Involvement of 1,25D3-MARRS (membrane associated, rapid response steroid-binding), a novel vitamin D receptor, in growth inhibition of breast cancer cells
In addition to classical roles in calcium homeostasis and bone development, 1,25 dihydroxyvitamin D3 [1,25(OH)2D3] inhibits the growth of several cancer types, including breast cancer. Although cellular effects of 1,25(OH)2D3 traditionally have been attributed to activation of a nuclear vitamin D re...
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| Veröffentlicht in: | Experimental cell research 2010-03, Vol.316 (5), p.695-703 |
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| creator | Richard, Cynthia L Farach-Carson, Mary C Rohe, Ben Nemere, Ilka Meckling, Kelly A |
| description | In addition to classical roles in calcium homeostasis and bone development, 1,25 dihydroxyvitamin D3 [1,25(OH)2D3] inhibits the growth of several cancer types, including breast cancer. Although cellular effects of 1,25(OH)2D3 traditionally have been attributed to activation of a nuclear vitamin D receptor (VDR), a novel receptor for 1,25(OH)2D3 called 1,25D3-MARRS (membrane-associated, rapid response steroid-binding) protein was identified recently. The purpose of this study was to determine if the level of 1,25D3-MARRS expression modulates 1,25(OH)2D3 activity in breast cancer cells. Relative levels of 1,25D3-MARRS protein in MCF-7, MDA MB 231, and MCF-10A cells were estimated by real-time RT-PCR and Western blotting. To determine if 1,25D3-MARRS receptor was involved in the growth inhibitory effects of 1,25(OH)2D3 in MCF-7 cells, a ribozyme construct designed to knock down 1,25D(3)-MARRS mRNA was stably transfected into MCF-7 cells. MCF-7 clones in which 1,25D3-MARRS receptor expression was reduced showed increased sensitivity to 1,25(OH)2D3 ( IC(50) 56+/-24 nM) compared to controls (319+/-181 nM; P |
| doi_str_mv | 10.1016/j.yexcr.2009.12.015 |
| format | Article |
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Although cellular effects of 1,25(OH)2D3 traditionally have been attributed to activation of a nuclear vitamin D receptor (VDR), a novel receptor for 1,25(OH)2D3 called 1,25D3-MARRS (membrane-associated, rapid response steroid-binding) protein was identified recently. The purpose of this study was to determine if the level of 1,25D3-MARRS expression modulates 1,25(OH)2D3 activity in breast cancer cells. Relative levels of 1,25D3-MARRS protein in MCF-7, MDA MB 231, and MCF-10A cells were estimated by real-time RT-PCR and Western blotting. To determine if 1,25D3-MARRS receptor was involved in the growth inhibitory effects of 1,25(OH)2D3 in MCF-7 cells, a ribozyme construct designed to knock down 1,25D(3)-MARRS mRNA was stably transfected into MCF-7 cells. MCF-7 clones in which 1,25D3-MARRS receptor expression was reduced showed increased sensitivity to 1,25(OH)2D3 ( IC(50) 56+/-24 nM) compared to controls (319+/-181 nM; P<0.05). Reduction in 1,25D3-MARRS receptor lengthened the doubling time in transfectants treated with 1,25(OH)2D3. Knockdown of 1,25D3-MARRS receptor also increased the sensitivity of MCF-7 cells to the vitamin D analogs KH1060 and MC903, but not to unrelated agents (all-trans retinoic acid, paclitaxel, serum/glucose starvation, or the isoflavone, pomiferin). These results suggest that 1,25D3-MARRS receptor expression interferes with the growth inhibitory activity of 1,25(OH)2D3 in breast cancer cells, possibly through the nuclear VDR. Further research should examine the potential for pharmacological or natural agents that modify 1,25D3-MARRS expression or activity as anticancer agents.