Modulation of retinoic acid receptor function alters the growth inhibitory response of oral SCC cells to retinoids
Retinoids have been shown to inhibit the growth of many human tumor cells including breast, ovarian and squamous cell carcinoma (SCC). While the exact mechanism of retinoid mediated growth suppression is not known, a role for the retinoic acid receptors (RARs) and retinoid X receptors (RXRs) has bee...
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| description | Retinoids have been shown to inhibit the growth of many human tumor cells including breast, ovarian and squamous cell carcinoma (SCC). While the exact mechanism of retinoid mediated growth suppression is not known, a role for the retinoic acid receptors (RARs) and retinoid X receptors (RXRs) has been established in both the breast and ovarian tumor cell models. We set out to determine if modulation of RAR/RXR function would alter the retinoid sensitivity of oral SCC cells. We found that the growth of SCC cells was significantly inhibited by treatment with either all-trans-retinoic acid (trans-RA) or the synthetic, conformationally restricted RARgamma selective retinoids MM11254 and MM11389. In order to demonstrate a role for RAR/RXR function in this process, stable oral SCC cell clones constitutively overexpressing the dominant negative mutant RARbeta2 (R269Q) were prepared and shown to exhibit reduced RAR/RXR transcriptional transactivation activity. We found that oral SCC cells exhibiting reduced RAR/RXR function became resistant to growth inhibition by all-trans-RA, MM11254 and MM11389. Likewise, treatment of oral SCC cells with the RARgamma antagonist MM11253 was found to block the ability of MM11254 and MM11389 to inhibit SCC cell growth. Thus, modulation of RAR function through the use of RAR-gamma selective agonists, an RAR-gamma selective antagonist or a pan-RAR dominant negative mutant significantly alters the growth inhibitory response of oral SCC cells to retinoids. |
| doi_str_mv | 10.1038/sj.onc.1203436 |
| format | Article |
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I ; SOPRANO, D. R ; SOPRANO, K. J</creator><creatorcontrib>QUAN LE ; DAWSON, M. I ; SOPRANO, D. R ; SOPRANO, K. J</creatorcontrib><description>Retinoids have been shown to inhibit the growth of many human tumor cells including breast, ovarian and squamous cell carcinoma (SCC). While the exact mechanism of retinoid mediated growth suppression is not known, a role for the retinoic acid receptors (RARs) and retinoid X receptors (RXRs) has been established in both the breast and ovarian tumor cell models. We set out to determine if modulation of RAR/RXR function would alter the retinoid sensitivity of oral SCC cells. We found that the growth of SCC cells was significantly inhibited by treatment with either all-trans-retinoic acid (trans-RA) or the synthetic, conformationally restricted RARgamma selective retinoids MM11254 and MM11389. In order to demonstrate a role for RAR/RXR function in this process, stable oral SCC cell clones constitutively overexpressing the dominant negative mutant RARbeta2 (R269Q) were prepared and shown to exhibit reduced RAR/RXR transcriptional transactivation activity. We found that oral SCC cells exhibiting reduced RAR/RXR function became resistant to growth inhibition by all-trans-RA, MM11254 and MM11389. Likewise, treatment of oral SCC cells with the RARgamma antagonist MM11253 was found to block the ability of MM11254 and MM11389 to inhibit SCC cell growth. Thus, modulation of RAR function through the use of RAR-gamma selective agonists, an RAR-gamma selective antagonist or a pan-RAR dominant negative mutant significantly alters the growth inhibitory response of oral SCC cells to retinoids.