Bufalin reduces the level of topoisomerase II in human leukemia cells and affects the cytotoxicity of anticancer drugs
When human leukemia HL-60 cells were treated with 10 −7 M bufalin, the amounts of both topoisomerase (topo) IIα and IIβ and the activity of topo II decreased markedly and were almost undetectable 18 h after the start of treatment. The level of topo II mRNA started to decrease immediately after the s...
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Veröffentlicht in: | Leukemia research 1997-09, Vol.21 (9), p.875-883 |
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creator | Hashimoto, Sachiko Jing, Yongkui Kawazoe, Nobuko Masuda, Yutaka Nakajo, Shigeo Yoshida, Takemi Kuroiwa, Yukio Nakaya, Kazuyasu |
description | When human leukemia HL-60 cells were treated with 10
−7 M bufalin, the amounts of both topoisomerase (topo) IIα and IIβ and the activity of topo II decreased markedly and were almost undetectable 18 h after the start of treatment. The level of topo II mRNA started to decrease immediately after the start of treatment with bufalin, with a subsequent decrease in the amount of topo IIα protein. These changes preceded the fragmentation of DNA, a typical feature of apoptosis. The results suggest that bufalin caused a marked decrease in the steady-state level of topo IIα mRNA, which led to a decrease in the amount and activity of the enzyme and to the induction of apoptosis. A reduction in the level of topo IIα by bufalin was also observed in other lines of human leukemia cells such as ML1 and U937. The results were exploited to potentiate the effects of cisplatin and retinoic acid (RA) on HL-60 cells: pretreatment of HL-60 cells with 10
−7 M bufalin for 6 h increased the inhibitory effects of cisplatin and RA on cell growth and enhanced the induction of cell death. |
doi_str_mv | 10.1016/S0145-2126(97)00061-1 |
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−7 M bufalin, the amounts of both topoisomerase (topo) IIα and IIβ and the activity of topo II decreased markedly and were almost undetectable 18 h after the start of treatment. The level of topo II mRNA started to decrease immediately after the start of treatment with bufalin, with a subsequent decrease in the amount of topo IIα protein. These changes preceded the fragmentation of DNA, a typical feature of apoptosis. The results suggest that bufalin caused a marked decrease in the steady-state level of topo IIα mRNA, which led to a decrease in the amount and activity of the enzyme and to the induction of apoptosis. A reduction in the level of topo IIα by bufalin was also observed in other lines of human leukemia cells such as ML1 and U937. The results were exploited to potentiate the effects of cisplatin and retinoic acid (RA) on HL-60 cells: pretreatment of HL-60 cells with 10
−7 M bufalin for 6 h increased the inhibitory effects of cisplatin and RA on cell growth and enhanced the induction of cell death.</description><identifier>ISSN: 0145-2126</identifier><identifier>EISSN: 1873-5835</identifier><identifier>DOI: 10.1016/S0145-2126(97)00061-1</identifier><identifier>PMID: 9393603</identifier><identifier>CODEN: LEREDD</identifier><language>eng</language><publisher>Oxford: Elsevier Ltd</publisher><subject>Antineoplastic agents ; Antineoplastic Agents - pharmacology ; apoptosis ; Apoptosis - drug effects ; Biological and medical sciences ; Bufalin ; Bufanolides - pharmacology ; Cisplatin - pharmacology ; DNA Fragmentation ; DNA Topoisomerases, Type II - biosynthesis ; DNA Topoisomerases, Type II - genetics ; DNA, Neoplasm - analysis ; Drug