Experiment study of PHI on histone methylation and acetylation in Molt-4 cells
To investigate the effect of phenyl-hexyl isothiocyanate (PHI) on acetylation and methylation of histone in acute lymphoblastic leukemia cell line Molt4. The inhibition of cell proliferation was observed by MTT method and clone suppression test. Apoptosis and cell cycle arrest were measured by flow...
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Veröffentlicht in: | Zhōnghuá xuèyèxué zázhì 2007-09, Vol.28 (9), p.612-615 |
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creator | Huang, Yi-Qun Ma, Xu-Dong Zhen, Rui-Ji Chiao, Jen-Wei Liu, De-Long |
description | To investigate the effect of phenyl-hexyl isothiocyanate (PHI) on acetylation and methylation of histone in acute lymphoblastic leukemia cell line Molt4.
The inhibition of cell proliferation was observed by MTT method and clone suppression test. Apoptosis and cell cycle arrest were measured by flow cytometry. The alterations in histone acetyltransferase and acetylation and methylation of histones were detected by Western blot.
PHI could up-regulate the expression of acetyltransferase (P300/CBP), markedly induced the accumulation of acetylated histone H3, H4 and methylated histone H3 lysine 4 (H3K4), and inhibited methylation on lysine 9 of H3 (H3K9). The epigenetic regulation resulted in cell cycle arrest at G0/G1 phase, and induction of apoptosis.
PHI can modulate both histone methylation and acetylation. It may serve as a histone deacetylase inhibitor, and might be a potential novel anti-leukemia agent. |
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The inhibition of cell proliferation was observed by MTT method and clone suppression test. Apoptosis and cell cycle arrest were measured by flow cytometry. The alterations in histone acetyltransferase and acetylation and methylation of histones were detected by Western blot.
PHI could up-regulate the expression of acetyltransferase (P300/CBP), markedly induced the accumulation of acetylated histone H3, H4 and methylated histone H3 lysine 4 (H3K4), and inhibited methylation on lysine 9 of H3 (H3K9). The epigenetic regulation resulted in cell cycle arrest at G0/G1 phase, and induction of apoptosis.
PHI can modulate both histone methylation and acetylation. It may serve as a histone deacetylase inhibitor, and might be a potential novel anti-leukemia agent.</description><identifier>ISSN: 0253-2727</identifier><identifier>PMID: 18246819</identifier><language>chi</language><publisher>China</publisher><subject>Acetylation - drug effects ; Apoptosis - drug effects ; Cell Cycle - drug effects ; Cell Line, Tumor ; Cell Proliferation - drug effects ; Epigenesis, Genetic ; Histone Deacetylases - metabolism ; Histones - metabolism ; Humans ; Isothiocyanates - pharmacology ; Methylation - drug effects</subject><ispartof>Zhōnghuá xuèyèxué zázhì, 2007-09, Vol.28 (9), p.612-615</ispartof><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18246819$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Huang, Yi-Qun</creatorcontrib><creatorcontrib>Ma, Xu-Dong</creatorcontrib><creatorcontrib>Zhen, Rui-Ji</creatorcontrib><creatorcontrib>Chiao, Jen-Wei</creatorcontrib><creatorcontrib>Liu, De-Long</creatorcontrib><title>Experiment study of PHI on histone methylation and acetylation in Molt-4 cells</title><title>Zhōnghuá xuèyèxué zázhì</title><addtitle>Zhonghua Xue Ye Xue Za Zhi</addtitle><description>To investigate the effect of phenyl-hexyl isothiocyanate (PHI) on acetylation and methylation of histone in acute lymphoblastic leukemia cell line Molt4.
The inhibition of cell proliferation was observed by MTT method and clone suppression test. Apoptosis and cell cycle arrest were measured by flow cytometry. The alterations in histone acetyltransferase and acetylation and methylation of histones were detected by Western blot.
PHI could up-regulate the expression of acetyltransferase (P300/CBP), markedly induced the accumulation of acetylated histone H3, H4 and methylated histone H3 lysine 4 (H3K4), and inhibited methylation on lysine 9 of H3 (H3K9). The epigenetic regulation resulted in cell cycle arrest at G0/G1 phase, and induction of apoptosis.
