The miR-371∼373 Cluster Represses Colon Cancer Initiation and Metastatic Colonization by Inhibiting the TGFBR2/ID1 Signaling Axis
The vast majority of colorectal cancer-related deaths can be attributed to metastatic spreading of the disease. Therefore, deciphering molecular mechanisms of metastatic dissemination is a key prerequisite to improve future treatment options. With this aim, we took advantage of different colorectal...
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| Veröffentlicht in: | Cancer research (Chicago, Ill.) Ill.), 2018-07, Vol.78 (14), p.3793-3808 |
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| creator | Ullmann, Pit Rodriguez, Fabien Schmitz, Martine Meurer, Steffen K Qureshi-Baig, Komal Felten, Paul Ginolhac, Aurélien Antunes, Laurent Frasquilho, Sonia Zügel, Nikolaus Weiskirchen, Ralf Haan, Serge Letellier, Elisabeth |
| description | The vast majority of colorectal cancer-related deaths can be attributed to metastatic spreading of the disease. Therefore, deciphering molecular mechanisms of metastatic dissemination is a key prerequisite to improve future treatment options. With this aim, we took advantage of different colorectal cancer cell lines and recently established primary cultures enriched in colon cancer stem cells, also known as tumor-initiating cells (TIC), to identify genes and miRNAs with regulatory functions in colorectal cancer progression. We show here that metastasis-derived TICs display increased capacity for self-renewal, TGFβ signaling activity, and reduced expression of the miR-371∼373 cluster compared with nonmetastatic cultures. TGFβ receptor 2 (
) and aldehyde dehydrogenase A1 (
) were identified as important target genes of the miR-371∼373 cluster. In addition, TGFBR2 repression, either by direct knockdown or indirectly via overexpression of the entire miR-371∼373 cluster, decreased tumor-initiating potential of TICs. We observed significantly reduced
self-renewal activity as well as lowered tumor initiation and metastatic outgrowth capacity
following stable overexpression of the miR-371∼373 cluster in different colon TIC cultures. Inhibitor of DNA binding 1 (ID1) was affected by both TGFBR2 and miR-371∼373 cluster alterations. Functional sphere and tumor formation as well as metastatic dissemination assays validated the link between miR-371∼373 and ID1. Altogether, our results establish the miR-371∼373/TGFBR2/ID1 signaling axis as a novel regulatory mechanism of TIC self-renewal and metastatic colonization.
These findings establish the miR-371∼373/TGFBR2/ID1 signaling axis as a novel mechanism regulating self-renewal of tumor-initiating cell and metastatic colonization, potentially opening new concepts for therapeutic targeting of cancer metastasis.
http://cancerres.aacrjournals.org/content/canres/78/14/3793/F1.large.jpg
. |
| doi_str_mv | 10.1158/0008-5472.CAN-17-3003 |
| format | Article |
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) and aldehyde dehydrogenase A1 (
) were identified as important target genes of the miR-371∼373 cluster. In addition, TGFBR2 repression, either by direct knockdown or indirectly via overexpression of the entire miR-371∼373 cluster, decreased tumor-initiating potential of TICs. We observed significantly reduced
self-renewal activity as well as lowered tumor initiation and metastatic outgrowth capacity
following stable overexpression of the miR-371∼373 cluster in different colon TIC cultures. Inhibitor of DNA binding 1 (ID1) was affected by both TGFBR2 and miR-371∼373 cluster alterations. Functional sphere and tumor formation as well as metastatic dissemination assays validated the link between miR-371∼373 and ID1. Altogether, our results establish the miR-371∼373/TGFBR2/ID1 signaling axis as a novel regulatory mechanism of TIC self-renewal and metastatic colonization.
