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Chemopreventive Agent 3,3′-Diindolylmethane Selectively Induces Proteasomal Degradation of Class I Histone Deacetylases

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Bibliographische Detailangaben
Zeitschriftentitel: Cancer Research
Personen und Körperschaften: Li, Yongming, Li, Xia, Guo, Bin
In: Cancer Research, 70, 2010, 2, S. 646-654
Medientyp: E-Article
Sprache: Englisch
veröffentlicht:
American Association for Cancer Research (AACR)
Schlagwörter:
author_facet Li, Yongming
Li, Xia
Guo, Bin
Li, Yongming
Li, Xia
Guo, Bin
author Li, Yongming
Li, Xia
Guo, Bin
spellingShingle Li, Yongming
Li, Xia
Guo, Bin
Cancer Research
Chemopreventive Agent 3,3′-Diindolylmethane Selectively Induces Proteasomal Degradation of Class I Histone Deacetylases
Cancer Research
Oncology
author_sort li, yongming
spelling Li, Yongming Li, Xia Guo, Bin 0008-5472 1538-7445 American Association for Cancer Research (AACR) Cancer Research Oncology http://dx.doi.org/10.1158/0008-5472.can-09-1924 <jats:title>Abstract</jats:title> <jats:p>3,3′-Diindolylmethane (DIM) is an anticancer agent that induces cell cycle arrest and apoptosis through unknown mechanisms. Here, we report that DIM can selectively induce proteasome-mediated degradation of class I histone deacetylases (HDAC1, HDAC2, HDAC3, and HDAC8) without affecting the class II HDAC proteins. DIM induced downregulation of class I HDACs in human colon cancer cells in vitro and in vivo in tumor xenografts. HDAC depletion relieved HDAC-mediated transcriptional inhibition of the cyclin-dependent kinase inhibitors p21WAF1 and p27KIP2, significantly increasing their expression and triggering cell cycle arrest in the G2 phase of the cell cycle. Additionally, HDAC depletion was associated with an induction of DNA damage that triggered apoptosis. Our findings indicate that DIM acts to selectively target the degradation of class I HDACs. Cancer Res; 70(2); 646–54</jats:p> Chemopreventive Agent 3,3′-Diindolylmethane Selectively Induces Proteasomal Degradation of Class I Histone Deacetylases Cancer Research
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imprint_str_mv American Association for Cancer Research (AACR), 2010
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title Chemopreventive Agent 3,3′-Diindolylmethane Selectively Induces Proteasomal Degradation of Class I Histone Deacetylases
title_unstemmed Chemopreventive Agent 3,3′-Diindolylmethane Selectively Induces Proteasomal Degradation of Class I Histone Deacetylases
title_full Chemopreventive Agent 3,3′-Diindolylmethane Selectively Induces Proteasomal Degradation of Class I Histone Deacetylases
title_fullStr Chemopreventive Agent 3,3′-Diindolylmethane Selectively Induces Proteasomal Degradation of Class I Histone Deacetylases
title_full_unstemmed Chemopreventive Agent 3,3′-Diindolylmethane Selectively Induces Proteasomal Degradation of Class I Histone Deacetylases
title_short Chemopreventive Agent 3,3′-Diindolylmethane Selectively Induces Proteasomal Degradation of Class I Histone Deacetylases
title_sort chemopreventive agent 3,3′-diindolylmethane selectively induces proteasomal degradation of class i histone deacetylases
topic Cancer Research
Oncology
url http://dx.doi.org/10.1158/0008-5472.can-09-1924
publishDate 2010
physical 646-654
description <jats:title>Abstract</jats:title> <jats:p>3,3′-Diindolylmethane (DIM) is an anticancer agent that induces cell cycle arrest and apoptosis through unknown mechanisms. Here, we report that DIM can selectively induce proteasome-mediated degradation of class I histone deacetylases (HDAC1, HDAC2, HDAC3, and HDAC8) without affecting the class II HDAC proteins. DIM induced downregulation of class I HDACs in human colon cancer cells in vitro and in vivo in tumor xenografts. HDAC depletion relieved HDAC-mediated transcriptional inhibition of the cyclin-dependent kinase inhibitors p21WAF1 and p27KIP2, significantly increasing their expression and triggering cell cycle arrest in the G2 phase of the cell cycle. Additionally, HDAC depletion was associated with an induction of DNA damage that triggered apoptosis. Our findings indicate that DIM acts to selectively target the degradation of class I HDACs. Cancer Res; 70(2); 646–54</jats:p>
