Activin A promotes multiple myeloma-induced osteolysis and is a promising target for myeloma bone disease
Understanding the pathogenesis of cancer-related bone disease is crucial to the discovery of new therapies. Here we identify activin A, a TGF-β family member, as a therapeutically amenable target exploited by multiple myeloma (MM) to alter its microenvironmental niche favoring osteolysis. Increased...
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| Veröffentlicht in: | Proceedings of the National Academy of Sciences - PNAS 2010-03, Vol.107 (11), p.5124-5129 |
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| creator | Vallet, Sonia Mukherjee, Siddhartha Vaghela, Nileshwari Hideshima, Teru Fulciniti, Mariateresa Pozzi, Samantha Santo, Loredana Cirstea, Diana Patel, Kishan Sohani, Aliyah R Guimaraes, Alex Xie, Wanling Chauhan, Dharminder Schoonmaker, Jesse A Attar, Eyal Churchill, Michael Weller, Edie Munshi, Nikhil Seehra, Jasbir S Weissleder, Ralph Anderson, Kenneth C Scadden, David T Raje, Noopur |
| description | Understanding the pathogenesis of cancer-related bone disease is crucial to the discovery of new therapies. Here we identify activin A, a TGF-β family member, as a therapeutically amenable target exploited by multiple myeloma (MM) to alter its microenvironmental niche favoring osteolysis. Increased bone marrow plasma activin A levels were found in MM patients with osteolytic disease. MM cell engagement of marrow stromal cells enhanced activin A secretion via adhesion-mediated JNK activation. Activin A, in turn, inhibited osteoblast differentiation via SMAD2-dependent distal-less homeobox-5 down-regulation. Targeting activin A by a soluble decoy receptor reversed osteoblast inhibition, ameliorated MM bone disease, and inhibited tumor growth in an in vivo humanized MM model, setting the stage for testing in human clinical trials. |
| doi_str_mv | 10.1073/pnas.0911929107 |
| format | Article |
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Here we identify activin A, a TGF-β family member, as a therapeutically amenable target exploited by multiple myeloma (MM) to alter its microenvironmental niche favoring osteolysis. Increased bone marrow plasma activin A levels were found in MM patients with osteolytic disease. MM cell engagement of marrow stromal cells enhanced activin A secretion via adhesion-mediated JNK activation. Activin A, in turn, inhibited osteoblast differentiation via SMAD2-dependent distal-less homeobox-5 down-regulation. Targeting activin A by a soluble decoy receptor reversed osteoblast inhibition, ameliorated MM bone disease, and inhibited tumor growth in an in vivo humanized MM model, setting the stage for testing in human clinical trials.</description><identifier>ISSN: 0027-8424</identifier><identifier>EISSN: 1091-6490</identifier><identifier>DOI: 10.1073/pnas.0911929107</identifier><identifier>PMID: 20194748</identifier><language>eng</language><publisher>United States: National Academy of Sciences</publisher><subject>Activins - antagonists & inhibitors ; Activins - metabolism ; Activins - secretion ; Animals ; Biological Sciences ; Bone diseases ; Bone marrow ; Bone Marrow Cells - pathology ; Bone Marrow Cells - secretion ; Bones ; Cancer ; Cancer therapies ; Cell Differentiation ; Cell Line, Tumor ; Cell lines ; Cells ; Cytokines ; Disease models ; Down-Regulation ; Enzyme Activation ; Homeodomain Proteins - metabolism ; Humans ; JNK Mitogen-Activated Protein Kinases - metabolism ; Mice ; Multiple Myeloma - complications ; Multiple Myeloma - enzymology ; Multiple Myeloma - pathology ; Osteoblasts - pathology ; Osteolysis ; Osteolysis - etiology ; Osteolysis - pathology ; Plasma ; Proteins ; Receptors ; Receptors, Cell Surface - metabolism ; Secretion ; Smad2 Protein - metabolism ; Stromal Cells - pathology ; Stromal Cells - secretion ; Tumors</subject><ispartof>Proceedings of the National Academy of Sciences - PNAS, 2010-03, Vol.107 (11), p.5124-5129</ispartof><rights>Copyright National Academy of Sciences Mar 16, 