miR-30-5p Functions as a Tumor Suppressor and Novel Therapeutic Tool by Targeting the Oncogenic Wnt/β-Catenin/BCL9 Pathway
Wnt/β-catenin signaling underlies the pathogenesis of a broad range of human cancers, including the deadly plasma cell cancer multiple myeloma. In this study, we report that downregulation of the tumor suppressor microRNA miR-30-5p is a frequent pathogenetic event in multiple myeloma. Evidence was d...
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| Veröffentlicht in: | Cancer research (Chicago, Ill.) Ill.), 2014-03, Vol.74 (6), p.1801-1813 |
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| creator | ZHAO, Jian-Jun JIANHONG LIN JIANGUO TAO TAI, Yu-Tzu TREON, Steven PINKUS, Geraldine KUO, Winston Patrick HIDESHIMA, Teru BOUXSEIN, Mary MUNSHI, Nikhil ANDERSON, Kenneth CARRASCO, Ruben DI ZHU XUJUN WANG BROOKS, Daniel MING CHEN CHU, Zhang-Bo TAKADA, Kohichi CICCARELLI, Bryan ADMIN, Samir |
| description | Wnt/β-catenin signaling underlies the pathogenesis of a broad range of human cancers, including the deadly plasma cell cancer multiple myeloma. In this study, we report that downregulation of the tumor suppressor microRNA miR-30-5p is a frequent pathogenetic event in multiple myeloma. Evidence was developed that miR-30-5p downregulation occurs as a result of interaction between multiple myeloma cells and bone marrow stromal cells, which in turn enhances expression of BCL9, a transcriptional coactivator of the Wnt signaling pathway known to promote multiple myeloma cell proliferation, survival, migration, drug resistance, and formation of multiple myeloma cancer stem cells. The potential for clinical translation of strategies to re-express miR-30-5p as a therapeutic approach was further encouraged by the capacity of miR-30c and miR-30 mix to reduce tumor burden and metastatic potential in vivo in three murine xenograft models of human multiple myeloma without adversely affecting associated bone disease. Together, our findings offer a preclinical rationale to explore miR-30-5p delivery as an effective therapeutic strategy to eradicate multiple myeloma cells in vivo. |
| doi_str_mv | 10.1158/0008-5472.CAN-13-3311-T |
| format | Article |
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In this study, we report that downregulation of the tumor suppressor microRNA miR-30-5p is a frequent pathogenetic event in multiple myeloma. Evidence was developed that miR-30-5p downregulation occurs as a result of interaction between multiple myeloma cells and bone marrow stromal cells, which in turn enhances expression of BCL9, a transcriptional coactivator of the Wnt signaling pathway known to promote multiple myeloma cell proliferation, survival, migration, drug resistance, and formation of multiple myeloma cancer stem cells. The potential for clinical translation of strategies to re-express miR-30-5p as a therapeutic approach was further encouraged by the capacity of miR-30c and miR-30 mix to reduce tumor burden and metastatic potential in vivo in three murine xenograft models of human multiple myeloma without adversely affecting associated bone disease. Together, our findings offer a preclinical rationale to explore miR-30-5p delivery as an effective therapeutic strategy to eradicate multiple myeloma cells in vivo.</description><identifier>ISSN: 0008-5472</identifier><identifier>EISSN: 1538-7445</identifier><identifier>DOI: 10.1158/0008-5472.CAN-13-3311-T</identifier><identifier>PMID: 24599134</identifier><identifier>CODEN: CNREA8</identifier><language>eng</language><publisher>Philadelphia, PA: American Association for Cancer Research</publisher><subject>3' Untranslated Regions ; Animals ; Antineoplastic agents ; Apoptosis ; Base Sequence ; Biological and medical sciences ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Down-Regulation ; Drug Resistance, Neoplasm ; Gene Expression Regulation, Neoplastic ; Genes, Tumor Suppressor ; HEK293 Cells ; Humans ; Medical sciences ; Mice ; Mice, Inbred NOD ; Mice, SCID ; MicroRNAs - genetics ; Multiple Myeloma - genetics ; Multiple Myeloma - metabolism ; Multiple Myeloma - pathology ; Neoplasm Invasiveness ; Neoplasm Proteins - genetics ; Neoplasm Proteins - metabolism ; Neoplasm Transplantation ; Neoplastic Stem Cells - metabolism ; Pharmacology. Drug treatments ; RNA Interference ; Tumor Burden ; Tumors ; Wnt Signaling Pathway</subject><ispartof>Cancer research (Chicago, Ill.), 2014-03, Vol.74 (6), p.1801-1813</ispartof><rights>2015 INIST-CNRS</rights><rights>2014 AACR.