</description><identifier>ISSN: 0014-4827</identifier><identifier>EISSN: 1090-2422</identifier><identifier>DOI: 10.1016/j.yexcr.2009.12.015</identifier><identifier>PMID: 20036234</identifier><language>eng</language><publisher>United States: Elsevier BV</publisher><subject>Animals ; Antineoplastic Agents - metabolism ; Antineoplastic Agents, Phytogenic - metabolism ; Benzopyrans - metabolism ; Breast cancer ; Breast Neoplasms - genetics ; Breast Neoplasms - metabolism ; Cell Line, Tumor ; Cellular biology ; Female ; Humans ; Isoflavones - metabolism ; Paclitaxel - metabolism ; Proteins ; Receptors, Calcitriol - genetics ; Receptors, Calcitriol - metabolism ; RNA, Catalytic - metabolism ; Steroids ; Tretinoin - metabolism ; Vitamin D ; Vitamin D - analogs & derivatives ; Vitamin D - metabolism</subject><ispartof>Experimental cell research, 2010-03, Vol.316 (5), p.695-703</ispartof><rights>2009 Elsevier Inc. All rights reserved.</rights><rights>Copyright © 2010 Elsevier B.V. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c246t-731a322d176db5e25fc54e6e9dcd4d88fb1601f00a283e5043a80ceeea9d1c203</citedby><cites>FETCH-LOGICAL-c246t-731a322d176db5e25fc54e6e9dcd4d88fb1601f00a283e5043a80ceeea9d1c203</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20036234$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Richard, Cynthia L</creatorcontrib><creatorcontrib>Farach-Carson, Mary C</creatorcontrib><creatorcontrib>Rohe, Ben</creatorcontrib><creatorcontrib>Nemere, Ilka</creatorcontrib><creatorcontrib>Meckling, Kelly A</creatorcontrib><title>Involvement of 1,25D3-MARRS (membrane associated, rapid response steroid-binding), a novel vitamin D receptor, in growth inhibition of breast cancer cells</title><title>Experimental cell research</title><addtitle>Exp Cell Res</addtitle><description>In addition to classical roles in calcium homeostasis and bone development, 1,25 dihydroxyvitamin D3 [1,25(OH)2D3] inhibits the growth of several cancer types, including breast cancer. Although cellular effects of 1,25(OH)2D3 traditionally have been attributed to activation of a nuclear vitamin D receptor (VDR), a novel receptor for 1,25(OH)2D3 called 1,25D3-MARRS (membrane-associated, rapid response steroid-binding) protein was identified recently. The purpose of this study was to determine if the level of 1,25D3-MARRS expression modulates 1,25(OH)2D3 activity in breast cancer cells. Relative levels of 1,25D3-MARRS protein in MCF-7, MDA MB 231, and MCF-10A cells were estimated by real-time RT-PCR and Western blotting. To determine if 1,25D3-MARRS receptor was involved in the growth inhibitory effects of 1,25(OH)2D3 in MCF-7 cells, a ribozyme construct designed to knock down 1,25D(3)-MARRS mRNA was stably transfected into MCF-7 cells. MCF-7 clones in which 1,25D3-MARRS receptor expression was reduced showed increased sensitivity to 1,25(OH)2D3 ( IC(50) 56+/-24 nM) compared to controls (319+/-181 nM; P<0.05). Reduction in 1,25D3-MARRS receptor lengthened the doubling time in transfectants treated with 1,25(OH)2D3. Knockdown of 1,25D3-MARRS receptor also increased the sensitivity of MCF-7 cells to the vitamin D analogs KH1060 and MC903, but not to unrelated agents (all-trans retinoic acid, paclitaxel, serum/glucose starvation, or the isoflavone, pomiferin). These results suggest that 1,25D3-MARRS receptor expression interferes with the growth inhibitory activity of 1,25(OH)2D3 in breast cancer cells, possibly through the nuclear VDR. Further research should examine the potential for pharmacological or natural agents that modify 1,25D3-MARRS expression or activity as anticancer agents.