Id2 gene-targeted crosstalk between Wnt and retinoid signaling regulates proliferation in human keratinocytes
We investigated the effect of all-trans-retinoic acid (atRA) on proliferation in several human skin cell lines and found that antiproliferative potency of atRA correlated with the endogenous activity of canonical Wnt signaling. In HaCaT keratinocytes, we found that atRA significantly suppressed the...
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| Veröffentlicht in: | Oncogene 2007-08, Vol.26 (35), p.5038-5045 |
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| creator | MEMEZAWA, A TAKADA, I TAKEYAMA, K IGARASHI, M ITO, S AIBA, S KATO, S KOUZMENKO, A. P |
| description | We investigated the effect of all-trans-retinoic acid (atRA) on proliferation in several human skin cell lines and found that antiproliferative potency of atRA correlated with the endogenous activity of canonical Wnt signaling. In HaCaT keratinocytes, we found that atRA significantly suppressed the expression of Id2, a member of the inhibitor of differentiation family of transcription factors that regulate cell growth and differentiation. However, no apparent change in the expression of other Wnt targets, like c-Myc or cyclin D1, was observed. Retinoid-induced Id2 gene suppression was associated with decreased levels of histone H3 and H4 acetylation and histone H3 Lys-4 methylation, and with recruitment of the LSD1 demethylase at the Wnt-response element (WRE) (TCF/LEF-binding site), in the Id2 gene promoter. None of such changes was detected at the WRE of c-Myc and cyclin D1 gene promoters. Inhibition of Id2 by short interfering RNA (siRNA) had a similar effect on the proliferation of HaCaT cells as exposure to atRA, whereas anti-beta-catenin siRNA significantly inhibited its antiproliferative effect. These data suggest that downregulation of Id2 gene expression through transcriptional convergence between Wnt and retinoid signaling pathways underlies the antiproliferative effect of retinoids in keratinocytes, and provide evidence of gene-targeted crosstalk between signaling pathways. |
| doi_str_mv | 10.1038/sj.onc.1210320 |
| format | Article |
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P</creator><creatorcontrib>MEMEZAWA, A ; TAKADA, I ; TAKEYAMA, K ; IGARASHI, M ; ITO, S ; AIBA, S ; KATO, S ; KOUZMENKO, A. P</creatorcontrib><description>We investigated the effect of all-trans-retinoic acid (atRA) on proliferation in several human skin cell lines and found that antiproliferative potency of atRA correlated with the endogenous activity of canonical Wnt signaling. In HaCaT keratinocytes, we found that atRA significantly suppressed the expression of Id2, a member of the inhibitor of differentiation family of transcription factors that regulate cell growth and differentiation. However, no apparent change in the expression of other Wnt targets, like c-Myc or cyclin D1, was observed. Retinoid-induced Id2 gene suppression was associated with decreased levels of histone H3 and H4 acetylation and histone H3 Lys-4 methylation, and with recruitment of the LSD1 demethylase at the Wnt-response element (WRE) (TCF/LEF-binding site), in the Id2 gene promoter. None of such changes was detected at the WRE of c-Myc and cyclin D1 gene promoters. Inhibition of Id2 by short interfering RNA (siRNA) had a similar effect on the proliferation of HaCaT cells as exposure to atRA, whereas anti-beta-catenin siRNA significantly inhibited its antiproliferative effect. These data suggest that downregulation of Id2 gene expression through transcriptional convergence between Wnt and retinoid signaling pathways underlies the antiproliferative effect of retinoids in keratinocytes, and provide evidence of gene-targeted crosstalk between signaling pathways.</description><identifier>ISSN: 0950-9232</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/sj.onc.1210320</identifier><identifier>PMID: 17310985</identifier><identifier>CODEN: ONCNES</identifier><language>eng</language><publisher>Basingstoke: Nature Publishing</publisher><subject>Acetylation ; Binding sites ; Biochemistry ; Biological and medical sciences ; c-Myc protein ; Cancer ; Cell differentiation ; Cell Line ; Cell lines ; Cell physiology ; Cell proliferation ; Cell Proliferation - drug effects ; Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes ; Cyclin D1 ; Cyclin D1 - metabolism ; Down-Regulation ; Fundamental and applied biological sciences. Psychology ; Gene expression ; Gene Expression Regulation ; Histone Demethylases ; Histone H3 ; Histones ; Histones - metabolism ; Humans ; Id2 protein ; Inhibitor of