These findings establish the miR-371∼373/TGFBR2/ID1 signaling axis as a novel mechanism regulating self-renewal of tumor-initiating cell and metastatic colonization, potentially opening new concepts for therapeutic targeting of cancer metastasis.
http://cancerres.aacrjournals.org/content/canres/78/14/3793/F1.large.jpg
.</description><identifier>ISSN: 0008-5472</identifier><identifier>EISSN: 1538-7445</identifier><identifier>DOI: 10.1158/0008-5472.CAN-17-3003</identifier><identifier>PMID: 29748374</identifier><language>eng</language><publisher>United States: American Association for Cancer Research, Inc</publisher><subject>Aldehyde dehydrogenase ; Animals ; Cell Line, Tumor ; Cell lines ; Cell Self Renewal - genetics ; Cell self-renewal ; Colon ; Colon cancer ; Colonic Neoplasms - genetics ; Colonic Neoplasms - pathology ; Colonization ; Colorectal cancer ; Colorectal carcinoma ; Culture ; Deoxyribonucleic acid ; DNA ; Gene Expression Profiling - methods ; Gene Expression Regulation, Neoplastic - genetics ; Genes ; HCT116 Cells ; HT29 Cells ; Humans ; Id1 protein ; Inhibitor of Differentiation Protein 1 - genetics ; Invasiveness ; Metastases ; Metastasis ; Mice ; Mice, Inbred NOD ; Mice, SCID ; MicroRNAs - genetics ; Molecular chains ; Molecular modelling ; Neoplastic Stem Cells - pathology ; Receptor, Transforming Growth Factor-beta Type II - genetics ; Self ; Signal Transduction - genetics ; Stem cells ; Therapeutic targets ; Tumor cell lines</subject><ispartof>Cancer research (Chicago, Ill.), 2018-07, Vol.78 (14), p.3793-3808</ispartof><rights>2018 American Association for Cancer Research.</rights><rights>Copyright American Association for Cancer Research, Inc. Jul 15, 2018</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c2293-559dbc343c3e622ca3919d365e45d85ef21cae3ba4e0247d4fe6fe4601cba20b3</citedby><cites>FETCH-LOGICAL-c2293-559dbc343c3e622ca3919d365e45d85ef21cae3ba4e0247d4fe6fe4601cba20b3</cites><orcidid>0000-0003-3888-0931</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3343,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29748374$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ullmann, Pit</creatorcontrib><creatorcontrib>Rodriguez, Fabien</creatorcontrib><creatorcontrib>Schmitz, Martine</creatorcontrib><creatorcontrib>Meurer, Steffen K</creatorcontrib><creatorcontrib>Qureshi-Baig, Komal</creatorcontrib><creatorcontrib>Felten, Paul</creatorcontrib><creatorcontrib>Ginolhac, Aurélien</creatorcontrib><creatorcontrib>Antunes, Laurent</creatorcontrib><creatorcontrib>Frasquilho, Sonia</creatorcontrib><creatorcontrib>Zügel, Nikolaus</creatorcontrib><creatorcontrib>Weiskirchen, Ralf</creatorcontrib><creatorcontrib>Haan, Serge</creatorcontrib><creatorcontrib>Letellier, Elisabeth</creatorcontrib><title>The miR-371∼373 Cluster Represses Colon Cancer Initiation and Metastatic Colonization by Inhibiting the TGFBR2/ID1 Signaling Axis</title><title>Cancer research (Chicago, Ill.)</title><addtitle>Cancer Res</addtitle><description>The vast majority of colorectal cancer-related deaths can be attributed to metastatic spreading of the disease. Therefore, deciphering molecular mechanisms of metastatic dissemination is a key prerequisite to improve future treatment options. With this aim, we took advantage of different colorectal cancer cell lines and recently established primary cultures enriched in colon cancer stem cells, also known as tumor-initiating cells (TIC), to identify genes and miRNAs with regulatory functions in colorectal cancer progression. We show here that metastasis-derived TICs display increased capacity for self-renewal, TGFβ signaling activity, and reduced expression of the miR-371∼373 cluster compared with nonmetastatic cultures. TGFβ receptor 2 (
) and aldehyde dehydrogenase A1 (
) were identified as important target genes of the miR-371∼373 cluster. In addition, TGFBR2 repression, either by direct knockdown or indirectly via overexpression of the entire miR-371∼373 cluster, decreased tumor-initiating potential of TICs. We observed significantly reduced
self-renewal activity as well as lowered tumor initiation and metastatic outgrowth capacity
following stable overexpression of the miR-371∼373 cluster in different colon TIC cultures. Inhibitor of DNA binding 1 (ID1) was affected by both TGFBR2 and miR-371∼373 cluster alterations. Functional sphere and tumor formation as well as metastatic dissemination assays validated the link between miR-371∼373 and ID1. Altogether, our results establish the miR-371∼373/TGFBR2/ID1 signaling axis as a novel regulatory mechanism of TIC self-renewal and metastatic colonization.