</description><identifier>ISSN: 0950-9232</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/sj.onc.1203436</identifier><identifier>PMID: 10723137</identifier><identifier>CODEN: ONCNES</identifier><language>eng</language><publisher>Basingstoke: Nature Publishing</publisher><subject>Acids ; Analysis ; Arginine - genetics ; Biological and medical sciences ; Breast ; Carcinoma, Squamous Cell - genetics ; Carcinoma, Squamous Cell - metabolism ; Carcinoma, Squamous Cell - pathology ; Cell culture ; Cell Division - drug effects ; Cell Division - genetics ; Cell growth ; Cell physiology ; Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes ; Fundamental and applied biological sciences. Psychology ; Gene Transfer Techniques ; Glutamine - genetics ; Growth ; Growth Inhibitors - genetics ; Growth Inhibitors - metabolism ; Growth Inhibitors - pharmacology ; Humans ; Immunology ; Medical research ; Medicine ; Molecular and cellular biology ; Mouth Neoplasms - genetics ; Mouth Neoplasms - metabolism ; Mouth Neoplasms - pathology ; Mutagenesis, Site-Directed ; Mutants ; Oral cancer ; Ovaries ; Receptors, Retinoic Acid - agonists ; Receptors, Retinoic Acid - antagonists & inhibitors ; Receptors, Retinoic Acid - biosynthesis ; Receptors, Retinoic Acid - genetics ; Receptors, Retinoic Acid - metabolism ; Receptors, Retinoic Acid - physiology ; Retinoic acid ; Retinoic Acid Receptor gamma ; Retinoic acid receptors ; Retinoid X receptors ; Retinoids ; Retinoids - chemical synthesis ; Retinoids - pharmacology ; Squamous cell carcinoma ; Transcription ; Tretinoin - pharmacology ; Tumor cells ; Tumor Cells, Cultured ; Tumors</subject><ispartof>Oncogene, 2000-03, Vol.19 (11), p.1457-1465</ispartof><rights>2000 INIST-CNRS</rights><rights>COPYRIGHT 2000 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Mar 9, 2000</rights><rights>Macmillan Publishers Limited 2000.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c539t-b88f498c0803cec98cf3b0650f09e22200d74fee196e0ca371981f71f21631573</citedby><cites>FETCH-LOGICAL-c539t-b88f498c0803cec98cf3b0650f09e22200d74fee196e0ca371981f71f21631573</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1304572$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10723137$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>QUAN LE</creatorcontrib><creatorcontrib>DAWSON, M. I</creatorcontrib><creatorcontrib>SOPRANO, D. R</creatorcontrib><creatorcontrib>SOPRANO, K. J</creatorcontrib><title>Modulation of retinoic acid receptor function alters the growth inhibitory response of oral SCC cells to retinoids</title><title>Oncogene</title><addtitle>Oncogene</addtitle><description>Retinoids have been shown to inhibit the growth of many human tumor cells including breast, ovarian and squamous cell carcinoma (SCC). While the exact mechanism of retinoid mediated growth suppression is not known, a role for the retinoic acid receptors (RARs) and retinoid X receptors (RXRs) has been established in both the breast and ovarian tumor cell models. We set out to determine if modulation of RAR/RXR function would alter the retinoid sensitivity of oral SCC cells. We found that the growth of SCC cells was significantly inhibited by treatment with either all-trans-retinoic acid (trans-RA) or the synthetic, conformationally restricted RARgamma selective retinoids MM11254 and MM11389. In order to demonstrate a role for RAR/RXR function in this process, stable oral SCC cell clones constitutively overexpressing the dominant negative mutant RARbeta2 (R269Q) were prepared and shown to exhibit reduced RAR/RXR transcriptional transactivation activity. We found that oral SCC cells exhibiting reduced RAR/RXR function became resistant to growth inhibition by all-trans-RA, MM11254 and MM11389. Likewise, treatment of oral SCC cells with the RARgamma antagonist MM11253 was found to block the ability of MM11254 and MM11389 to inhibit SCC cell growth. Thus, modulation of RAR function through the use of RAR-gamma selective agonists, an RAR-gamma selective antagonist or a pan-RAR dominant negative mutant significantly alters the growth inhibitory response of oral SCC cells to retinoids.