</description><subject>Animals</subject><subject>Antineoplastic Agents - metabolism</subject><subject>Antineoplastic Agents, Phytogenic - metabolism</subject><subject>Benzopyrans - metabolism</subject><subject>Breast cancer</subject><subject>Breast Neoplasms - genetics</subject><subject>Breast Neoplasms - metabolism</subject><subject>Cell Line, Tumor</subject><subject>Cellular biology</subject><subject>Female</subject><subject>Humans</subject><subject>Isoflavones - metabolism</subject><subject>Paclitaxel - metabolism</subject><subject>Proteins</subject><subject>Receptors, Calcitriol - genetics</subject><subject>Receptors, Calcitriol - metabolism</subject><subject>RNA, Catalytic - metabolism</subject><subject>Steroids</subject><subject>Tretinoin - metabolism</subject><subject>Vitamin D</subject><subject>Vitamin D - analogs & derivatives</subject><subject>Vitamin D - metabolism</subject><issn>0014-4827</issn><issn>1090-2422</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkVtrFDEUx4Modlv9BIIEX6ywM55c5vZYWi-FilD1OWSSM22WmWRNsqv9Kn5as7b64FNO4Pc_F36EvGBQM2Dt2019hz9NrDnAUDNeA2sekRWDASouOX9MVgBMVrLn3RE5TmkDAH3P2qfkqEREy4VckV-Xfh_mPS7oMw0TZWveXIjq09n19Rd6uuAyRu2R6pSCcTqjXdOot87SiGkbfEKaMsbgbDU6b52_ebOmmvqwx5nuXdaL8_SiwAa3OcQ1Ld-bGH7k21LdutFlF_xh7hhRp0yN9gYjNTjP6Rl5Muk54fOH94R8e__u6_nH6urzh8vzs6vKcNnmqhNMC84t61o7NsibyTQSWxyssdL2_TSyFtgEoHkvsAEpdA8GEfVgmeEgTsjr-77bGL7vMGW1uHTYoBwedkl1QvTQcykK-eo_chN20ZflFBtk27dDxwsk7iETQ0oRJ7WNbtHxTjFQB3Fqo_6IUwdxinFVxJXUy4fWu3FB-y_z15T4DU8oli4</recordid><startdate>20100310</startdate><enddate>20100310</enddate><creator>Richard, Cynthia L</creator><creator>Farach-Carson, Mary C</creator><creator>Rohe, Ben</creator><creator>Nemere, Ilka</creator><creator>Meckling, Kelly A</creator><general>Elsevier BV</general><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>7TK</scope><scope>7TM</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20100310</creationdate><title>Involvement of 1,25D3-MARRS (membrane associated, rapid response steroid-binding), a novel vitamin D receptor, in growth inhibition of breast cancer cells</title><author>Richard, Cynthia L ; Farach-Carson, Mary C ; Rohe, Ben ; Nemere, Ilka ; Meckling, Kelly A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c246t-731a322d176db5e25fc54e6e9dcd4d88fb1601f00a283e5043a80ceeea9d1c203</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Animals</topic><topic>Antineoplastic Agents - metabolism</topic><topic>Antineoplastic Agents, Phytogenic - metabolism</topic><topic>Benzopyrans - metabolism</topic><topic>Breast cancer</topic><topic>Breast Neoplasms - genetics</topic><topic>Breast Neoplasms - metabolism</topic><topic>Cell Line, Tumor</topic><topic>Cellular biology</topic><topic>Female</topic><topic>Humans</topic><topic>Isoflavones - metabolism</topic><topic>Paclitaxel - metabolism</topic><topic>Proteins</topic><topic>Receptors, Calcitriol - genetics</topic><topic>Receptors, Calcitriol - metabolism</topic><topic>RNA, Catalytic - metabolism</topic><topic>Steroids</topic><topic>Tretinoin - metabolism</topic><topic>Vitamin D</topic><topic>Vitamin D - analogs & derivatives</topic><topic>Vitamin D - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Richard, Cynthia L</creatorcontrib><creatorcontrib>Farach-Carson, Mary C</creatorcontrib><creatorcontrib>Rohe, Ben</creatorcontrib><creatorcontrib>Nemere, Ilka</creatorcontrib><creatorcontrib>Meckling, Kelly A</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Experimental