Differentiation Protein 2 - antagonists & inhibitors ; Inhibitor of Differentiation Protein 2 - genetics ; Keratinocytes ; Keratinocytes - drug effects ; Keratinocytes - metabolism ; Kinases ; LEF/TCF protein ; Methylation ; Molecular and cellular biology ; Myc protein ; Oncology ; Oxidoreductases, N-Demethylating - metabolism ; Physiological aspects ; Proto-Oncogene Proteins c-myc - metabolism ; Response Elements ; Retinoic acid ; Retinoids ; Retinoids - pharmacology ; Ribonucleic acid ; RNA ; RNA, Small Interfering - pharmacology ; Signal transduction ; siRNA ; Transcription factors ; Tretinoin - pharmacology ; Wnt protein ; Wnt Proteins - metabolism ; β-Catenin</subject><ispartof>Oncogene, 2007-08, Vol.26 (35), p.5038-5045</ispartof><rights>2007 INIST-CNRS</rights><rights>COPYRIGHT 2007 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Aug 2 2007</rights><rights>Nature Publishing Group 2007.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c529t-6b49f4665691c88859b39fa58a0e10853c97beca2eb0de34344214f7ba7219523</citedby><cites>FETCH-LOGICAL-c529t-6b49f4665691c88859b39fa58a0e10853c97beca2eb0de34344214f7ba7219523</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785,2728,27928,27929</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18970009$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17310985$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>MEMEZAWA, A</creatorcontrib><creatorcontrib>TAKADA, I</creatorcontrib><creatorcontrib>TAKEYAMA, K</creatorcontrib><creatorcontrib>IGARASHI, M</creatorcontrib><creatorcontrib>ITO, S</creatorcontrib><creatorcontrib>AIBA, S</creatorcontrib><creatorcontrib>KATO, S</creatorcontrib><creatorcontrib>KOUZMENKO, A. P</creatorcontrib><title>Id2 gene-targeted crosstalk between Wnt and retinoid signaling regulates proliferation in human keratinocytes</title><title>Oncogene</title><addtitle>Oncogene</addtitle><description>We investigated the effect of all-trans-retinoic acid (atRA) on proliferation in several human skin cell lines and found that antiproliferative potency of atRA correlated with the endogenous activity of canonical Wnt signaling. In HaCaT keratinocytes, we found that atRA significantly suppressed the expression of Id2, a member of the inhibitor of differentiation family of transcription factors that regulate cell growth and differentiation. However, no apparent change in the expression of other Wnt targets, like c-Myc or cyclin D1, was observed. Retinoid-induced Id2 gene suppression was associated with decreased levels of histone H3 and H4 acetylation and histone H3 Lys-4 methylation, and with recruitment of the LSD1 demethylase at the Wnt-response element (WRE) (TCF/LEF-binding site), in the Id2 gene promoter. None of such changes was detected at the WRE of c-Myc and cyclin D1 gene promoters. Inhibition of Id2 by short interfering RNA (siRNA) had a similar effect on the proliferation of HaCaT cells as exposure to atRA, whereas anti-beta-catenin siRNA significantly inhibited its antiproliferative effect. These data suggest that downregulation of Id2 gene expression through transcriptional convergence between Wnt and retinoid signaling pathways underlies the antiproliferative effect of retinoids in keratinocytes, and provide evidence of gene-targeted crosstalk between signaling pathways.</description><subject>Acetylation</subject><subject>Binding sites</subject><subject>Biochemistry</subject><subject>Biological and medical sciences</subject><subject>c-Myc protein</subject><subject>Cancer</subject><subject>Cell differentiation</subject><subject>Cell Line</subject><subject>Cell lines</subject><subject>Cell physiology</subject><subject>Cell proliferation</subject><subject>Cell Proliferation - drug effects</subject><subject>Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes</subject><subject>Cyclin D1</subject><subject>Cyclin D1 - metabolism</subject><subject>Down-Regulation</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene expression</subject><subject>Gene Expression Regulation</subject><subject>Histone Demethylases</subject><subject>Histone H3</subject><subject>Histones</subject><subject>Histones - metabolism</subject><subject>Humans</subject><subject>Id2 protein</subject><subject>Inhibitor of Differentiation Protein 2 - antagonists & inhibitors</subject><subject>Inhibitor of Differentiation Protein 2 - genetics</subject><subject>Keratinocytes</subject><subject>Keratinocytes - drug effects</subject><subject>Keratinocytes - metabolism</subject><subject>Kinases</subject><subject>LEF/TCF protein</subject><subject>Methylation</subject><subject>Molecular and cellular biology</subject><subject>Myc