eb22d101556c3</originalsourceid><addsrcrecordid>eNqFkEtPAjEQgBujEUT_gvboZddp98mREBUTEi_item2s1Lc3WK7S8K_twTk6mmSmW9eHyEPDGIGLH_axBvTWfdVGRvzkIgZjwH4BRmzskiiJEnTSzIOBR4BS9IRufF-AwBZlhbXZMTLkIU8H5PPWdebBodvbI2iUvVmZ_o9tTWVHZXOY2db2-wrLXukpqP9Gul6aENxsYxyCJSmq2lS0NMMSRU2jb8lV7VsPN6d4oSsXp4_5oto-f76Np8tI5VC2UccoNSZZqh0PS0AIUNe5ypVWYq6AkgZLxMmlaw0K6TECnSJFec6SMiyXCUT8nicu3X2Z0Dfi9b4wwWyQzt4wcpsWoSncwhocUSVs947rMXWmVa6vWAgDlLFRpylioNUwbgIUkPn_WnJULWoz31_FgMwOwIYXt0ZdMIrg51CbRyqXmhr_l3yCxhcjBc</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1859755460</pqid></control><display><type>article</type><title>Antileukemic activity of an arsenomolybdate in the human HL-60 and U937 leukemia cells</title><source>Elsevier</source><creator>Li, Chunyan ; Cao, Hongqian ; Sun, Jiaheng ; Tian, Rui ; Li, Dongbei ; Qi, Yanfei ; Yang, Wei ; Li, Juan</creator><creatorcontrib>Li, Chunyan ; Cao, Hongqian ; Sun, Jiaheng ; Tian, Rui ; Li, Dongbei ; Qi, Yanfei ; Yang, Wei ; Li, Juan</creatorcontrib><description>The antileukemic activity, mechanisms and serum albumin interactions of an arsenomolybdate, K2Na[AsMo6O21(O2CCH2NH3)3]·6H2O (1), was evaluated in the human leukemia HL-60 and U937 cells. The results indicated that 1 could inhibit the proliferation of both leukemia cell lines in a dose-dependent manner with the 50% lethal concentration (IC50) value of 8.61μM for HL-60 and 14.50μM for U937 at 24h, compare to the positive controls, all-trans retinoic acid (ATRA) with IC50 value of 20.76μM and 14.85μM,and As2O3 with IC50 value of 6.40μM and 8.75μM at 24h, respectively (P<0.05). Furthermore, the anti-leukemia activity of compound 1 might be medicated by arresting the leukemic cells in the G1 phase and inducing apoptosis via caspase-3 and bcl-2 regulatory proteins. Spectroscopic techniques results showed that the fluorescence of human serum albumin was quenched by compound 1, and the quenching mechanism was mainly static quenching. Compound 1 might be a potential medicinal candidate against acute promyelocytic leukemia.