Synergism ; Enzyme Induction - drug effects ; Enzyme Inhibitors - pharmacology ; General aspects ; HL-60 Cells - drug effects ; HL-60 Cells - enzymology ; Humans ; Isoenzymes - antagonists & inhibitors ; Isoenzymes - biosynthesis ; Isoenzymes - genetics ; leukemia cell ; Medical sciences ; Neoplasm Proteins - antagonists & inhibitors ; Neoplasm Proteins - biosynthesis ; Neoplasm Proteins - genetics ; Pharmacology. Drug treatments ; RNA, Messenger - biosynthesis ; RNA, Neoplasm - biosynthesis ; Tetradecanoylphorbol Acetate - pharmacology ; topoisomerase II ; Topoisomerase II Inhibitors ; Tretinoin - pharmacology</subject><ispartof>Leukemia research, 1997-09, Vol.21 (9), p.875-883</ispartof><rights>1997</rights><rights>1998 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c538t-7d8daabe84da6cc48de3ac9e5affa1d76ccba68346981a25caf265589609875e3</citedby><cites>FETCH-LOGICAL-c538t-7d8daabe84da6cc48de3ac9e5affa1d76ccba68346981a25caf265589609875e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/S0145-2126(97)00061-1$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2060043$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9393603$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hashimoto, Sachiko</creatorcontrib><creatorcontrib>Jing, Yongkui</creatorcontrib><creatorcontrib>Kawazoe, Nobuko</creatorcontrib><creatorcontrib>Masuda, Yutaka</creatorcontrib><creatorcontrib>Nakajo, Shigeo</creatorcontrib><creatorcontrib>Yoshida, Takemi</creatorcontrib><creatorcontrib>Kuroiwa, Yukio</creatorcontrib><creatorcontrib>Nakaya, Kazuyasu</creatorcontrib><title>Bufalin reduces the level of topoisomerase II in human leukemia cells and affects the cytotoxicity of anticancer drugs</title><title>Leukemia research</title><addtitle>Leuk Res</addtitle><description>When human leukemia HL-60 cells were treated with 10
−7 M bufalin, the amounts of both topoisomerase (topo) IIα and IIβ and the activity of topo II decreased markedly and were almost undetectable 18 h after the start of treatment. The level of topo II mRNA started to decrease immediately after the start of treatment with bufalin, with a subsequent decrease in the amount of topo IIα protein. These changes preceded the fragmentation of DNA, a typical feature of apoptosis. The results suggest that bufalin caused a marked decrease in the steady-state level of topo IIα mRNA, which led to a decrease in the amount and activity of the enzyme and to the induction of apoptosis. A reduction in the level of topo IIα by bufalin was also observed in other lines of human leukemia cells such as ML1 and U937. The results were exploited to potentiate the effects of cisplatin and retinoic acid (RA) on HL-60 cells: pretreatment of HL-60 cells with 10
−7 M bufalin for 6 h increased the inhibitory effects of cisplatin and RA on cell growth and enhanced the induction of cell death.</description><subject>Antineoplastic agents</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Biological and medical sciences</subject><subject>Bufalin</subject><subject>Bufanolides - pharmacology</subject><subject>Cisplatin - pharmacology</subject><subject>DNA Fragmentation</subject><subject>DNA Topoisomerases, Type II - biosynthesis</subject><subject>DNA Topoisomerases, Type II - genetics</subject><subject>DNA, Neoplasm - analysis</subject><subject>Drug Synergism</subject><subject>Enzyme Induction - drug effects</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>General aspects</subject><subject>HL-60 Cells - drug effects</subject><subject>HL-60 Cells - enzymology</subject><subject>Humans</subject><subject>Isoenzymes - antagonists & inhibitors</subject><subject>Isoenzymes - biosynthesis</subject><subject>Isoenzymes - genetics</subject><subject>leukemia cell</subject><subject>Medical sciences</subject><subject>Neoplasm Proteins - antagonists & inhibitors</subject><subject>Neoplasm Proteins - biosynthesis</subject><subject>Neoplasm Proteins - genetics</subject><subject>Pharmacology. Drug treatments</subject><subject>RNA, Messenger - biosynthesis</subject><subject>RNA, Neoplasm - biosynthesis</subject><subject>Tetradecanoylphorbol Acetate - pharmacology</subject><subject>topoisomerase II</subject><subject>Topoisomerase II Inhibitors</subject><subject>Tretinoin - pharmacology</subject><issn>0145-2126</issn><issn>1873-5835</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1997</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkE1v1DAQhi0EKtvSn1DJB4ToIdSOY8c-oVLxsVKlHqBna9aeUEMSL3ayYv89Tne1V06WPM-87-gh5IqzD5xxdfOd8UZWNa_Ve9NeM8YUr_gLsuK6FZXUQr4kqxPympzn_KtA0nBzRs6MMEIxsSK7T3MHfRhpQj87zHR6QtrjDnsaOzrFbQw5DpggI12vaQGf5gHGgsy_cQhAHfZ9pjB6Cl2HbjokuP0Up_g3uDDtlyAYp-BgdJioT_PP_Ia8KrUZL4_vBXn88vnH3bfq_uHr-u72vnJS6KlqvfYAG9SNB-Vcoz0KcAZl6QLu2_K3AaVFo4zmUEsHXa2k1EYxo1uJ4oK8O-RuU_wzY57sEPJyMowY52y5EkxLoQooD6BLMeeEnd2mMEDaW87s4ts--7aLTGta--zb8rJ3dSyYNwP609ZRcJm_Pc4hO-i7VCSEfMJqphhrFuzjAcMiYxcw2ewCFl8-pCLV-hj-c8g_QCqeiA</recordid><startdate>19970901</startdate><enddate>19970901</enddate><creator>Hashimoto, Sachiko</creator><creator>Jing, Yongkui</creator><creator>Kawazoe, Nobuko</creator><creator>Masuda, Yutaka</creator><creator>Nakajo, Shigeo</creator><creator>Yoshida, Takemi</creator><creator>Kuroiwa, Yukio</creator><creator>Nakaya, Kazuyasu</creator><general>Elsevier Ltd</general><general>Elsevier Science</general><scope>IQODW</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>7T5</scope><scope>H94</scope></search><sort><creationdate>19970901</creationdate><title>Bufalin reduces the level of topoisomerase II in human leukemia cells and affects the cytotoxicity of anticancer drugs</title><author>Hashimoto, Sachiko ; Jing, Yongkui ; Kawazoe, Nobuko ; Masuda, Yutaka ; Nakajo, Shigeo ; Yoshida, Takemi ; Kuroiwa, Yukio ; Nakaya, Kazuyasu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c538t-7d8daabe84da6cc48de3ac9e5affa1d76ccba68346981a25caf265589609875e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1997</creationdate><topic>Antineoplastic agents</topic><topic>Antineoplastic Agents - pharmacology</topic><topic>apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Biological and medical sciences</topic><topic>Bufalin</topic><topic>Bufanolides - pharmacology</topic><topic>Cisplatin - pharmacology</topic><topic>DNA Fragmentation</topic><topic>DNA Topoisomerases, Type II - biosynthesis</topic><topic>DNA Topoisomerases, Type II - genetics</topic><topic>DNA, Neoplasm - analysis</topic><topic>Drug Synergism</topic><topic>Enzyme Induction - drug effects</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>General aspects</topic><topic>HL-60 Cells - drug effects</topic><topic>HL-60 Cells - enzymology</topic><topic>Humans</topic><topic>Isoenzymes - antagonists & inhibitors</topic><topic>Isoenzymes - biosynthesis</topic><topic>Isoenzymes - genetics</topic><topic>leukemia cell</topic><topic>Medical sciences</topic><topic>Neoplasm Proteins - antagonists & inhibitors</topic><topic>Neoplasm Proteins - biosynthesis</topic><topic>Neoplasm Proteins - genetics</topic><topic>Pharmacology. Drug treatments</topic><topic>RNA, Messenger - biosynthesis</topic><topic>RNA, Neoplasm - biosynthesis</topic><topic>Tetradecanoylphorbol Acetate - pharmacology</topic><topic>topoisomerase