These findings establish the miR-371∼373/TGFBR2/ID1 signaling axis as a novel mechanism regulating self-renewal of tumor-initiating cell and metastatic colonization, potentially opening new concepts for therapeutic targeting of cancer metastasis.
http://cancerres.aacrjournals.org/content/canres/78/14/3793/F1.large.jpg
.</description><subject>Aldehyde dehydrogenase</subject><subject>Animals</subject><subject>Cell Line, Tumor</subject><subject>Cell lines</subject><subject>Cell Self Renewal - genetics</subject><subject>Cell self-renewal</subject><subject>Colon</subject><subject>Colon cancer</subject><subject>Colonic Neoplasms - genetics</subject><subject>Colonic Neoplasms - pathology</subject><subject>Colonization</subject><subject>Colorectal cancer</subject><subject>Colorectal carcinoma</subject><subject>Culture</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>Gene Expression Profiling - methods</subject><subject>Gene Expression Regulation, Neoplastic - genetics</subject><subject>Genes</subject><subject>HCT116 Cells</subject><subject>HT29 Cells</subject><subject>Humans</subject><subject>Id1 protein</subject><subject>Inhibitor of Differentiation Protein 1 - genetics</subject><subject>Invasiveness</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>Mice</subject><subject>Mice, Inbred NOD</subject><subject>Mice, SCID</subject><subject>MicroRNAs - genetics</subject><subject>Molecular chains</subject><subject>Molecular modelling</subject><subject>Neoplastic Stem Cells - pathology</subject><subject>Receptor, Transforming Growth Factor-beta Type II - genetics</subject><subject>Self</subject><subject>Signal Transduction - genetics</subject><subject>Stem cells</subject><subject>Therapeutic targets</subject><subject>Tumor cell lines</subject><issn>0008-5472</issn><issn>1538-7445</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkc1O4zAQgC0EWgrsI4AiceESsD12nBxLWNhK_Ejd7tlynAkYpUmJE2nLlQsPxdPwJOuowIHTaGa--ZE-Qg4ZPWVMpmeU0jSWQvHTfHobMxUDpbBFJkxCGish5DaZfDG7ZM_7x5BKRuUPssszJVJQYkJeFg8YLd08BsXeX99AQZTXg--xi-a46tB79FHe1m0T5aaxoTxrXO9M70LFNGV0g73xfcjtBnPPm16xDuSDKwLc3Ed9uLK4ujyf87PZBYv-uPvG1GNj-s_5A7JTmdrjz4-4T_5e_lrkv-Pru6tZPr2OLecZxFJmZWFBgAVMOLcGMpaVkEgUskwlVpxZg1AYgZQLVYoKkwpFQpktDKcF7JOTzd5V1z4N6Hu9dN5iXZsG28FrTiHlCWdZEtDjb-hjO3Th55FSlIokUzxQckPZrvW-w0qvOrc03VozqkdLejSgRwM6WNJM6dFSmDv62D4USyy_pj61wH-Zt4zo</recordid><startdate>20180715</startdate><enddate>20180715</enddate><creator>Ullmann, Pit</creator><creator>Rodriguez, Fabien</creator><creator>Schmitz, Martine</creator><creator>Meurer, Steffen K</creator><creator>Qureshi-Baig, Komal</creator><creator>Felten, Paul</creator><creator>Ginolhac, Aurélien</creator><creator>Antunes, Laurent</creator><creator>Frasquilho, Sonia</creator><creator>Zügel, Nikolaus</creator><creator>Weiskirchen, Ralf</creator><creator>Haan, Serge</creator><creator>Letellier, Elisabeth</creator><general>American Association for Cancer Research, Inc</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>7T5</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0003-3888-0931</orcidid></search><sort><creationdate>20180715</creationdate><title>The miR-371∼373 Cluster Represses Colon Cancer Initiation and Metastatic Colonization by Inhibiting the TGFBR2/ID1 Signaling Axis</title><author>Ullmann, Pit ; Rodriguez, Fabien ; Schmitz, Martine ; Meurer, Steffen K ; Qureshi-Baig, Komal ; Felten, Paul ; Ginolhac, Aurélien ; Antunes, Laurent ; Frasquilho, Sonia ; Zügel, Nikolaus ; Weiskirchen, Ralf ; Haan, Serge ; Letellier, Elisabeth</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c2293-559dbc343c3e622ca3919d365e45d85ef21cae3ba4e0247d4fe6fe4601cba20b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Aldehyde dehydrogenase</topic><topic>Animals</topic><topic>Cell Line, Tumor</topic><topic>Cell lines</topic><topic>Cell Self Renewal - genetics</topic><topic>Cell self-renewal</topic><topic>Colon</topic><topic>Colon cancer</topic><topic>Colonic Neoplasms - genetics</topic><topic>Colonic Neoplasms - pathology</topic><topic>Colonization</topic><topic>Colorectal cancer</topic><topic>Colorectal carcinoma</topic><topic>Culture</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>Gene Expression Profiling - methods</topic><topic>Gene Expression Regulation, Neoplastic - genetics</topic><topic>Genes</topic><topic>HCT116 Cells</topic><topic>HT29 Cells</topic><topic>Humans</topic><topic>Id1 protein</topic><topic>Inhibitor of Differentiation Protein 1 - genetics</topic><topic>Invasiveness</topic><topic>Metastases</topic><topic>Metastasis</topic><topic>Mice</topic><topic>Mice, Inbred NOD</topic><topic>Mice, SCID</topic><topic>MicroRNAs - genetics</topic><topic>Molecular chains</topic><topic>Molecular modelling</topic><topic>Neoplastic Stem Cells - pathology</topic><topic>Receptor, Transforming Growth Factor-beta Type II - genetics</topic><topic>Self</topic><topic>Signal Transduction - genetics</topic><topic>Stem cells</topic><topic>Therapeutic targets</topic><topic>Tumor cell lines</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ullmann, Pit</creatorcontrib><creatorcontrib>Rodriguez, Fabien</creatorcontrib><creatorcontrib>Schmitz, Martine</creatorcontrib><creatorcontrib>Meurer, Steffen K</creatorcontrib><creatorcontrib>Qureshi-Baig, Komal</creatorcontrib><creatorcontrib>Felten, Paul</creatorcontrib><creatorcontrib>Ginolhac, Aurélien</creatorcontrib><creatorcontrib>Antunes, Laurent</creatorcontrib><creatorcontrib>Frasquilho, Sonia</creatorcontrib><creatorcontrib>Zügel, Nikolaus</creatorcontrib><creatorcontrib>Weiskirchen, Ralf</creatorcontrib><creatorcontrib>Haan, Serge</creatorcontrib><creatorcontrib>Letellier, Elisabeth</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Cancer research (Chicago, Ill.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ullmann, Pit</au><au>Rodriguez, Fabien</au><au>Schmitz, Martine</au><au>Meurer, Steffen K</au><au>Qureshi-Baig, Komal</au><au>Felten, Paul</au><au>Ginolhac, Aurélien</au><au>Antunes, Laurent</au><au>Frasquilho, Sonia</au><au>Zügel, Nikolaus</au><au>Weiskirchen, Ralf</au><au>Haan, Serge</au><au>Letellier, Elisabeth</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The miR-371∼373 Cluster Represses Colon Cancer Initiation and Metastatic Colonization by Inhibiting the TGFBR2/ID1 Signaling Axis</atitle><jtitle>Cancer research (Chicago, Ill.)