The antileukemic activity of an arsenomolybdate, K2Na[AsMo6O21 (O2CCH2NH3)3]·6H2O 1 has been investigated. The results indicated that 1 could inhibit the proliferation of HL-60 and U937 cells, arrest the leukemic cells in the G1 phase and induce apoptosis. Compound 1 might be a potential candidate against acute promyelocytic leukemia. [Display omitted]
•Arsenomolybdate-induced apoptosis in leukemia cells via caspase-3 regulatory protein•Arsenomolybdate-induced apoptosis in leukemia cells via the bcl-2 regulatory protein•Arsenomolybdate arrests the leukemic cells in the G1 phase.•The main quenching mechanism for arsenomolybdate and human serum albumin was static quenching.</description><identifier>ISSN: 0162-0134</identifier><identifier>EISSN: 1873-3344</identifier><identifier>DOI: 10.1016/j.jinorgbio.2016.12.002</identifier><identifier>PMID: 28013066</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Acute promyelocytic leukemia ; Antineoplastic Agents - chemical synthesis ; Antineoplastic Agents - chemistry ; Antineoplastic Agents - pharmacology ; Apoptosis ; Apoptosis - drug effects ; Arsenicals - chemical synthesis ; Arsenicals - chemistry ; Arsenicals - pharmacology ; Arsenomolybdate ; Blotting, Western ; Caspase 3 - drug effects ; Cell Cycle - drug effects ; Cell Proliferation - drug effects ; Drug Stability ; Flow Cytometry ; Fluorescence ; HL-60 Cells ; Humans ; Inhibitory Concentration 50 ; Leukemia, Promyelocytic, Acute - drug therapy ; Molybdenum - chemistry ; Molybdenum - pharmacology ; Polyoxometalates ; U937 Cells</subject><ispartof>Journal of inorganic biochemistry, 2017-03, Vol.168, p.67-75</ispartof><rights>2016 Elsevier Inc.</rights><rights>Copyright © 2016 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c408t-2008d5d1ecdf970e05e2f6c4c54edb00412831acabd17aaeb0d8eb22d101556c3</citedby><cites>FETCH-LOGICAL-c408t-2008d5d1ecdf970e05e2f6c4c54edb00412831acabd17aaeb0d8eb22d101556c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781,27905,27906</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28013066$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Chunyan</creatorcontrib><creatorcontrib>Cao, Hongqian</creatorcontrib><creatorcontrib>Sun, Jiaheng</creatorcontrib><creatorcontrib>Tian, Rui</creatorcontrib><creatorcontrib>Li, Dongbei</creatorcontrib><creatorcontrib>Qi, Yanfei</creatorcontrib><creatorcontrib>Yang, Wei</creatorcontrib><creatorcontrib>Li, Juan</creatorcontrib><title>Antileukemic activity of an arsenomolybdate in the human HL-60 and U937 leukemia cells</title><title>Journal of inorganic biochemistry</title><addtitle>J Inorg Biochem</addtitle><description>The antileukemic activity, mechanisms and serum albumin interactions of an arsenomolybdate, K2Na[AsMo6O21(O2CCH2NH3)3]·6H2O (1), was evaluated in the human leukemia HL-60 and U937 cells. The results indicated that 1 could inhibit the proliferation of both leukemia cell lines in a dose-dependent manner with the 50% lethal concentration (IC50) value of 8.61μM for HL-60 and 14.50μM for U937 at 24h, compare to the positive controls, all-trans retinoic acid (ATRA) with IC50 value of 20.76μM and 14.85μM,and As2O3 with IC50 value of 6.40μM and 8.75μM at 24h, respectively (P<0.05). Furthermore, the anti-leukemia activity of compound 1 might be medicated by arresting the leukemic cells in the G1 phase and inducing apoptosis via caspase-3 and bcl-2 regulatory proteins. Spectroscopic techniques results showed that the fluorescence of human serum albumin was quenched by compound 1, and the quenching mechanism was mainly static quenching. Compound 1 might be a potential medicinal candidate against acute promyelocytic leukemia.
