The Yin and Yang of vitamin D receptor (VDR) signaling in neoplastic progression: Operational networks and tissue-specific growth control
Substantive evidence implicates vitamin D receptor (VDR) or its natural ligand 1α,25-(OH)2 D3 in modulation of tumor growth. However, both human and animal studies indicate tissue-specificity of effect. Epidemiological studies show both inverse and direct relationships between serum 25(OH)D levels a...
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| Veröffentlicht in: | Biochemical pharmacology 2010-01, Vol.79 (1), p.1-9 |
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| creator | Campbell, F.C. Xu, Haibo El-Tanani, M. Crowe, P. Bingham, V. |
| description | Substantive evidence implicates vitamin D receptor (VDR) or its natural ligand 1α,25-(OH)2 D3 in modulation of tumor growth. However, both human and animal studies indicate tissue-specificity of effect. Epidemiological studies show both inverse and direct relationships between serum 25(OH)D levels and common solid cancers. VDR ablation affects carcinogen-induced tumorigenesis in a tissue-specific manner in model systems. Better understanding of the tissue-specificity of vitamin D-dependent molecular networks may provide insight into selective growth control by the seco-steroid, 1α,25-(OH)2 D3. This commentary considers complex factors that may influence the cell- or tissue-specificity of 1α,25-(OH)2 D3/VDR growth effects, including local synthesis, metabolism and transport of vitamin D and its metabolites, vitamin D receptor (VDR) expression and ligand-interactions, 1α,25-(OH)2 D3 genomic and non-genomic actions, Ca2+ flux, kinase activation, VDR interactions with activating and inhibitory vitamin D responsive elements (VDREs) within target gene promoters, VDR coregulator recruitment and differential effects on key downstream growth regulatory genes. We highlight some differences of VDR growth control relevant to colonic, esophageal, prostate, pancreatic and other cancers and assess the potential for development of selective prevention or treatment strategies. |
| doi_str_mv | 10.1016/j.bcp.2009.09.005 |
| format | Article |
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However, both human and animal studies indicate tissue-specificity of effect. Epidemiological studies show both inverse and direct relationships between serum 25(OH)D levels and common solid cancers. VDR ablation affects carcinogen-induced tumorigenesis in a tissue-specific manner in model systems. Better understanding of the tissue-specificity of vitamin D-dependent molecular networks may provide insight into selective growth control by the seco-steroid, 1α,25-(OH)2 D3. This commentary considers complex factors that may influence the cell- or tissue-specificity of 1α,25-(OH)2 D3/VDR growth effects, including local synthesis, metabolism and transport of vitamin D and its metabolites, vitamin D receptor (VDR) expression and ligand-interactions, 1α,25-(OH)2 D3 genomic and non-genomic actions, Ca2+ flux, kinase activation, VDR interactions with activating and inhibitory vitamin D responsive elements (VDREs) within target gene promoters, VDR coregulator recruitment and differential effects on key downstream growth regulatory genes. We highlight some differences of VDR growth control relevant to colonic, esophageal, prostate, pancreatic and other cancers and assess the potential for development of selective prevention or treatment strategies.</description><identifier>ISSN: 0006-2952</identifier><identifier>EISSN: 1873-2968</identifier><identifier>DOI: 10.1016/j.bcp.2009.09.005</identifier><identifier>PMID: 19737544</identifier><identifier>CODEN: BCPCA6</identifier><language>eng</language><publisher>Amsterdam: Elsevier Inc</publisher><subject>1α,25-(OH)2 D3 ; Animals ; Biological and medical sciences ; Cancer ; Cholecalciferol - metabolism ; Cholecalciferol - physiology ; Dimerization ; Disease Progression ; Gene Targeting ; Humans ; Ligands ; Medical sciences ; Neoplasms - drug therapy ; Neoplasms - genetics ; Neoplasms - metabolism ; Neoplasms - pathology ; Organ Specificity - genetics ; Organ Specificity - physiology ; Pharmacology. 