miR-193b-Regulated Signaling Networks Serve as Tumor Suppressors in Liposarcoma and Promote Adipogenesis in Adipose-Derived Stem Cells
Well-differentiated and dedifferentiated liposarcomas (WDLS/DDLS) account for approximately 13% of all soft tissue sarcoma in adults and cause substantial morbidity or mortality in the majority of patients. In this study, we evaluated the functions of miRNA (miR-193b) in liposarcoma and Deep RNA seq...
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| Veröffentlicht in: | Cancer research (Chicago, Ill.) Ill.), 2017-11, Vol.77 (21), p.5728-5740 |
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| creator | Mazzu, Ying Z Hu, Yulan Soni, Rajesh K Mojica, Kelly M Qin, Li-Xuan Agius, Phaedra Waxman, Zachary M Mihailovic, Aleksandra Socci, Nicholas D Hendrickson, Ronald C Tuschl, Thomas Singer, Samuel |
| description | Well-differentiated and dedifferentiated liposarcomas (WDLS/DDLS) account for approximately 13% of all soft tissue sarcoma in adults and cause substantial morbidity or mortality in the majority of patients. In this study, we evaluated the functions of miRNA (miR-193b) in liposarcoma
and
Deep RNA sequencing on 93 WDLS, 145 DDLS, and 12 normal fat samples demonstrated that miR-193b was significantly underexpressed in DDLS compared with normal fat. Reintroduction of miR-193b induced apoptosis in liposarcoma cells and promoted adipogenesis in human adipose-derived stem cells (ASC). Integrative transcriptomic and proteomic analysis of miR-193b-target networks identified novel direct targets, including CRK-like proto-oncogene (CRKL) and focal adhesion kinase (FAK). miR-193b was found to regulate FAK-SRC-CRKL signaling through CRKL and FAK. miR-193b also stimulated reactive oxygen species signaling by targeting the antioxidant methionine sulfoxide reductase A to modulate liposarcoma cell survival and ASC differentiation state. Expression of miR-193b in liposarcoma cells was downregulated by promoter methylation, resulting at least in part from increased expression of the DNA methyltransferase DNMT1 in WDLS/DDLS.
, miR-193b mimetics and FAK inhibitor (PF-562271) each inhibited liposarcoma xenograft growth. In summary, miR-193b not only functions as a tumor suppressor in liposarcoma but also promotes adipogenesis in ASC. Furthermore, this study reveals key tyrosine kinase and DNA methylation pathways in liposarcoma, some with immediate implications for therapeutic exploration.
. |
| doi_str_mv | 10.1158/0008-5472.CAN-16-2253 |
| format | Article |
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and
Deep RNA sequencing on 93 WDLS, 145 DDLS, and 12 normal fat samples demonstrated that miR-193b was significantly underexpressed in DDLS compared with normal fat. Reintroduction of miR-193b induced apoptosis in liposarcoma cells and promoted adipogenesis in human adipose-derived stem cells (ASC). Integrative transcriptomic and proteomic analysis of miR-193b-target networks identified novel direct targets, including CRK-like proto-oncogene (CRKL) and focal adhesion kinase (FAK). miR-193b was found to regulate FAK-SRC-CRKL signaling through CRKL and FAK. miR-193b also stimulated reactive oxygen species signaling by targeting the antioxidant methionine sulfoxide reductase A to modulate liposarcoma cell survival and ASC differentiation state. Expression of miR-193b in liposarcoma cells was downregulated by promoter methylation, resulting at least in part from increased expression of the DNA methyltransferase DNMT1 in WDLS/DDLS.
, miR-193b mimetics and FAK inhibitor (PF-562271) each inhibited liposarcoma xenograft growth. In summary, miR-193b not only functions as a tumor suppressor in liposarcoma but also promotes adipogenesis in ASC. Furthermore, this study reveals key tyrosine kinase and DNA methylation pathways in liposarcoma, some with immediate implications for therapeutic exploration.