2010</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c587t-9b4d27998a8609da034c57cc2a2ea608eff7306f4952662f7e2a0b9d459656223</citedby><cites>FETCH-LOGICAL-c587t-9b4d27998a8609da034c57cc2a2ea608eff7306f4952662f7e2a0b9d459656223</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://www.pnas.org/content/107/11.cover.gif</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/25664937$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/25664937$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>230,314,723,776,780,799,881,27901,27902,53766,53768,57992,58225</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20194748$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Vallet, Sonia</creatorcontrib><creatorcontrib>Mukherjee, Siddhartha</creatorcontrib><creatorcontrib>Vaghela, Nileshwari</creatorcontrib><creatorcontrib>Hideshima, Teru</creatorcontrib><creatorcontrib>Fulciniti, Mariateresa</creatorcontrib><creatorcontrib>Pozzi, Samantha</creatorcontrib><creatorcontrib>Santo, Loredana</creatorcontrib><creatorcontrib>Cirstea, Diana</creatorcontrib><creatorcontrib>Patel, Kishan</creatorcontrib><creatorcontrib>Sohani, Aliyah R</creatorcontrib><creatorcontrib>Guimaraes, Alex</creatorcontrib><creatorcontrib>Xie, Wanling</creatorcontrib><creatorcontrib>Chauhan, Dharminder</creatorcontrib><creatorcontrib>Schoonmaker, Jesse A</creatorcontrib><creatorcontrib>Attar, Eyal</creatorcontrib><creatorcontrib>Churchill, Michael</creatorcontrib><creatorcontrib>Weller, Edie</creatorcontrib><creatorcontrib>Munshi, Nikhil</creatorcontrib><creatorcontrib>Seehra, Jasbir S</creatorcontrib><creatorcontrib>Weissleder, Ralph</creatorcontrib><creatorcontrib>Anderson, Kenneth C</creatorcontrib><creatorcontrib>Scadden, David T</creatorcontrib><creatorcontrib>Raje, Noopur</creatorcontrib><title>Activin A promotes multiple myeloma-induced osteolysis and is a promising target for myeloma bone disease</title><title>Proceedings of the National Academy of Sciences - PNAS</title><addtitle>Proc Natl Acad Sci U S A</addtitle><description>Understanding the pathogenesis of cancer-related bone disease is crucial to the discovery of new therapies. Here we identify activin A, a TGF-β family member, as a therapeutically amenable target exploited by multiple myeloma (MM) to alter its microenvironmental niche favoring osteolysis. Increased bone marrow plasma activin A levels were found in MM patients with osteolytic disease. MM cell engagement of marrow stromal cells enhanced activin A secretion via adhesion-mediated JNK activation. Activin A, in turn, inhibited osteoblast differentiation via SMAD2-dependent distal-less homeobox-5 down-regulation. Targeting activin A by a soluble decoy receptor reversed osteoblast inhibition, ameliorated MM bone disease, and inhibited tumor growth in an in vivo humanized MM model, setting the stage for testing in human clinical trials.</description><subject>Activins - antagonists & inhibitors</subject><subject>Activins - metabolism</subject><subject>Activins - secretion</subject><subject>Animals</subject><subject>Biological Sciences</subject><subject>Bone diseases</subject><subject>Bone marrow</subject><subject>Bone Marrow Cells - pathology</subject><subject>Bone Marrow Cells - secretion</subject><subject>Bones</subject><subject>Cancer</subject><subject>Cancer therapies</subject><subject>Cell Differentiation</subject><subject>Cell Line, Tumor</subject><subject>Cell lines</subject><subject>Cells</subject><subject>Cytokines</subject><subject>Disease models</subject><subject>Down-Regulation</subject><subject>Enzyme Activation</subject><subject>Homeodomain Proteins - metabolism</subject><subject>Humans</subject><subject>JNK Mitogen-Activated Protein Kinases - metabolism</subject><subject>Mice</subject><subject>Multiple Myeloma - complications</subject><subject>Multiple Myeloma - enzymology</subject><subject>Multiple Myeloma - pathology</subject><subject>Osteoblasts - pathology</subject><subject>Osteolysis</subject><subject>Osteolysis - etiology</subject><subject>Osteolysis - pathology</subject><subject>Plasma</subject><subject>Proteins</subject><subject>Receptors</subject><subject>Receptors, Cell Surface - metabolism</subject><subject>Secretion</subject><subject>Smad2 Protein - metabolism</subject><subject>Stromal Cells - pathology</subject><subject>Stromal Cells - secretion</subject><subject>Tumors</subject><issn>0027-8424</issn><issn>1091-6490</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkTtvFDEUhS0EIptATQVYNFST-DV-NEiriABSJApIbXk9nsWrGXuwPZH23-NhN1mgobqy_Z0jn3sAeIXRJUaCXk3B5EukMFZE1YsnYIXrqeFMoadghRARjWSEnYHznHcIIdVK9BycEYQVE0yugF_b4u99gGs4pTjG4jIc56H4aXBw3LshjqbxoZut62DMxcVhn32GJnRwGb9VPvuwhcWkrSuwj-lBCDcxONj57Ex2L8Cz3gzZvTzOC3B38_H79efm9uunL9fr28a2UpRGbVhHhFLSSI5UZxBlthXWEkOc4Ui6vhcU8Z6plnBOeuGIQRvVsVbxlhNCL8CHg-80b0bXWRdKMoOekh9N2utovP77JfgfehvvNZGsrnExeH80SPHn7HLRNaB1w2CCi3PWgnFCMefs_ySlghLKaSXf_UPu4pxC3YOuXTCKGBcVujpANsWck-sfP42RXurWS936VHdVvPkz6yP_0G8F3h6BRXmyExpj3WKyZHh9IHa5xHRyaGtARcXJoTdRm23yWd99q_4UYYm5bDH9BSsUxB8</recordid><startdate>20100316</startdate><enddate>20100316</enddate><creator>Vallet, Sonia</creator><creator>Mukherjee, Siddhartha</creator><creator>Vaghela, Nileshwari</creator><creator>Hideshima, Teru</creator><creator>Fulciniti, Mariateresa</creator><creator>Pozzi, Samantha</creator><creator>Santo, Loredana</creator><creator>Cirstea, Diana</creator><creator>Patel, Kishan</creator><creator>Sohani, Aliyah R</creator><creator>Guimaraes, Alex</creator><creator>Xie, Wanling</creator><creator>Chauhan, Dharminder</creator><creator>Schoonmaker, Jesse A</creator><creator>Attar, Eyal</creator><creator>Churchill, Michael</creator><creator>Weller, Edie</creator><creator>Munshi, Nikhil</creator><creator>Seehra, Jasbir S</creator><creator>Weissleder, Ralph</creator><creator>Anderson, Kenneth C</creator><creator>Scadden, David T</creator><creator>Raje, Noopur</creator><general>National Academy of Sciences</general><general>National Acad Sciences</general><scope>FBQ</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>7QG</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20100316</creationdate><title>Activin A promotes multiple myeloma-induced osteolysis and is a promising target for myeloma bone disease</title><author>Vallet, Sonia ; Mukherjee, Siddhartha ; Vaghela, Nileshwari ; Hideshima, Teru ; Fulciniti, Mariateresa ; Pozzi, Samantha ; Santo, Loredana ; Cirstea, Diana ; Patel, Kishan ; Sohani, Aliyah R ; Guimaraes, Alex ; Xie, Wanling ; Chauhan, Dharminder ; Schoonmaker, Jesse A ; Attar, Eyal ; Churchill, Michael ; Weller, Edie ; Munshi, Nikhil ; Seehra, Jasbir S ; Weissleder, Ralph ; Anderson, Kenneth C ; Scadden, David T ; Raje, Noopur</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c587t-9b4d27998a8609da034c57cc2a2ea608eff7306f4952662f7e2a0b9d459656223</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Activins - 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Here we identify activin A, a TGF-β family member, as a therapeutically amenable target exploited by multiple myeloma (MM) to alter its microenvironmental niche favoring osteolysis. Increased bone marrow plasma activin A levels were found in MM patients with osteolytic disease. MM cell engagement of marrow stromal cells enhanced activin A secretion via adhesion-mediated JNK activation. Activin A, in turn, inhibited osteoblast differentiation via SMAD2-dependent distal-less homeobox-5 down-regulation. Targeting activin A by a soluble decoy receptor reversed osteoblast inhibition, ameliorated MM bone disease, and inhibited tumor growth in an in vivo humanized MM model, setting the stage for testing in human clinical trials.</abstract><cop>United States</cop><pub>National Academy of Sciences</pub><pmid>20194748</pmid><doi>10.1073/pnas.0911929107</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Activins - antagonists & inhibitors Activins - metabolism Activins - secretion Animals Biological Sciences Bone diseases Bone marrow Bone Marrow Cells - pathology Bone Marrow Cells - secretion Bones Cancer Cancer therapies Cell Differentiation Cell Line, Tumor Cell lines Cells Cytokines Disease models Down-Regulation Enzyme Activation Homeodomain Proteins - metabolism Humans JNK Mitogen-Activated Protein Kinases - metabolism Mice Multiple Myeloma - complications Multiple Myeloma - enzymology Multiple Myeloma - pathology Osteoblasts - pathology Osteolysis Osteolysis - etiology Osteolysis - pathology Plasma Proteins Receptors Receptors, Cell Surface - metabolism Secretion Smad2 Protein - metabolism Stromal Cells - pathology Stromal Cells - secretion Tumors |
| title | Activin A promotes multiple myeloma-induced osteolysis and is a promising target for myeloma bone disease |
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