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author Li, Yongming, Li, Xia, Guo, Bin
author_facet Li, Yongming, Li, Xia, Guo, Bin, Li, Yongming, Li, Xia, Guo, Bin
author_sort li, yongming
container_issue 2
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container_title Cancer Research
container_volume 70
description <jats:title>Abstract</jats:title> <jats:p>3,3′-Diindolylmethane (DIM) is an anticancer agent that induces cell cycle arrest and apoptosis through unknown mechanisms. Here, we report that DIM can selectively induce proteasome-mediated degradation of class I histone deacetylases (HDAC1, HDAC2, HDAC3, and HDAC8) without affecting the class II HDAC proteins. DIM induced downregulation of class I HDACs in human colon cancer cells in vitro and in vivo in tumor xenografts. HDAC depletion relieved HDAC-mediated transcriptional inhibition of the cyclin-dependent kinase inhibitors p21WAF1 and p27KIP2, significantly increasing their expression and triggering cell cycle arrest in the G2 phase of the cell cycle. Additionally, HDAC depletion was associated with an induction of DNA damage that triggered apoptosis. Our findings indicate that DIM acts to selectively target the degradation of class I HDACs. Cancer Res; 70(2); 646–54</jats:p>
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imprint American Association for Cancer Research (AACR), 2010
imprint_str_mv American Association for Cancer Research (AACR), 2010
institution DE-D275, DE-Bn3, DE-Brt1, DE-Zwi2, DE-D161, DE-Gla1, DE-Zi4, DE-15, DE-Pl11, DE-Rs1, DE-105, DE-14, DE-Ch1, DE-L229
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spelling Li, Yongming Li, Xia Guo, Bin 0008-5472 1538-7445 American Association for Cancer Research (AACR) Cancer Research Oncology http://dx.doi.org/10.1158/0008-5472.can-09-1924 <jats:title>Abstract</jats:title> <jats:p>3,3′-Diindolylmethane (DIM) is an anticancer agent that induces cell cycle arrest and apoptosis through unknown mechanisms. Here, we report that DIM can selectively induce proteasome-mediated degradation of class I histone deacetylases (HDAC1, HDAC2, HDAC3, and HDAC8) without affecting the class II HDAC proteins. DIM induced downregulation of class I HDACs in human colon cancer cells in vitro and in vivo in tumor xenografts. HDAC depletion relieved HDAC-mediated transcriptional inhibition of the cyclin-dependent kinase inhibitors p21WAF1 and p27KIP2, significantly increasing their expression and triggering cell cycle arrest in the G2 phase of the cell cycle. Additionally, HDAC depletion was associated with an induction of DNA damage that triggered apoptosis. Our findings indicate that DIM acts to selectively target the degradation of class I HDACs. Cancer Res; 70(2); 646–54</jats:p> Chemopreventive Agent 3,3′-Diindolylmethane Selectively Induces Proteasomal Degradation of Class I Histone Deacetylases Cancer Research
spellingShingle Li, Yongming, Li, Xia, Guo, Bin, Cancer Research, Chemopreventive Agent 3,3′-Diindolylmethane Selectively Induces Proteasomal Degradation of Class I Histone Deacetylases, Cancer Research, Oncology
title Chemopreventive Agent 3,3′-Diindolylmethane Selectively Induces Proteasomal Degradation of Class I Histone Deacetylases
title_full Chemopreventive Agent 3,3′-Diindolylmethane Selectively Induces Proteasomal Degradation of Class I Histone Deacetylases
title_fullStr Chemopreventive Agent 3,3′-Diindolylmethane Selectively Induces Proteasomal Degradation of Class I Histone Deacetylases
title_full_unstemmed Chemopreventive Agent 3,3′-Diindolylmethane Selectively Induces Proteasomal Degradation of Class I Histone Deacetylases
title_short Chemopreventive Agent 3,3′-Diindolylmethane Selectively Induces Proteasomal Degradation of Class I Histone Deacetylases
title_sort chemopreventive agent 3,3′-diindolylmethane selectively induces proteasomal degradation of class i histone deacetylases
title_unstemmed Chemopreventive Agent 3,3′-Diindolylmethane Selectively Induces Proteasomal Degradation of Class I Histone Deacetylases
topic Cancer Research, Oncology
url http://dx.doi.org/10.1158/0008-5472.can-09-1924