PHI can modulate both histone methylation and acetylation. It may serve as a histone deacetylase inhibitor, and might be a potential novel anti-leukemia agent.</description><subject>Acetylation - drug effects</subject><subject>Apoptosis - drug effects</subject><subject>Cell Cycle - drug effects</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation - drug effects</subject><subject>Epigenesis, Genetic</subject><subject>Histone Deacetylases - metabolism</subject><subject>Histones - metabolism</subject><subject>Humans</subject><subject>Isothiocyanates - pharmacology</subject><subject>Methylation - drug effects</subject><issn>0253-2727</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo1UEtrwzAY82FjLV3_wvBpt8DnR2L7OEq3FrrHYTsHx_lCDUmcxQ4s_34Za09CQghJN2QNPBcZV1ytyDZGX0HORKGFgDuyYprLQjOzJm_7nwFH32GfaExTPdPQ0I_DkYaenn1MoUfaYTrPrU1-0WxfU-swXbnv6WtoUyapw7aN9-S2sW3E7QU35Ot5_7k7ZKf3l-Pu6ZQNjMuUuZwbbhwHmUsH3NbWMGhAA0qmXN0oJTQAcmmZBemMMmBNVSlT6IqJXIkNefzPHcbwPWFMZefjXwPbY5hiqQBUwaVZjA8X41R1WJfDstWOc3l9QPwCH8dWCA</recordid><startdate>200709</startdate><enddate>200709</enddate><creator>Huang, Yi-Qun</creator><creator>Ma, Xu-Dong</creator><creator>Zhen, Rui-Ji</creator><creator>Chiao, Jen-Wei</creator><creator>Liu, De-Long</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>200709</creationdate><title>Experiment study of PHI on histone methylation and acetylation in Molt-4 cells</title><author>Huang, Yi-Qun ; Ma, Xu-Dong ; Zhen, Rui-Ji ; Chiao, Jen-Wei ; Liu, De-Long</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p124t-c52929c20454c02ada910f080e417cdf773800e24a1a04c9790a9bb7968b13573</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>chi</language><creationdate>2007</creationdate><topic>Acetylation - drug effects</topic><topic>Apoptosis - drug effects</topic><topic>Cell Cycle - drug effects</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation - drug effects</topic><topic>Epigenesis, Genetic</topic><topic>Histone Deacetylases - metabolism</topic><topic>Histones - metabolism</topic><topic>Humans</topic><topic>Isothiocyanates - pharmacology</topic><topic>Methylation - drug effects</topic><toplevel>online_resources</toplevel><creatorcontrib>Huang, Yi-Qun</creatorcontrib><creatorcontrib>Ma, Xu-Dong</creatorcontrib><creatorcontrib>Zhen, Rui-Ji</creatorcontrib><creatorcontrib>Chiao, Jen-Wei</creatorcontrib><creatorcontrib>Liu, De-Long</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Zhōnghuá xuèyèxué zázhì</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Huang, Yi-Qun</au><au>Ma, Xu-Dong</au><au>Zhen, Rui-Ji</au><au>Chiao, Jen-Wei</au><au>Liu, De-Long</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Experiment study of PHI on histone methylation and acetylation in Molt-4 cells</atitle><jtitle>Zhōnghuá xuèyèxué zázhì</jtitle><addtitle>Zhonghua Xue Ye Xue Za Zhi</addtitle><date>2007-09</date><risdate>2007</risdate><volume>28</volume><issue>9</issue><spage>612</spage><epage>615</epage><pages>612-615</pages><issn>0253-2727</issn><abstract>To investigate the effect of phenyl-hexyl isothiocyanate (PHI) on acetylation and methylation of histone in acute lymphoblastic leukemia cell line Molt4.
The inhibition of cell proliferation was observed by MTT method and clone suppression test. Apoptosis and cell cycle arrest were measured by flow cytometry. The alterations in histone acetyltransferase and acetylation and methylation of histones were detected by Western blot.
PHI could up-regulate the expression of acetyltransferase (P300/CBP), markedly induced the accumulation of acetylated histone H3, H4 and methylated histone H3 lysine 4 (H3K4), and inhibited methylation on lysine 9 of H3 (H3K9). The epigenetic regulation resulted in cell cycle arrest at G0/G1 phase, and induction of apoptosis.
PHI can modulate both histone methylation and acetylation. It may serve as a histone deacetylase inhibitor, and might be a potential novel anti-leukemia agent.</abstract><cop>China</cop><pmid>18246819</pmid><tpages>4</tpages></addata></record> |
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subjects | Acetylation - drug effects Apoptosis - drug effects Cell Cycle - drug effects Cell Line, Tumor Cell Proliferation - drug effects Epigenesis, Genetic Histone Deacetylases - metabolism Histones - metabolism Humans Isothiocyanates - pharmacology Methylation - drug effects |
title | Experiment study of PHI on histone methylation and acetylation in Molt-4 cells |
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