.</description><identifier>ISSN: 0008-5472</identifier><identifier>EISSN: 1538-7445</identifier><identifier>DOI: 10.1158/0008-5472.CAN-16-2253</identifier><identifier>PMID: 28882999</identifier><language>eng</language><publisher>United States: American Association for Cancer Research, Inc</publisher><subject>Adaptor Proteins, Signal Transducing - genetics ; Adaptor Proteins, Signal Transducing - metabolism ; Adipogenesis ; Adipogenesis - genetics ; Adipose Tissue - cytology ; Animals ; Antioxidants ; Apoptosis ; Cell Line, Tumor ; Cell survival ; DNA methylation ; DNA methyltransferase ; DNMT1 protein ; Exploration ; Focal adhesion kinase ; Focal Adhesion Kinase 1 - genetics ; Focal Adhesion Kinase 1 - metabolism ; Gene Expression Profiling - methods ; Gene Expression Regulation, Neoplastic ; Genes, Tumor Suppressor ; Humans ; Indoles - pharmacology ; Liposarcoma ; Liposarcoma - drug therapy ; Liposarcoma - genetics ; Liposarcoma - pathology ; Methionine ; Methionine Sulfoxide Reductases - genetics ; Methionine Sulfoxide Reductases - metabolism ; Methylation ; Mice, Inbred ICR ; Mice, SCID ; MicroRNAs - genetics ; miRNA ; Morbidity ; Nuclear Proteins - genetics ; Nuclear Proteins - metabolism ; Protein-tyrosine kinase ; Proteomics ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Reductase ; Reintroduction ; Sarcoma ; Signal transduction ; Signal Transduction - genetics ; Soft tissue sarcoma ; Stem cells ; Stem Cells - metabolism ; Sulfonamides - pharmacology ; Tumor suppressor genes ; Xenograft Model Antitumor Assays ; Xenografts</subject><ispartof>Cancer research (Chicago, Ill.), 2017-11, Vol.77 (21), p.5728-5740</ispartof><rights>2017 American Association for Cancer Research.</rights><rights>Copyright American Association for Cancer Research, Inc. Nov 1, 2017</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c488t-46e60ef8c0ef6a3306d363decba4ae760ae234b9d6c5e5ce8745971ef123a8e93</citedby><cites>FETCH-LOGICAL-c488t-46e60ef8c0ef6a3306d363decba4ae760ae234b9d6c5e5ce8745971ef123a8e93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785,3357,27929,27930</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28882999$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mazzu, Ying Z</creatorcontrib><creatorcontrib>Hu, Yulan</creatorcontrib><creatorcontrib>Soni, Rajesh K</creatorcontrib><creatorcontrib>Mojica, Kelly M</creatorcontrib><creatorcontrib>Qin, Li-Xuan</creatorcontrib><creatorcontrib>Agius, Phaedra</creatorcontrib><creatorcontrib>Waxman, Zachary M</creatorcontrib><creatorcontrib>Mihailovic, Aleksandra</creatorcontrib><creatorcontrib>Socci, Nicholas D</creatorcontrib><creatorcontrib>Hendrickson, Ronald C</creatorcontrib><creatorcontrib>Tuschl, Thomas</creatorcontrib><creatorcontrib>Singer, Samuel</creatorcontrib><title>miR-193b-Regulated Signaling Networks Serve as Tumor Suppressors in Liposarcoma and Promote Adipogenesis in Adipose-Derived Stem Cells</title><title>Cancer research (Chicago, Ill.)</title><addtitle>Cancer Res</addtitle><description>Well-differentiated and dedifferentiated liposarcomas (WDLS/DDLS) account for approximately 13% of all soft tissue sarcoma in adults and cause substantial morbidity or mortality in the majority of patients. In this study, we evaluated the functions of miRNA (miR-193b) in liposarcoma
and
Deep RNA sequencing on 93 WDLS, 145 DDLS, and 12 normal fat samples demonstrated that miR-193b was significantly underexpressed in DDLS compared with normal fat. Reintroduction of miR-193b induced apoptosis in liposarcoma cells and promoted adipogenesis in human adipose-derived stem cells (ASC). Integrative transcriptomic and proteomic analysis of miR-193b-target networks identified novel direct targets, including CRK-like proto-oncogene (CRKL) and focal adhesion kinase (FAK). miR-193b was found to regulate FAK-SRC-CRKL signaling through CRKL and FAK. miR-193b also stimulated reactive oxygen species signaling by targeting the antioxidant methionine sulfoxide reductase A to modulate liposarcoma cell survival and ASC differentiation state. Expression of miR-193b in liposarcoma cells was downregulated by promoter methylation, resulting at least in part from increased expression of the DNA methyltransferase DNMT1 in WDLS/DDLS.