</description><subject>Acids</subject><subject>Analysis</subject><subject>Arginine - genetics</subject><subject>Biological and medical sciences</subject><subject>Breast</subject><subject>Carcinoma, Squamous Cell - genetics</subject><subject>Carcinoma, Squamous Cell - metabolism</subject><subject>Carcinoma, Squamous Cell - pathology</subject><subject>Cell culture</subject><subject>Cell Division - drug effects</subject><subject>Cell Division - genetics</subject><subject>Cell growth</subject><subject>Cell physiology</subject><subject>Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes</subject><subject>Fundamental and applied biological sciences. 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I</au><au>SOPRANO, D. R</au><au>SOPRANO, K. J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Modulation of retinoic acid receptor function alters the growth inhibitory response of oral SCC cells to retinoids</atitle><jtitle>Oncogene</jtitle><addtitle>Oncogene</addtitle><date>2000-03-09</date><risdate>2000</risdate><volume>19</volume><issue>11</issue><spage>1457</spage><epage>1465</epage><pages>1457-1465</pages><issn>0950-9232</issn><eissn>1476-5594</eissn><coden>ONCNES</coden><abstract>Retinoids have been shown to inhibit the growth of many human tumor cells including breast, ovarian and squamous cell carcinoma (SCC). While the exact mechanism of retinoid mediated growth suppression is not known, a role for the retinoic acid receptors (RARs) and retinoid X receptors (RXRs) has been established in both the breast and ovarian tumor cell models. We set out to determine if modulation of RAR/RXR function would alter the retinoid sensitivity of oral SCC cells. We found that the growth of SCC cells was significantly inhibited by treatment with either all-trans-retinoic acid (trans-RA) or the synthetic, conformationally restricted RARgamma selective retinoids MM11254 and MM11389. In order to demonstrate a role for RAR/RXR function in this process, stable oral SCC cell clones constitutively overexpressing the dominant negative mutant RARbeta2 (R269Q) were prepared and shown to exhibit reduced RAR/RXR transcriptional transactivation activity. We found that oral SCC cells exhibiting reduced RAR/RXR function became resistant to growth inhibition by all-trans-RA, MM11254 and MM11389. Likewise, treatment of oral SCC cells with the RARgamma antagonist MM11253 was found to block the ability of MM11254 and MM11389 to inhibit SCC cell growth. Thus, modulation of RAR function through the use of RAR-gamma selective agonists, an RAR-gamma selective antagonist or a pan-RAR dominant negative mutant significantly alters the growth inhibitory response of oral SCC cells to retinoids.</abstract><cop>Basingstoke</cop><pub>Nature Publishing</pub><pmid>10723137</pmid><doi>10.1038/sj.onc.1203436</doi><tpages>9</tpages></addata></record> |
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| subjects | Acids Analysis Arginine - genetics Biological and medical sciences Breast Carcinoma, Squamous Cell - genetics Carcinoma, Squamous Cell - metabolism Carcinoma, Squamous Cell - pathology Cell culture Cell Division - drug effects Cell Division - genetics Cell growth Cell physiology Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes Fundamental and applied biological sciences. Psychology Gene Transfer Techniques Glutamine - genetics Growth Growth Inhibitors - genetics Growth Inhibitors - metabolism Growth Inhibitors - pharmacology Humans Immunology Medical research Medicine Molecular and cellular biology Mouth Neoplasms - genetics Mouth Neoplasms - metabolism Mouth Neoplasms - pathology Mutagenesis, Site-Directed Mutants Oral cancer Ovaries Receptors, Retinoic Acid - agonists Receptors, Retinoic Acid - antagonists & inhibitors Receptors, Retinoic Acid - biosynthesis Receptors, Retinoic Acid - genetics Receptors, Retinoic Acid - metabolism Receptors, Retinoic Acid - physiology Retinoic acid Retinoic Acid Receptor gamma Retinoic acid receptors Retinoid X receptors Retinoids Retinoids - chemical synthesis Retinoids - pharmacology Squamous cell carcinoma Transcription Tretinoin - pharmacology Tumor cells Tumor Cells, Cultured Tumors |
| title | Modulation of retinoic acid receptor function alters the growth inhibitory response of oral SCC cells to retinoids |
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