protein</subject><subject>Oncology</subject><subject>Oxidoreductases, N-Demethylating - metabolism</subject><subject>Physiological aspects</subject><subject>Proto-Oncogene Proteins c-myc - metabolism</subject><subject>Response Elements</subject><subject>Retinoic acid</subject><subject>Retinoids</subject><subject>Retinoids - pharmacology</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>RNA, Small Interfering - pharmacology</subject><subject>Signal transduction</subject><subject>siRNA</subject><subject>Transcription factors</subject><subject>Tretinoin - pharmacology</subject><subject>Wnt protein</subject><subject>Wnt Proteins - metabolism</subject><subject>β-Catenin</subject><issn>0950-9232</issn><issn>1476-5594</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqFks9rFTEQxxdR7LN69aYERW_7zOTHJjmW4o9CwYvicclmZ9e87svWJEvpf29eu_BAKiWHkOEz853MfKvqNdAtUK4_pd12Dm4LrLwYfVJtQKimltKIp9WGGklrwzg7qV6ktKOUKkPZ8-oEFAdqtNxU-4uekRED1tnGETP2xMU5pWynK9JhvkEM5FfIxIaeRMw-zL4nyY_BTj6MJTQuk82YyHWcJz9gtNnPgfhAfi97G8jVXSTM7rZAL6tng50Svlrv0-rnl88_zr_Vl9-_XpyfXdZOMpPrphNmEE0jGwNOay1Nx81gpbYUgWrJnVEdOsuwoz1ywYVgIAbVWcXASMZPq4_3dUtTfxZMud375HCabMB5SW2jgVFZRvYYyIADNFI_CoJRXAqQBXz_D7ibl1imVYo1AriiRphCvfsvxRRvgCp1LDXaCVsfhjlH6w667RnoBoCXjRZq-wBVTo977-aAgy_xhxLuFh1xaK-j39t42wJtD6Zq064tpmpXU5WEt2uzS7fH_oivLirAhxWwydlpiDY4n46cNqoIH3795p4LNi8Rj8Aq9Bcdw9w0</recordid><startdate>20070802</startdate><enddate>20070802</enddate><creator>MEMEZAWA, A</creator><creator>TAKADA, I</creator><creator>TAKEYAMA, K</creator><creator>IGARASHI, M</creator><creator>ITO, S</creator><creator>AIBA, S</creator><creator>KATO, S</creator><creator>KOUZMENKO, A. 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P</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Id2 gene-targeted crosstalk between Wnt and retinoid signaling regulates proliferation in human keratinocytes</atitle><jtitle>Oncogene</jtitle><addtitle>Oncogene</addtitle><date>2007-08-02</date><risdate>2007</risdate><volume>26</volume><issue>35</issue><spage>5038</spage><epage>5045</epage><pages>5038-5045</pages><issn>0950-9232</issn><eissn>1476-5594</eissn><coden>ONCNES</coden><abstract>We investigated the effect of all-trans-retinoic acid (atRA) on proliferation in several human skin cell lines and found that antiproliferative potency of atRA correlated with the endogenous activity of canonical Wnt signaling. In HaCaT keratinocytes, we found that atRA significantly suppressed the expression of Id2, a member of the inhibitor of differentiation family of transcription factors that regulate cell growth and differentiation. However, no apparent change in the expression of other Wnt targets, like c-Myc or cyclin D1, was observed. Retinoid-induced Id2 gene suppression was associated with decreased levels of histone H3 and H4 acetylation and histone H3 Lys-4 methylation, and with recruitment of the LSD1 demethylase at the Wnt-response element (WRE) (TCF/LEF-binding site), in the Id2 gene promoter. None of such changes was detected at the WRE of c-Myc and cyclin D1 gene promoters. Inhibition of Id2 by short interfering RNA (siRNA) had a similar effect on the proliferation of HaCaT cells as exposure to atRA, whereas anti-beta-catenin siRNA significantly inhibited its antiproliferative effect. 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| subjects | Acetylation Binding sites Biochemistry Biological and medical sciences c-Myc protein Cancer Cell differentiation Cell Line Cell lines Cell physiology Cell proliferation Cell Proliferation - drug effects Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes Cyclin D1 Cyclin D1 - metabolism Down-Regulation Fundamental and applied biological sciences. Psychology Gene expression Gene Expression Regulation Histone Demethylases Histone H3 Histones Histones - metabolism Humans Id2 protein Inhibitor of Differentiation Protein 2 - antagonists & inhibitors Inhibitor of Differentiation Protein 2 - genetics Keratinocytes Keratinocytes - drug effects Keratinocytes - metabolism Kinases LEF/TCF protein Methylation Molecular and cellular biology Myc protein Oncology Oxidoreductases, N-Demethylating - metabolism Physiological aspects Proto-Oncogene Proteins c-myc - metabolism Response Elements Retinoic acid Retinoids Retinoids - pharmacology Ribonucleic acid RNA RNA, Small Interfering - pharmacology Signal transduction siRNA Transcription factors Tretinoin - pharmacology Wnt protein Wnt Proteins - metabolism β-Catenin |
| title | Id2 gene-targeted crosstalk between Wnt and retinoid signaling regulates proliferation in human keratinocytes |
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