, miR-193b mimetics and FAK inhibitor (PF-562271) each inhibited liposarcoma xenograft growth. In summary, miR-193b not only functions as a tumor suppressor in liposarcoma but also promotes adipogenesis in ASC. Furthermore, this study reveals key tyrosine kinase and DNA methylation pathways in liposarcoma, some with immediate implications for therapeutic exploration.
.</description><subject>Adaptor Proteins, Signal Transducing - genetics</subject><subject>Adaptor Proteins, Signal Transducing - metabolism</subject><subject>Adipogenesis</subject><subject>Adipogenesis - genetics</subject><subject>Adipose Tissue - cytology</subject><subject>Animals</subject><subject>Antioxidants</subject><subject>Apoptosis</subject><subject>Cell Line, Tumor</subject><subject>Cell survival</subject><subject>DNA methylation</subject><subject>DNA methyltransferase</subject><subject>DNMT1 protein</subject><subject>Exploration</subject><subject>Focal adhesion kinase</subject><subject>Focal Adhesion Kinase 1 - genetics</subject><subject>Focal Adhesion Kinase 1 - metabolism</subject><subject>Gene Expression Profiling - methods</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genes, Tumor Suppressor</subject><subject>Humans</subject><subject>Indoles - pharmacology</subject><subject>Liposarcoma</subject><subject>Liposarcoma - drug therapy</subject><subject>Liposarcoma - genetics</subject><subject>Liposarcoma - pathology</subject><subject>Methionine</subject><subject>Methionine Sulfoxide Reductases - genetics</subject><subject>Methionine Sulfoxide Reductases - metabolism</subject><subject>Methylation</subject><subject>Mice, Inbred ICR</subject><subject>Mice, SCID</subject><subject>MicroRNAs - genetics</subject><subject>miRNA</subject><subject>Morbidity</subject><subject>Nuclear Proteins - genetics</subject><subject>Nuclear Proteins - metabolism</subject><subject>Protein-tyrosine kinase</subject><subject>Proteomics</subject><subject>Reactive oxygen species</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Reductase</subject><subject>Reintroduction</subject><subject>Sarcoma</subject><subject>Signal transduction</subject><subject>Signal Transduction - genetics</subject><subject>Soft tissue sarcoma</subject><subject>Stem cells</subject><subject>Stem Cells - metabolism</subject><subject>Sulfonamides - pharmacology</subject><subject>Tumor suppressor genes</subject><subject>Xenograft Model Antitumor Assays</subject><subject>Xenografts</subject><issn>0008-5472</issn><issn>1538-7445</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkc1u1DAQgC0EokvhEUCWuHBx8X-c42pLAWlVULecLW8yu3JJ4uBJiniBPjdOW3rgMqORv5mx5iPkreBnQhj3kXPumNGVPNusL5mwTEqjnpGVMMqxSmvznKyemBPyCvGmlEZw85KcSOecrOt6Re76eMVErfbsCo5zFyZo6S4eh9DF4UgvYfqd8k-kO8i3QAPS67lPme7mccyAmDLSONBtHBOG3KQ-0DC09HtOfZqArtvycIQBMN5z9zUCO4ccb5dFE_R0A12Hr8mLQ-gQ3jzmU_Lj4tP15gvbfvv8dbPeskY7NzFtwXI4uKYEG5TitlVWtdDsgw5QWR5AKr2vW9sYMA24Spu6EnAQUgUHtTolHx7mjjn9mgEn30dsyg_CAGlGXy5RGemUVAV9_x96k-ZcDrNQhTC10bxQ5oFqckLMcPBjjn3If7zgfhHlFwl-keCLKC-sX0SVvneP0-d9D-1T1z8z6i9Dx4-n</recordid><startdate>20171101</startdate><enddate>20171101</enddate><creator>Mazzu, Ying Z</creator><creator>Hu, Yulan</creator><creator>Soni, Rajesh K</creator><creator>Mojica, Kelly M</creator><creator>Qin, Li-Xuan</creator><creator>Agius, Phaedra</creator><creator>Waxman, Zachary M</creator><creator>Mihailovic, Aleksandra</creator><creator>Socci, Nicholas D</creator><creator>Hendrickson, Ronald