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However, both human and animal studies indicate tissue-specificity of effect. Epidemiological studies show both inverse and direct relationships between serum 25(OH)D levels and common solid cancers. VDR ablation affects carcinogen-induced tumorigenesis in a tissue-specific manner in model systems. Better understanding of the tissue-specificity of vitamin D-dependent molecular networks may provide insight into selective growth control by the seco-steroid, 1α,25-(OH)2 D3. This commentary considers complex factors that may influence the cell- or tissue-specificity of 1α,25-(OH)2 D3/VDR growth effects, including local synthesis, metabolism and transport of vitamin D and its metabolites, vitamin D receptor (VDR) expression and ligand-interactions, 1α,25-(OH)2 D3 genomic and non-genomic actions, Ca2+ flux, kinase activation, VDR interactions with activating and inhibitory vitamin D responsive elements (VDREs) within target gene promoters, VDR coregulator recruitment and differential effects on key downstream growth regulatory genes. We highlight some differences of VDR growth control relevant to colonic, esophageal, prostate, pancreatic and other cancers and assess the potential for development of selective prevention or treatment strategies.</description><subject>1α,25-(OH)2 D3</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cancer</subject><subject>Cholecalciferol - metabolism</subject><subject>Cholecalciferol - physiology</subject><subject>Dimerization</subject><subject>Disease Progression</subject><subject>Gene Targeting</subject><subject>Humans</subject><subject>Ligands</subject><subject>Medical sciences</subject><subject>Neoplasms - drug therapy</subject><subject>Neoplasms - genetics</subject><subject>Neoplasms - metabolism</subject><subject>Neoplasms - pathology</subject><subject>Organ Specificity - genetics</subject><subject>Organ Specificity - physiology</subject><subject>Pharmacology. Drug treatments</subject><subject>Protein Isoforms - physiology</subject><subject>Receptors, Calcitriol - metabolism</subject><subject>Receptors, Calcitriol - physiology</subject><subject>Response Elements - genetics</subject><subject>Retinoid X Receptors - physiology</subject><subject>Signal Transduction - genetics</subject><subject>Signaling</subject><subject>Transcription, Genetic</subject><subject>Vitamin D receptor</subject><issn>0006-2952</issn><issn>1873-2968</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9UV1rFDEUDaLYtfoDfJG8CPZh1iSTmUkUhNJWKywUpAp9CtnszWzW2WRI0i3-BP91M-5SPx6EC7kf55x7yUHoJSVzSmj7djNfmnHOCJHzKUjzCM2o6OqKyVY8RjNCSFvyhh2hZyltplK09Ck6orKru4bzGfp5vQZ84zzWfoVvtO9xsHjnst6W3jmOYGDMIeI3386_nODkeq8HV1Bl6iGMg07ZGTzG0EdIyQX_Dl-NEHUuqR4KJt-F-D39ks8upVuo0gjG2cLqY7jLa2yCzzEMz9ETq4cELw7vMfr68eL67LJaXH36fHa6qEwjSK7auq0FIdB1VtqmE5LVjAPhspSkq1sNhjOQTPAlr1eWE05tZ5tGW0kMIbQ-Rh_2uuPtcgsrA2W7HtQY3VbHHypop_6eeLdWfdgpJhgXXBaBk73A-h_a5elCTb1iBJPFoN20jO6xJoaUItgHAiVq8lBtVPFQTR6qKUhTOK_-PPA342BaAbw-AHQyerBRe-PSA44xSgRvWMG93-OgfOfOQVTJOPAGVq74mtUquP-ccQ-v3bsS</recordid><startdate>20100101</startdate><enddate>20100101</enddate><creator>Campbell, F.C.</creator><creator>Xu, Haibo</creator><creator>El-Tanani, M.</creator><creator>Crowe, P.</creator><creator>Bingham, V.</creator><general>Elsevier Inc</general><general>Elsevier</general><general>Elsevier Science</general><scope>6I.</scope><scope>AAFTH</scope><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>1XC</scope><scope>VOOES</scope><scope>5PM</scope></search><sort><creationdate>20100101</creationdate><title>The Yin and Yang of vitamin D receptor (VDR) signaling in neoplastic progression: Operational networks and tissue-specific growth control</title><author>Campbell, F.C. ; Xu, Haibo ; El-Tanani, M. ; Crowe, P. ; Bingham, V.