II</topic><topic>Topoisomerase II Inhibitors</topic><topic>Tretinoin - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hashimoto, Sachiko</creatorcontrib><creatorcontrib>Jing, Yongkui</creatorcontrib><creatorcontrib>Kawazoe, Nobuko</creatorcontrib><creatorcontrib>Masuda, Yutaka</creatorcontrib><creatorcontrib>Nakajo, Shigeo</creatorcontrib><creatorcontrib>Yoshida, Takemi</creatorcontrib><creatorcontrib>Kuroiwa, Yukio</creatorcontrib><creatorcontrib>Nakaya, Kazuyasu</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>Leukemia research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hashimoto, Sachiko</au><au>Jing, Yongkui</au><au>Kawazoe, Nobuko</au><au>Masuda, Yutaka</au><au>Nakajo, Shigeo</au><au>Yoshida, Takemi</au><au>Kuroiwa, Yukio</au><au>Nakaya, Kazuyasu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Bufalin reduces the level of topoisomerase II in human leukemia cells and affects the cytotoxicity of anticancer drugs</atitle><jtitle>Leukemia research</jtitle><addtitle>Leuk Res</addtitle><date>1997-09-01</date><risdate>1997</risdate><volume>21</volume><issue>9</issue><spage>875</spage><epage>883</epage><pages>875-883</pages><issn>0145-2126</issn><eissn>1873-5835</eissn><coden>LEREDD</coden><abstract>When human leukemia HL-60 cells were treated with 10
−7 M bufalin, the amounts of both topoisomerase (topo) IIα and IIβ and the activity of topo II decreased markedly and were almost undetectable 18 h after the start of treatment. The level of topo II mRNA started to decrease immediately after the start of treatment with bufalin, with a subsequent decrease in the amount of topo IIα protein. These changes preceded the fragmentation of DNA, a typical feature of apoptosis. The results suggest that bufalin caused a marked decrease in the steady-state level of topo IIα mRNA, which led to a decrease in the amount and activity of the enzyme and to the induction of apoptosis. A reduction in the level of topo IIα by bufalin was also observed in other lines of human leukemia cells such as ML1 and U937. The results were exploited to potentiate the effects of cisplatin and retinoic acid (RA) on HL-60 cells: pretreatment of HL-60 cells with 10
−7 M bufalin for 6 h increased the inhibitory effects of cisplatin and RA on cell growth and enhanced the induction of cell death.</abstract><cop>Oxford</cop><pub>Elsevier Ltd</pub><pmid>9393603</pmid><doi>10.1016/S0145-2126(97)00061-1</doi><tpages>9</tpages></addata></record> |
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subjects | Antineoplastic agents Antineoplastic Agents - pharmacology apoptosis Apoptosis - drug effects Biological and medical sciences Bufalin Bufanolides - pharmacology Cisplatin - pharmacology DNA Fragmentation DNA Topoisomerases, Type II - biosynthesis DNA Topoisomerases, Type II - genetics DNA, Neoplasm - analysis Drug Synergism Enzyme Induction - drug effects Enzyme Inhibitors - pharmacology General aspects HL-60 Cells - drug effects HL-60 Cells - enzymology Humans Isoenzymes - antagonists & inhibitors Isoenzymes - biosynthesis Isoenzymes - genetics leukemia cell Medical sciences Neoplasm Proteins - antagonists & inhibitors Neoplasm Proteins - biosynthesis Neoplasm Proteins - genetics Pharmacology. Drug treatments RNA, Messenger - biosynthesis RNA, Neoplasm - biosynthesis Tetradecanoylphorbol Acetate - pharmacology topoisomerase II Topoisomerase II Inhibitors Tretinoin - pharmacology |
title | Bufalin reduces the level of topoisomerase II in human leukemia cells and affects the cytotoxicity of anticancer drugs |
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