C</creator><creator>Tuschl, Thomas</creator><creator>Singer, Samuel</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></search><sort><creationdate>20171101</creationdate><title>miR-193b-Regulated Signaling Networks Serve as Tumor Suppressors in Liposarcoma and Promote Adipogenesis in Adipose-Derived Stem Cells</title><author>Mazzu, Ying Z ; Hu, Yulan ; Soni, Rajesh K ; Mojica, Kelly M ; Qin, Li-Xuan ; Agius, Phaedra ; Waxman, Zachary M ; Mihailovic, Aleksandra ; Socci, Nicholas D ; Hendrickson, Ronald C ; Tuschl, Thomas ; Singer, Samuel</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c488t-46e60ef8c0ef6a3306d363decba4ae760ae234b9d6c5e5ce8745971ef123a8e93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Adaptor Proteins, Signal Transducing - genetics</topic><topic>Adaptor Proteins, Signal Transducing - metabolism</topic><topic>Adipogenesis</topic><topic>Adipogenesis - genetics</topic><topic>Adipose Tissue - cytology</topic><topic>Animals</topic><topic>Antioxidants</topic><topic>Apoptosis</topic><topic>Cell Line, Tumor</topic><topic>Cell survival</topic><topic>DNA methylation</topic><topic>DNA methyltransferase</topic><topic>DNMT1 protein</topic><topic>Exploration</topic><topic>Focal adhesion kinase</topic><topic>Focal Adhesion Kinase 1 - genetics</topic><topic>Focal Adhesion Kinase 1 - metabolism</topic><topic>Gene Expression Profiling - methods</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Genes, Tumor Suppressor</topic><topic>Humans</topic><topic>Indoles - pharmacology</topic><topic>Liposarcoma</topic><topic>Liposarcoma - drug therapy</topic><topic>Liposarcoma - genetics</topic><topic>Liposarcoma - pathology</topic><topic>Methionine</topic><topic>Methionine Sulfoxide Reductases - genetics</topic><topic>Methionine Sulfoxide Reductases - metabolism</topic><topic>Methylation</topic><topic>Mice, Inbred ICR</topic><topic>Mice, SCID</topic><topic>MicroRNAs - genetics</topic><topic>miRNA</topic><topic>Morbidity</topic><topic>Nuclear Proteins - genetics</topic><topic>Nuclear Proteins - metabolism</topic><topic>Protein-tyrosine kinase</topic><topic>Proteomics</topic><topic>Reactive oxygen species</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Reductase</topic><topic>Reintroduction</topic><topic>Sarcoma</topic><topic>Signal transduction</topic><topic>Signal Transduction - genetics</topic><topic>Soft tissue sarcoma</topic><topic>Stem cells</topic><topic>Stem Cells - metabolism</topic><topic>Sulfonamides - pharmacology</topic><topic>Tumor suppressor genes</topic><topic>Xenograft Model Antitumor Assays</topic><topic>Xenografts</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Mazzu, Ying Z</creatorcontrib><creatorcontrib>Hu, Yulan</creatorcontrib><creatorcontrib>Soni, Rajesh K</creatorcontrib><creatorcontrib>Mojica, Kelly M</creatorcontrib><creatorcontrib>Qin, Li-Xuan</creatorcontrib><creatorcontrib>Agius, Phaedra</creatorcontrib><creatorcontrib>Waxman, Zachary M</creatorcontrib><creatorcontrib>Mihailovic, Aleksandra</creatorcontrib><creatorcontrib>Socci, Nicholas D</creatorcontrib><creatorcontrib>Hendrickson, Ronald C</creatorcontrib><creatorcontrib>Tuschl, Thomas</creatorcontrib><creatorcontrib>Singer, Samuel</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>Mazzu, Ying Z</au><au>Hu, Yulan</au><au>Soni, Rajesh K</au><au>Mojica, Kelly M</au><au>Qin, Li-Xuan</au><au>Agius, Phaedra</au><au>Waxman, Zachary M</au><au>Mihailovic, Aleksandra</au><au>Socci, Nicholas D</au><au>Hendrickson, Ronald C</au><au>Tuschl, Thomas</au><au>Singer, Samuel</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>miR-193b-Regulated Signaling Networks Serve as Tumor Suppressors in Liposarcoma and Promote Adipogenesis in Adipose-Derived Stem Cells</atitle><jtitle>Cancer research (Chicago, Ill.)