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c377t-623318734781c1a879bdd3923286f32a0cf2eb33a83dac7827c38e6af5c8bc9b3</citedby><cites>FETCH-LOGICAL-c377t-623318734781c1a879bdd3923286f32a0cf2eb33a83dac7827c38e6af5c8bc9b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,3356,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=28398975$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24599134$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>ZHAO, Jian-Jun</creatorcontrib><creatorcontrib>JIANHONG LIN</creatorcontrib><creatorcontrib>JIANGUO TAO</creatorcontrib><creatorcontrib>TAI, Yu-Tzu</creatorcontrib><creatorcontrib>TREON, Steven</creatorcontrib><creatorcontrib>PINKUS, Geraldine</creatorcontrib><creatorcontrib>KUO, Winston Patrick</creatorcontrib><creatorcontrib>HIDESHIMA, Teru</creatorcontrib><creatorcontrib>BOUXSEIN, Mary</creatorcontrib><creatorcontrib>MUNSHI, Nikhil</creatorcontrib><creatorcontrib>ANDERSON, Kenneth</creatorcontrib><creatorcontrib>CARRASCO, Ruben</creatorcontrib><creatorcontrib>DI ZHU</creatorcontrib><creatorcontrib>XUJUN WANG</creatorcontrib><creatorcontrib>BROOKS, Daniel</creatorcontrib><creatorcontrib>MING CHEN</creatorcontrib><creatorcontrib>CHU, Zhang-Bo</creatorcontrib><creatorcontrib>TAKADA, Kohichi</creatorcontrib><creatorcontrib>CICCARELLI, Bryan</creatorcontrib><creatorcontrib>ADMIN, Samir</creatorcontrib><title>miR-30-5p Functions as a Tumor Suppressor and Novel Therapeutic Tool by Targeting the Oncogenic Wnt/β-Catenin/BCL9 Pathway</title><title>Cancer research (Chicago, Ill.)</title><addtitle>Cancer Res</addtitle><description>Wnt/β-catenin signaling underlies the pathogenesis of a broad range of human cancers, including the deadly plasma cell cancer multiple myeloma. In this study, we report that downregulation of the tumor suppressor microRNA miR-30-5p is a frequent pathogenetic event in multiple myeloma. Evidence was developed that miR-30-5p downregulation occurs as a result of interaction between multiple myeloma cells and bone marrow stromal cells, which in turn enhances expression of BCL9, a transcriptional coactivator of the Wnt signaling pathway known to promote multiple myeloma cell proliferation, survival, migration, drug resistance, and formation of multiple myeloma cancer stem cells. The potential for clinical translation of strategies to re-express miR-30-5p as a therapeutic approach was further encouraged by the capacity of miR-30c and miR-30 mix to reduce tumor burden and metastatic potential in vivo in three murine xenograft models of human multiple myeloma without adversely affecting associated bone disease. Together, our findings offer a preclinical rationale to explore miR-30-5p delivery as an effective therapeutic strategy to eradicate multiple myeloma cells in vivo.</description><subject>3' Untranslated Regions</subject><subject>Animals</subject><subject>Antineoplastic agents</subject><subject>Apoptosis</subject><subject>Base Sequence</subject><subject>Biological and medical sciences</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement</subject><subject>Cell Proliferation</subject><subject>Down-Regulation</subject><subject>Drug Resistance, Neoplasm</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genes, Tumor Suppressor</subject><subject>HEK293 Cells</subject><subject>Humans</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred NOD</subject><subject>Mice, SCID</subject><subject>MicroRNAs - genetics</subject><subject>Multiple Myeloma - genetics</subject><subject>Multiple Myeloma - metabolism</subject><subject>Multiple Myeloma - pathology</subject><subject>Neoplasm Invasiveness</subject><subject>Neoplasm Proteins - genetics</subject><subject>Neoplasm Proteins - metabolism</subject><subject>Neoplasm Transplantation</subject><subject>Neoplastic Stem Cells - metabolism</subject><subject>Pharmacology. Drug treatments</subject><subject>RNA Interference</subject><subject>Tumor Burden</subject><subject>Tumors</subject><subject>Wnt Signaling Pathway</subject><issn>0008-5472</issn><issn>1538-7445</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkd-OEyEUh4nRuHX1FZQbE2_Y8mcocGOyTlw1aXaNjvGSMJRpx8zACMyaxrfyQXwmqVurJiRwcr7zA_IB8IzgC0K4XGKMJeKVoBf15TUiDDFGCGrugQXhTCJRVfw-WJyoM_AopS-l5ATzh-CMVlwpwqoF-D72HxDDiE_wavY298EnaMqCzTyGCD_O0xRdSuVo_AZeh1s3wGbnopncnHsLmxAG2O5hY-LW5d5vYd45eONt2Dpf-p99Xv78gWqTS-mXr-q1gu9N3n0z-8fgQWeG5J4c93Pw6ep1U79F65s37-rLNbJMiIxWtHxOClYJSSwxUqh2s2GKMipXHaMG2466ljEj2cZYIamwTLqV6biVrVUtOwcv73KnuR3dxjqfoxn0FPvRxL0Optf_d3y_09twq5niakVFCXhxDIjh6-xS1mOfrBsG412YkyYcy4pS_BsVd6iNIaXoutM1BOuDOn2Qog9SdFGnCdMHdbopk0__feVp7o-rAjw_AiZZM3TReNunv5xkSirB2S869aOP</recordid><startdate>20140315</startdate><enddate>20140315</enddate><creator>ZHAO, Jian-Jun</creator><creator>JIANHONG LIN</creator><creator>JIANGUO