cell research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Richard, Cynthia L</au><au>Farach-Carson, Mary C</au><au>Rohe, Ben</au><au>Nemere, Ilka</au><au>Meckling, Kelly A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Involvement of 1,25D3-MARRS (membrane associated, rapid response steroid-binding), a novel vitamin D receptor, in growth inhibition of breast cancer cells</atitle><jtitle>Experimental cell research</jtitle><addtitle>Exp Cell Res</addtitle><date>2010-03-10</date><risdate>2010</risdate><volume>316</volume><issue>5</issue><spage>695</spage><epage>703</epage><pages>695-703</pages><issn>0014-4827</issn><eissn>1090-2422</eissn><abstract>In addition to classical roles in calcium homeostasis and bone development, 1,25 dihydroxyvitamin D3 [1,25(OH)2D3] inhibits the growth of several cancer types, including breast cancer. Although cellular effects of 1,25(OH)2D3 traditionally have been attributed to activation of a nuclear vitamin D receptor (VDR), a novel receptor for 1,25(OH)2D3 called 1,25D3-MARRS (membrane-associated, rapid response steroid-binding) protein was identified recently. The purpose of this study was to determine if the level of 1,25D3-MARRS expression modulates 1,25(OH)2D3 activity in breast cancer cells. Relative levels of 1,25D3-MARRS protein in MCF-7, MDA MB 231, and MCF-10A cells were estimated by real-time RT-PCR and Western blotting. To determine if 1,25D3-MARRS receptor was involved in the growth inhibitory effects of 1,25(OH)2D3 in MCF-7 cells, a ribozyme construct designed to knock down 1,25D(3)-MARRS mRNA was stably transfected into MCF-7 cells. MCF-7 clones in which 1,25D3-MARRS receptor expression was reduced showed increased sensitivity to 1,25(OH)2D3 ( IC(50) 56+/-24 nM) compared to controls (319+/-181 nM; P<0.05). Reduction in 1,25D3-MARRS receptor lengthened the doubling time in transfectants treated with 1,25(OH)2D3. Knockdown of 1,25D3-MARRS receptor also increased the sensitivity of MCF-7 cells to the vitamin D analogs KH1060 and MC903, but not to unrelated agents (all-trans retinoic acid, paclitaxel, serum/glucose starvation, or the isoflavone, pomiferin). These results suggest that 1,25D3-MARRS receptor expression interferes with the growth inhibitory activity of 1,25(OH)2D3 in breast cancer cells, possibly through the nuclear VDR. Further research should examine the potential for pharmacological or natural agents that modify 1,25D3-MARRS expression or activity as anticancer agents.</abstract><cop>United States</cop><pub>Elsevier BV</pub><pmid>20036234</pmid><doi>10.1016/j.yexcr.2009.12.015</doi><tpages>9</tpages></addata></record> |
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| ispartof | Experimental cell research, 2010-03, Vol.316 (5), p.695-703 |
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| subjects | Animals Antineoplastic Agents - metabolism Antineoplastic Agents, Phytogenic - metabolism Benzopyrans - metabolism Breast cancer Breast Neoplasms - genetics Breast Neoplasms - metabolism Cell Line, Tumor Cellular biology Female Humans Isoflavones - metabolism Paclitaxel - metabolism Proteins Receptors, Calcitriol - genetics Receptors, Calcitriol - metabolism RNA, Catalytic - metabolism Steroids Tretinoin - metabolism Vitamin D Vitamin D - analogs & derivatives Vitamin D - metabolism |
| title | Involvement of 1,25D3-MARRS (membrane associated, rapid response steroid-binding), a novel vitamin D receptor, in growth inhibition of breast cancer cells |
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