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chrysin, cells, histone, cell, stat, hdac, pubmed, article, google, scholar, tsa, figure, cas, treated, waf, activity, promoter, protein, chromatin, proteins, hack, cycle, inhibitor, cancer, acetylation, methylation, control, deacetylase, lysine, analysis, induction, apoptosis, effect, incubated, expression, arrest, transcriptional, min, modifications, level, binding, assay, increase, inhibitors, authors, cdk, treatment, central, represents, dmso,

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author information authors springer nature abbreviations hdac references peltonen merge figures conclusions supplementary information mut-p21-luc promoter plasmid statistical profile demonstrated pre-publication history methods chemical structure quantitative real-time pcr shows dna content authors’ original file cmv-βgal plasmid combinations hplc methods information methods effect cell cycle arrest authors scientific editing post-translational histone modifications cmv-β-galactosidase plasmid nf-kb dependent genes p21waf1 promoter apoptotic inducing nature cell growth arrest arrest cell growth p21waf1/ cip1 pre-incubated a375 cells induce growth arrest cell cycle analysis sds-page article pal-bhadra vitro anti-cancer activity real-time pcr sp1/sp3 binding sites control growth arrest cell cycle progression potent hdac-8 inhibitor privacy choices/manage cookies garlic-derived organosulfur compound content ice-cold ripa buffer regulating cell cycle stat3 transcription factor histone deacetylase inhibitor multimode varioskan flash supplementary protocol full size image rnase free dnase

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• Gray SG, Teh BT: Histone acetylation/deacetylation and cancer: an "open" and "shut" case?

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WebPage:
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         headline:Plant HDAC inhibitor chrysin arrest cell growth and induce p21 WAF1 by altering chromatin of STAT response element in A375 cells
         description:Chrysin and its analogues, belongs to flavonoid family and possess potential anti-tumour activity. The aim of this study is to determine the molecular mechanism by which chrysin controls cell growth and induce apoptosis in A375 cells. Effect of chrysin and its analogues on cell viability and cell cycle analysis was determined by MTT assay and flowcytometry. A series of Western blots was performed to determine the effect of chrysin on important cell cycle regulatory proteins (Cdk2, cyclin D1, p53, p21, p27). The fluorimetry and calorimetry based assays was conducted for characterization of chrysin as HDAC inhibitor. The changes in histone tail modification such as acetylation and methylation was studied after chrysin treatment was estimated by immuno-fluorescence and western blot analysis. The expression of Bcl-xL, survivin and caspase-3 was estimated in chrysin treated cells. The effect of chrysin on p21 promoter activity was studied by luciferase and ChIP assays. Chrysin cause G1 cell cycle arrest and found to inhibit HDAC-2 and HDAC-8. Chrysin treated cells have shown increase in the levels of H3acK14, H4acK12, H4acK16 and decrease in H3me2K9 methylation. The p21 induction by chrysin treatment was found to be independent of p53 status. The chromatin remodelling at p21WAF1 promoter induces p21 activity, increased STAT-1 expression and epigenetic modifications that are responsible for ultimate cell cycle arrest and apoptosis. Chrysin shows in vitro anti-cancer activity that is correlated with induction of histone hyperacetylation and possible recruitment of STAT-1, 3, 5 proteins at STAT (−692 to −684) region of p21 promoter. Our results also support an unexpected action of chrysin on the chromatin organization of p21 WAF1 promoter through histone methylation and hyper-acetylation. It proposes previously unknown sequence specific chromatin modulations in the STAT responsive elements for regulating cell cycle progression negatively via the induction of the CDK inhibitor p21 WAF1 .
         datePublished:2012-05-16T00:00:00Z
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            HDAC inhibitor
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            STAT
            Apoptosis
            Cancer Research
            Oncology
            Surgical Oncology
            Health Promotion and Disease Prevention
            Biomedicine
            general
            Medicine/Public Health
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      headline:Plant HDAC inhibitor chrysin arrest cell growth and induce p21 WAF1 by altering chromatin of STAT response element in A375 cells
      description:Chrysin and its analogues, belongs to flavonoid family and possess potential anti-tumour activity. The aim of this study is to determine the molecular mechanism by which chrysin controls cell growth and induce apoptosis in A375 cells. Effect of chrysin and its analogues on cell viability and cell cycle analysis was determined by MTT assay and flowcytometry. A series of Western blots was performed to determine the effect of chrysin on important cell cycle regulatory proteins (Cdk2, cyclin D1, p53, p21, p27). The fluorimetry and calorimetry based assays was conducted for characterization of chrysin as HDAC inhibitor. The changes in histone tail modification such as acetylation and methylation was studied after chrysin treatment was estimated by immuno-fluorescence and western blot analysis. The expression of Bcl-xL, survivin and caspase-3 was estimated in chrysin treated cells. The effect of chrysin on p21 promoter activity was studied by luciferase and ChIP assays. Chrysin cause G1 cell cycle arrest and found to inhibit HDAC-2 and HDAC-8. Chrysin treated cells have shown increase in the levels of H3acK14, H4acK12, H4acK16 and decrease in H3me2K9 methylation. The p21 induction by chrysin treatment was found to be independent of p53 status. The chromatin remodelling at p21WAF1 promoter induces p21 activity, increased STAT-1 expression and epigenetic modifications that are responsible for ultimate cell cycle arrest and apoptosis. Chrysin shows in vitro anti-cancer activity that is correlated with induction of histone hyperacetylation and possible recruitment of STAT-1, 3, 5 proteins at STAT (−692 to −684) region of p21 promoter. Our results also support an unexpected action of chrysin on the chromatin organization of p21 WAF1 promoter through histone methylation and hyper-acetylation. It proposes previously unknown sequence specific chromatin modulations in the STAT responsive elements for regulating cell cycle progression negatively via the induction of the CDK inhibitor p21 WAF1 .
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      dateModified:2012-05-16T00:00:00Z
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      pageEnd:17
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         HDAC-8
         Chrysin
         A375 cells
         HDAC inhibitor
         p21WAF1
         Cell cycle arrest
         p21 promoter
         STAT
         Apoptosis
         Cancer Research
         Oncology
         Surgical Oncology
         Health Promotion and Disease Prevention
         Biomedicine
         general
         Medicine/Public Health
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      name:Department of Chemical Biology, Indian Institute of Chemical Technology, Hyderabad, India
      name:Functional Genomics and Gene silencing Group, Centre for Cellular and Molecular Biology, Hyderabad, India
      name:Department of Chemical Biology, Indian Institute of Chemical Technology, Hyderabad, India
      name:Department of Chemical Biology, Indian Institute of Chemical Technology, Hyderabad, India
      name:Functional Genomics and Gene silencing Group, Centre for Cellular and Molecular Biology, Hyderabad, India
      name:Department of Chemical Biology, Indian Institute of Chemical Technology, Hyderabad, India
      name:Department of Natural Product, Indian Institute of Chemical Technology, Hyderabad, India
      name:Department of Pharmacology, Indian Institute of Chemical Technology, Hyderabad, India
      name:Department of Natural Product, Indian Institute of Chemical Technology, Hyderabad, India
      name:Department of Chemical Biology, Indian Institute of Chemical Technology, Hyderabad, India
      name:Functional Genomics and Gene silencing Group, Centre for Cellular and Molecular Biology, Hyderabad, India

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