TAO</creator><creator>TAI, Yu-Tzu</creator><creator>TREON, Steven</creator><creator>PINKUS, Geraldine</creator><creator>KUO, Winston Patrick</creator><creator>HIDESHIMA, Teru</creator><creator>BOUXSEIN, Mary</creator><creator>MUNSHI, Nikhil</creator><creator>ANDERSON, Kenneth</creator><creator>CARRASCO, Ruben</creator><creator>DI ZHU</creator><creator>XUJUN WANG</creator><creator>BROOKS, Daniel</creator><creator>MING CHEN</creator><creator>CHU, Zhang-Bo</creator><creator>TAKADA, Kohichi</creator><creator>CICCARELLI, Bryan</creator><creator>ADMIN, Samir</creator><general>American Association for Cancer Research</general><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>7X8</scope><scope>5PM</scope></search><sort><creationdate>20140315</creationdate><title>miR-30-5p Functions as a Tumor Suppressor and Novel Therapeutic Tool by Targeting the Oncogenic Wnt/β-Catenin/BCL9 Pathway</title><author>ZHAO, Jian-Jun ; JIANHONG LIN ; JIANGUO TAO ; TAI, Yu-Tzu ; TREON, Steven ; PINKUS, Geraldine ; KUO, Winston Patrick ; HIDESHIMA, Teru ; BOUXSEIN, Mary ; MUNSHI, Nikhil ; ANDERSON, Kenneth ; CARRASCO, Ruben ; DI ZHU ; XUJUN WANG ; BROOKS, Daniel ; MING CHEN ; CHU, Zhang-Bo ; TAKADA, Kohichi ; CICCARELLI, Bryan ; ADMIN, Samir</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c377t-623318734781c1a879bdd3923286f32a0cf2eb33a83dac7827c38e6af5c8bc9b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>3' Untranslated Regions</topic><topic>Animals</topic><topic>Antineoplastic agents</topic><topic>Apoptosis</topic><topic>Base Sequence</topic><topic>Biological and medical sciences</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement</topic><topic>Cell Proliferation</topic><topic>Down-Regulation</topic><topic>Drug Resistance, Neoplasm</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Genes, Tumor Suppressor</topic><topic>HEK293 Cells</topic><topic>Humans</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred NOD</topic><topic>Mice, SCID</topic><topic>MicroRNAs - genetics</topic><topic>Multiple Myeloma - genetics</topic><topic>Multiple Myeloma - metabolism</topic><topic>Multiple Myeloma - pathology</topic><topic>Neoplasm Invasiveness</topic><topic>Neoplasm Proteins - genetics</topic><topic>Neoplasm Proteins - metabolism</topic><topic>Neoplasm Transplantation</topic><topic>Neoplastic Stem Cells - metabolism</topic><topic>Pharmacology. 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In this study, we report that downregulation of the tumor suppressor microRNA miR-30-5p is a frequent pathogenetic event in multiple myeloma. Evidence was developed that miR-30-5p downregulation occurs as a result of interaction between multiple myeloma cells and bone marrow stromal cells, which in turn enhances expression of BCL9, a transcriptional coactivator of the Wnt signaling pathway known to promote multiple myeloma cell proliferation, survival, migration, drug resistance, and formation of multiple myeloma cancer stem cells. The potential for clinical translation of strategies to re-express miR-30-5p as a therapeutic approach was further encouraged by the capacity of miR-30c and miR-30 mix to reduce tumor burden and metastatic potential in vivo in three murine xenograft models of human multiple myeloma without adversely affecting associated bone disease. Together, our findings offer a preclinical rationale to explore miR-30-5p delivery as an effective therapeutic strategy to eradicate multiple myeloma cells in vivo.</abstract><cop>Philadelphia, PA</cop><pub>American Association for Cancer Research</pub><pmid>24599134</pmid><doi>10.1158/0008-5472.CAN-13-3311-T</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Cancer research (Chicago, Ill.), 2014-03, Vol.74 (6), p.1801-1813 |
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| subjects | 3' Untranslated Regions Animals Antineoplastic agents Apoptosis Base Sequence Biological and medical sciences Cell Line, Tumor Cell Movement Cell Proliferation Down-Regulation Drug Resistance, Neoplasm Gene Expression Regulation, Neoplastic Genes, Tumor Suppressor HEK293 Cells Humans Medical sciences Mice Mice, Inbred NOD Mice, SCID MicroRNAs - genetics Multiple Myeloma - genetics Multiple Myeloma - metabolism Multiple Myeloma - pathology Neoplasm Invasiveness Neoplasm Proteins - genetics Neoplasm Proteins - metabolism Neoplasm Transplantation Neoplastic Stem Cells - metabolism Pharmacology. Drug treatments RNA Interference Tumor Burden Tumors Wnt Signaling Pathway |
| title | miR-30-5p Functions as a Tumor Suppressor and Novel Therapeutic Tool by Targeting the Oncogenic Wnt/β-Catenin/BCL9 Pathway |
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