</jtitle><addtitle>Cancer Res</addtitle><date>2017-11-01</date><risdate>2017</risdate><volume>77</volume><issue>21</issue><spage>5728</spage><epage>5740</epage><pages>5728-5740</pages><issn>0008-5472</issn><eissn>1538-7445</eissn><abstract>Well-differentiated and dedifferentiated liposarcomas (WDLS/DDLS) account for approximately 13% of all soft tissue sarcoma in adults and cause substantial morbidity or mortality in the majority of patients. In this study, we evaluated the functions of miRNA (miR-193b) in liposarcoma
and
Deep RNA sequencing on 93 WDLS, 145 DDLS, and 12 normal fat samples demonstrated that miR-193b was significantly underexpressed in DDLS compared with normal fat. Reintroduction of miR-193b induced apoptosis in liposarcoma cells and promoted adipogenesis in human adipose-derived stem cells (ASC). Integrative transcriptomic and proteomic analysis of miR-193b-target networks identified novel direct targets, including CRK-like proto-oncogene (CRKL) and focal adhesion kinase (FAK). miR-193b was found to regulate FAK-SRC-CRKL signaling through CRKL and FAK. miR-193b also stimulated reactive oxygen species signaling by targeting the antioxidant methionine sulfoxide reductase A to modulate liposarcoma cell survival and ASC differentiation state. Expression of miR-193b in liposarcoma cells was downregulated by promoter methylation, resulting at least in part from increased expression of the DNA methyltransferase DNMT1 in WDLS/DDLS.
, miR-193b mimetics and FAK inhibitor (PF-562271) each inhibited liposarcoma xenograft growth. In summary, miR-193b not only functions as a tumor suppressor in liposarcoma but also promotes adipogenesis in ASC. Furthermore, this study reveals key tyrosine kinase and DNA methylation pathways in liposarcoma, some with immediate implications for therapeutic exploration.
.</abstract><cop>United States</cop><pub>American Association for Cancer Research, Inc</pub><pmid>28882999</pmid><doi>10.1158/0008-5472.CAN-16-2253</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adaptor Proteins, Signal Transducing - genetics Adaptor Proteins, Signal Transducing - metabolism Adipogenesis Adipogenesis - genetics Adipose Tissue - cytology Animals Antioxidants Apoptosis Cell Line, Tumor Cell survival DNA methylation DNA methyltransferase DNMT1 protein Exploration Focal adhesion kinase Focal Adhesion Kinase 1 - genetics Focal Adhesion Kinase 1 - metabolism Gene Expression Profiling - methods Gene Expression Regulation, Neoplastic Genes, Tumor Suppressor Humans Indoles - pharmacology Liposarcoma Liposarcoma - drug therapy Liposarcoma - genetics Liposarcoma - pathology Methionine Methionine Sulfoxide Reductases - genetics Methionine Sulfoxide Reductases - metabolism Methylation Mice, Inbred ICR Mice, SCID MicroRNAs - genetics miRNA Morbidity Nuclear Proteins - genetics Nuclear Proteins - metabolism Protein-tyrosine kinase Proteomics Reactive oxygen species Reactive Oxygen Species - metabolism Reductase Reintroduction Sarcoma Signal transduction Signal Transduction - genetics Soft tissue sarcoma Stem cells Stem Cells - metabolism Sulfonamides - pharmacology Tumor suppressor genes Xenograft Model Antitumor Assays Xenografts |
| title | miR-193b-Regulated Signaling Networks Serve as Tumor Suppressors in Liposarcoma and Promote Adipogenesis in Adipose-Derived Stem Cells |
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