The antileukemic activity of an arsenomolybdate, K2Na[AsMo6O21 (O2CCH2NH3)3]·6H2O 1 has been investigated. The results indicated that 1 could inhibit the proliferation of HL-60 and U937 cells, arrest the leukemic cells in the G1 phase and induce apoptosis. Compound 1 might be a potential candidate against acute promyelocytic leukemia. [Display omitted]
•Arsenomolybdate-induced apoptosis in leukemia cells via caspase-3 regulatory protein•Arsenomolybdate-induced apoptosis in leukemia cells via the bcl-2 regulatory protein•Arsenomolybdate arrests the leukemic cells in the G1 phase.•The main quenching mechanism for arsenomolybdate and human serum albumin was static quenching.</description><subject>Acute promyelocytic leukemia</subject><subject>Antineoplastic Agents - chemical synthesis</subject><subject>Antineoplastic Agents - chemistry</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Arsenicals - chemical synthesis</subject><subject>Arsenicals - chemistry</subject><subject>Arsenicals - pharmacology</subject><subject>Arsenomolybdate</subject><subject>Blotting, Western</subject><subject>Caspase 3 - drug effects</subject><subject>Cell Cycle - drug effects</subject><subject>Cell Proliferation - drug effects</subject><subject>Drug Stability</subject><subject>Flow Cytometry</subject><subject>Fluorescence</subject><subject>HL-60 Cells</subject><subject>Humans</subject><subject>Inhibitory Concentration 50</subject><subject>Leukemia, Promyelocytic, Acute - drug therapy</subject><subject>Molybdenum - chemistry</subject><subject>Molybdenum - pharmacology</subject><subject>Polyoxometalates</subject><subject>U937 Cells</subject><issn>0162-0134</issn><issn>1873-3344</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><recordid>eNqFkEtPAjEQgBujEUT_gvboZddp98mREBUTEi_item2s1Lc3WK7S8K_twTk6mmSmW9eHyEPDGIGLH_axBvTWfdVGRvzkIgZjwH4BRmzskiiJEnTSzIOBR4BS9IRufF-AwBZlhbXZMTLkIU8H5PPWdebBodvbI2iUvVmZ_o9tTWVHZXOY2db2-wrLXukpqP9Gul6aENxsYxyCJSmq2lS0NMMSRU2jb8lV7VsPN6d4oSsXp4_5oto-f76Np8tI5VC2UccoNSZZqh0PS0AIUNe5ypVWYq6AkgZLxMmlaw0K6TECnSJFec6SMiyXCUT8nicu3X2Z0Dfi9b4wwWyQzt4wcpsWoSncwhocUSVs947rMXWmVa6vWAgDlLFRpylioNUwbgIUkPn_WnJULWoz31_FgMwOwIYXt0ZdMIrg51CbRyqXmhr_l3yCxhcjBc</recordid><startdate>20170301</startdate><enddate>20170301</enddate><creator>Li, Chunyan</creator><creator>Cao, Hongqian</creator><creator>Sun, Jiaheng</creator><creator>Tian, Rui</creator><creator>Li, Dongbei</creator><creator>Qi, Yanfei</creator><creator>Yang, Wei</creator><creator>Li, Juan</creator><general>Elsevier Inc</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>7X8</scope></search><sort><creationdate>20170301</creationdate><title>Antileukemic activity of an arsenomolybdate in the human HL-60 and U937 leukemia cells</title><author>Li, Chunyan ; Cao, Hongqian ; Sun, Jiaheng ; Tian, Rui ; Li, Dongbei ; Qi, Yanfei ; Yang, Wei ; Li, Juan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c408t-2008d5d1ecdf970e05e2f6c4c54edb00412831acabd17aaeb0d8eb22d101556c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Acute promyelocytic leukemia</topic><topic>Antineoplastic Agents - chemical synthesis</topic><topic>Antineoplastic Agents - chemistry</topic><topic>Antineoplastic Agents - pharmacology</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Arsenicals - chemical synthesis</topic><topic>Arsenicals - chemistry</topic><topic>Arsenicals - pharmacology</topic><topic>Arsenomolybdate</topic><topic>Blotting, Western</topic><topic>Caspase 3 - drug effects</topic><topic>Cell Cycle - drug effects</topic><topic>Cell Proliferation - drug effects</topic><topic>Drug Stability</topic><topic>Flow Cytometry</topic><topic>Fluorescence</topic><topic>HL-60 Cells</topic><topic>Humans</topic><topic>Inhibitory Concentration 50</topic><topic>Leukemia, Promyelocytic, Acute - drug therapy</topic><topic>Molybdenum - chemistry</topic><topic>Molybdenum - pharmacology</topic><topic>Polyoxometalates</topic><topic>U937 Cells</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Chunyan</creatorcontrib><creatorcontrib>Cao, Hongqian</creatorcontrib><creatorcontrib>Sun, Jiaheng</creatorcontrib><creatorcontrib>Tian, Rui</creatorcontrib><creatorcontrib>Li, Dongbei</creatorcontrib><creatorcontrib>Qi, Yanfei</creatorcontrib><creatorcontrib>Yang, Wei</creatorcontrib><creatorcontrib>Li, Juan</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of inorganic biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Chunyan</au><au>Cao, Hongqian</au><au>Sun, Jiaheng</au><au>Tian, Rui</au><au>Li, Dongbei</au><au>Qi, Yanfei</au><au>Yang, Wei</au><au>Li, Juan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Antileukemic activity of an arsenomolybdate in the human HL-60 and U937 leukemia cells</atitle><jtitle>Journal of inorganic biochemistry</jtitle><addtitle>J Inorg Biochem</addtitle><date>2017-03-01</date><risdate>2017</risdate><volume>168</volume><spage>67</spage><epage>75</epage><pages>67-75</pages><issn>0162-0134</issn><eissn>1873-3344</eissn><abstract>The antileukemic activity, mechanisms and serum albumin interactions of an arsenomolybdate, K2Na[AsMo6O21(O2CCH2NH3)3]·6H2O (1), was evaluated in the human leukemia HL-60 and U937 cells. The results indicated that 1 could inhibit the proliferation of both leukemia cell lines in a dose-dependent manner with the 50% lethal concentration (IC50) value of 8.61μM for HL-60 and 14.50μM for U937 at 24h, compare to the positive controls, all-trans retinoic acid (ATRA) with IC50 value of 20.76μM and 14.85μM,and As2O3 with IC50 value of 6.40μM and 8.75μM at 24h, respectively (P<0.05). Furthermore, the anti-leukemia activity of compound 1 might be medicated by arresting the leukemic cells in the G1 phase and inducing apoptosis via caspase-3 and bcl-2 regulatory proteins. Spectroscopic techniques results showed that the fluorescence of human serum albumin was quenched by compound 1, and the quenching mechanism was mainly static quenching. Compound 1 might be a potential medicinal candidate against acute promyelocytic leukemia.
The antileukemic activity of an arsenomolybdate, K2Na[AsMo6O21 (O2CCH2NH3)3]·6H2O 1 has been investigated. The results indicated that 1 could inhibit the proliferation of HL-60 and U937 cells, arrest the leukemic cells in the G1 phase and induce apoptosis. Compound 1 might be a potential candidate against acute promyelocytic leukemia. [Display omitted]
•Arsenomolybdate-induced apoptosis in leukemia cells via caspase-3 regulatory protein•Arsenomolybdate-induced apoptosis in leukemia cells via the bcl-2 regulatory protein•Arsenomolybdate arrests the leukemic cells in the G1 phase.•The main quenching mechanism for arsenomolybdate and human serum albumin was static quenching.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>28013066</pmid><doi>10.1016/j.jinorgbio.2016.12.002</doi><tpages>9</tpages></addata></record> |
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| subjects | Acute promyelocytic leukemia Antineoplastic Agents - chemical synthesis Antineoplastic Agents - chemistry Antineoplastic Agents - pharmacology Apoptosis Apoptosis - drug effects Arsenicals - chemical synthesis Arsenicals - chemistry Arsenicals - pharmacology Arsenomolybdate Blotting, Western Caspase 3 - drug effects Cell Cycle - drug effects Cell Proliferation - drug effects Drug Stability Flow Cytometry Fluorescence HL-60 Cells Humans Inhibitory Concentration 50 Leukemia, Promyelocytic, Acute - drug therapy Molybdenum - chemistry Molybdenum - pharmacology Polyoxometalates U937 Cells |
| title | Antileukemic activity of an arsenomolybdate in the human HL-60 and U937 leukemia cells |
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