</jtitle><addtitle>Cancer Res</addtitle><date>2018-07-15</date><risdate>2018</risdate><volume>78</volume><issue>14</issue><spage>3793</spage><epage>3808</epage><pages>3793-3808</pages><issn>0008-5472</issn><eissn>1538-7445</eissn><abstract>The vast majority of colorectal cancer-related deaths can be attributed to metastatic spreading of the disease. Therefore, deciphering molecular mechanisms of metastatic dissemination is a key prerequisite to improve future treatment options. With this aim, we took advantage of different colorectal cancer cell lines and recently established primary cultures enriched in colon cancer stem cells, also known as tumor-initiating cells (TIC), to identify genes and miRNAs with regulatory functions in colorectal cancer progression. We show here that metastasis-derived TICs display increased capacity for self-renewal, TGFβ signaling activity, and reduced expression of the miR-371∼373 cluster compared with nonmetastatic cultures. TGFβ receptor 2 (
) and aldehyde dehydrogenase A1 (
) were identified as important target genes of the miR-371∼373 cluster. In addition, TGFBR2 repression, either by direct knockdown or indirectly via overexpression of the entire miR-371∼373 cluster, decreased tumor-initiating potential of TICs. We observed significantly reduced
self-renewal activity as well as lowered tumor initiation and metastatic outgrowth capacity
following stable overexpression of the miR-371∼373 cluster in different colon TIC cultures. Inhibitor of DNA binding 1 (ID1) was affected by both TGFBR2 and miR-371∼373 cluster alterations. Functional sphere and tumor formation as well as metastatic dissemination assays validated the link between miR-371∼373 and ID1. Altogether, our results establish the miR-371∼373/TGFBR2/ID1 signaling axis as a novel regulatory mechanism of TIC self-renewal and metastatic colonization.
These findings establish the miR-371∼373/TGFBR2/ID1 signaling axis as a novel mechanism regulating self-renewal of tumor-initiating cell and metastatic colonization, potentially opening new concepts for therapeutic targeting of cancer metastasis.
http://cancerres.aacrjournals.org/content/canres/78/14/3793/F1.large.jpg
.</abstract><cop>United States</cop><pub>American Association for Cancer Research, Inc</pub><pmid>29748374</pmid><doi>10.1158/0008-5472.CAN-17-3003</doi><tpages>16</tpages><orcidid>https://orcid.org/0000-0003-3888-0931</orcidid><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; American Association for Cancer Research; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals |
| subjects | Aldehyde dehydrogenase Animals Cell Line, Tumor Cell lines Cell Self Renewal - genetics Cell self-renewal Colon Colon cancer Colonic Neoplasms - genetics Colonic Neoplasms - pathology Colonization Colorectal cancer Colorectal carcinoma Culture Deoxyribonucleic acid DNA Gene Expression Profiling - methods Gene Expression Regulation, Neoplastic - genetics Genes HCT116 Cells HT29 Cells Humans Id1 protein Inhibitor of Differentiation Protein 1 - genetics Invasiveness Metastases Metastasis Mice Mice, Inbred NOD Mice, SCID MicroRNAs - genetics Molecular chains Molecular modelling Neoplastic Stem Cells - pathology Receptor, Transforming Growth Factor-beta Type II - genetics Self Signal Transduction - genetics Stem cells Therapeutic targets Tumor cell lines |
| title | The miR-371∼373 Cluster Represses Colon Cancer Initiation and Metastatic Colonization by Inhibiting the TGFBR2/ID1 Signaling Axis |
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