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c580t-6363800e77f9f57892324e049f9f0736aec42e9284b43df4041f7f55af90c0013</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>1α,25-(OH)2 D3</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cancer</topic><topic>Cholecalciferol - metabolism</topic><topic>Cholecalciferol - physiology</topic><topic>Dimerization</topic><topic>Disease Progression</topic><topic>Gene Targeting</topic><topic>Humans</topic><topic>Ligands</topic><topic>Medical sciences</topic><topic>Neoplasms - drug therapy</topic><topic>Neoplasms - genetics</topic><topic>Neoplasms - metabolism</topic><topic>Neoplasms - pathology</topic><topic>Organ Specificity - genetics</topic><topic>Organ Specificity - physiology</topic><topic>Pharmacology. Drug treatments</topic><topic>Protein Isoforms - physiology</topic><topic>Receptors, Calcitriol - metabolism</topic><topic>Receptors, Calcitriol - physiology</topic><topic>Response Elements - genetics</topic><topic>Retinoid X Receptors - physiology</topic><topic>Signal Transduction - genetics</topic><topic>Signaling</topic><topic>Transcription, Genetic</topic><topic>Vitamin D receptor</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Campbell, F.C.</creatorcontrib><creatorcontrib>Xu, Haibo</creatorcontrib><creatorcontrib>El-Tanani, M.</creatorcontrib><creatorcontrib>Crowe, P.</creatorcontrib><creatorcontrib>Bingham, V.</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><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>Hyper Article en Ligne (HAL)</collection><collection>Hyper Article en Ligne (HAL) (Open Access)</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Biochemical pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Campbell, F.C.</au><au>Xu, Haibo</au><au>El-Tanani, M.</au><au>Crowe, P.</au><au>Bingham, V.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Yin and Yang of vitamin D receptor (VDR) signaling in neoplastic progression: Operational networks and tissue-specific growth control</atitle><jtitle>Biochemical pharmacology</jtitle><addtitle>Biochem Pharmacol</addtitle><date>2010-01-01</date><risdate>2010</risdate><volume>79</volume><issue>1</issue><spage>1</spage><epage>9</epage><pages>1-9</pages><issn>0006-2952</issn><eissn>1873-2968</eissn><coden>BCPCA6</coden><abstract>Substantive evidence implicates vitamin D receptor (VDR) or its natural ligand 1α,25-(OH)2 D3 in modulation of tumor growth. However, both human and animal studies indicate tissue-specificity of effect. Epidemiological studies show both inverse and direct relationships between serum 25(OH)D levels and common solid cancers. VDR ablation affects carcinogen-induced tumorigenesis in a tissue-specific manner in model systems. Better understanding of the tissue-specificity of vitamin D-dependent molecular networks may provide insight into selective growth control by the seco-steroid, 1α,25-(OH)2 D3. This commentary considers complex factors that may influence the cell- or tissue-specificity of 1α,25-(OH)2 D3/VDR growth effects, including local synthesis, metabolism and transport of vitamin D and its metabolites, vitamin D receptor (VDR) expression and ligand-interactions, 1α,25-(OH)2 D3 genomic and non-genomic actions, Ca2+ flux, kinase activation, VDR interactions with activating and inhibitory vitamin D responsive elements (VDREs) within target gene promoters, VDR coregulator recruitment and differential effects on key downstream growth regulatory genes. We highlight some differences of VDR growth control relevant to colonic, esophageal, prostate, pancreatic and other cancers and assess the potential for development of selective prevention or treatment strategies.</abstract><cop>Amsterdam</cop><pub>Elsevier Inc</pub><pmid>19737544</pmid><doi>10.1016/j.bcp.2009.09.005</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Biochemical pharmacology, 2010-01, Vol.79 (1), p.1-9 |
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| source | MEDLINE; Elsevier ScienceDirect Journals Complete |
| subjects | 1α,25-(OH)2 D3 Animals Biological and medical sciences Cancer Cholecalciferol - metabolism Cholecalciferol - physiology Dimerization Disease Progression Gene Targeting Humans Ligands Medical sciences Neoplasms - drug therapy Neoplasms - genetics Neoplasms - metabolism Neoplasms - pathology Organ Specificity - genetics Organ Specificity - physiology Pharmacology. Drug treatments Protein Isoforms - physiology Receptors, Calcitriol - metabolism Receptors, Calcitriol - physiology Response Elements - genetics Retinoid X Receptors - physiology Signal Transduction - genetics Signaling Transcription, Genetic Vitamin D receptor |
| title | The Yin and Yang of vitamin D receptor (VDR) signaling in neoplastic progression: Operational networks and tissue-specific growth control |
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