MiR-93 enhances angiogenesis and metastasis by targeting LATS2
Here we report that miR-93, a miRNA in the miR-106B~25 cluster, a paralog of the miR-17-92 cluster, was significantly upregulated in human breast carcinoma tissues. We stably expressed miR-93 in the MT-1 human breast carcinoma cell line and found that tumors formed by the miR-93 cells contained more...
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| Veröffentlicht in: | Cell cycle (Georgetown, Tex.) Tex.), 2012-12, Vol.11 (23), p.4352-4365 |
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| creator | Fang, Ling Du, William W. Yang, Weining Rutnam, Zina Jeyapalan Peng, Chun Li, Haoran O'Malley, Yunxia Q. Askeland, Ryan W. Sugg, Sonia Liu, Mingyao Mehta, Tanvi Deng, Zhaoqun Yang, Burton B. |
| description | Here we report that miR-93, a miRNA in the miR-106B~25 cluster, a paralog of the miR-17-92 cluster, was significantly upregulated in human breast carcinoma tissues. We stably expressed miR-93 in the MT-1 human breast carcinoma cell line and found that tumors formed by the miR-93 cells contained more blood vessels than those formed by the control cells. Co-culture experiments indicated that the MT-1 cells displayed a high activity of adhesion with endothelial cells and could form larger and more tube-like structures with endothelial cells. Lung metastasis assays were performed in a mouse metastatic model, and it was found that expression of miR-93 promoted tumor cell metastasis to lung tissue. In cell culture, expression of miR-93 enhanced cell survival and invasion. We examined the potential target that mediated miR-93's effects and found that the large tumor suppressor, homology 2 (LATS2) was a target of miR-93. Higher levels of LATS2 were associated with cell death in the tumor mass. Silencing LATS2 expression promoted cell survival, tube formation and invasion, while ectopic expression of LATS2 decreased cell survival and invasion. These findings demonstrated that miR-93 promoted tumor angiogenesis and metastasis by suppressing LATS2 expression. Our results suggest that the inhibition of miR-93 function may be a feasible approach to repress tumor metastasis. |
| doi_str_mv | 10.4161/cc.22670 |
| format | Article |
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We stably expressed miR-93 in the MT-1 human breast carcinoma cell line and found that tumors formed by the miR-93 cells contained more blood vessels than those formed by the control cells. Co-culture experiments indicated that the MT-1 cells displayed a high activity of adhesion with endothelial cells and could form larger and more tube-like structures with endothelial cells. Lung metastasis assays were performed in a mouse metastatic model, and it was found that expression of miR-93 promoted tumor cell metastasis to lung tissue. In cell culture, expression of miR-93 enhanced cell survival and invasion. We examined the potential target that mediated miR-93's effects and found that the large tumor suppressor, homology 2 (LATS2) was a target of miR-93. Higher levels of LATS2 were associated with cell death in the tumor mass. Silencing LATS2 expression promoted cell survival, tube formation and invasion, while ectopic expression of LATS2 decreased cell survival and invasion. These findings demonstrated that miR-93 promoted tumor angiogenesis and metastasis by suppressing LATS2 expression. Our results suggest that the inhibition of miR-93 function may be a feasible approach to repress tumor metastasis.</description><identifier>ISSN: 1538-4101</identifier><identifier>EISSN: 1551-4005</identifier><identifier>DOI: 10.4161/cc.22670</identifier><identifier>PMID: 23111389</identifier><language>eng</language><publisher>United States: Taylor & Francis</publisher><subject>angiogenesis ; Animals ; Base Sequence ; Breast Neoplasms - blood supply ; Breast Neoplasms - metabolism ; Breast Neoplasms - pathology ; Cell Line ; Cell Movement ; Cell Survival ; Coculture Techniques ; Disease Models, Animal ; Endothelial Cells - cytology ; Endothelial Cells - metabolism ; Female ; Humans ; KPM ; Lung Neoplasms - pathology ; Lung Neoplasms - secondary ; Mice ; Mice, Nude ; Mice, SCID ; microRNA ; MicroRNAs - metabolism ; Neovascularization, Pathologic ; Protein-Serine-Threonine Kinases - antagonists & inhibitors ; Protein-Serine-Threonine Kinases - genetics ; Protein-Serine-Threonine Kinases - metabolism ; RNA Interference ; RNA, Small Interfering - metabolism ; siRNA ; Transplantation, Heterologous ; Tumor Suppressor Proteins - antagonists & inhibitors ; Tumor Suppressor Proteins - genetics ; Tumor Suppressor Proteins - metabolism ; tumorigenesis</subject><ispartof>Cell cycle (Georgetown, Tex.), 2012-12, Vol.11 (23), p.4352-4365</ispartof><rights>Copyright © 2012 Landes Bioscience 2012</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c416t-2a72db656ff3474a58015485129b6be0d41f4ca3213484c5034477920733a01e3</citedby><cites>FETCH-LOGICAL-c416t-2a72db656ff3474a58015485129b6be0d41f4ca3213484c5034477920733a01e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3552918/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3552918/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23111389$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Fang, Ling</creatorcontrib><creatorcontrib>Du, William W.</creatorcontrib><creatorcontrib>Yang, Weining</creatorcontrib><creatorcontrib>Rutnam, Zina Jeyapalan</creatorcontrib><creatorcontrib>Peng, Chun</creatorcontrib><creatorcontrib>Li, Haoran</creatorcontrib><creatorcontrib>O'Malley, Yunxia Q.</creatorcontrib><creatorcontrib>Askeland, Ryan W.</creatorcontrib><creatorcontrib>Sugg, Sonia</creatorcontrib><creatorcontrib>Liu, Mingyao</creatorcontrib><creatorcontrib>Mehta, Tanvi</creatorcontrib><creatorcontrib>Deng, Zhaoqun</creatorcontrib><creatorcontrib>Yang, Burton B.</creatorcontrib><title>MiR-93 enhances angiogenesis and metastasis by targeting LATS2</title><title>Cell cycle (Georgetown, Tex.)</title><addtitle>Cell Cycle</addtitle><description>Here we report that miR-93, a miRNA in the miR-106B~25 cluster, a paralog of the miR-17-92 cluster, was significantly upregulated in human breast carcinoma tissues. We stably expressed miR-93 in the MT-1 human breast carcinoma cell line and found that tumors formed by the miR-93 cells contained more blood vessels than those formed by the control cells. Co-culture experiments indicated that the MT-1 cells displayed a high activity of adhesion with endothelial cells and could form larger and more tube-like structures with endothelial cells. Lung metastasis assays were performed in a mouse metastatic model, and it was found that expression of miR-93 promoted tumor cell metastasis to lung tissue. In cell culture, expression of miR-93 enhanced cell survival and invasion. We examined the potential target that mediated miR-93's effects and found that the large tumor suppressor, homology 2 (LATS2) was a target of miR-93. Higher levels of LATS2 were associated with cell death in the tumor mass. Silencing LATS2 expression promoted cell survival, tube formation and invasion, while ectopic expression of LATS2 decreased cell survival and invasion. These findings demonstrated that miR-93 promoted tumor angiogenesis and metastasis by suppressing LATS2 expression. Our results suggest that the inhibition of miR-93 function may be a feasible approach to repress tumor metastasis.</description><subject>angiogenesis</subject><subject>Animals</subject><subject>Base Sequence</subject><subject>Breast Neoplasms - blood supply</subject><subject>Breast Neoplasms - metabolism</subject><subject>Breast Neoplasms - pathology</subject><subject>Cell Line</subject><subject>Cell Movement</subject><subject>Cell Survival</subject><subject>Coculture Techniques</subject><subject>Disease Models, Animal</subject><subject>Endothelial Cells - cytology</subject><subject>Endothelial Cells - metabolism</subject><subject>Female</subject><subject>Humans</subject><subject>KPM</subject><subject>Lung Neoplasms - pathology</subject><subject>Lung Neoplasms - secondary</subject><subject>Mice</subject><subject>Mice, Nude</subject><subject>Mice, SCID</subject><subject>microRNA</subject><subject>MicroRNAs - metabolism</subject><subject>Neovascularization, Pathologic</subject><subject>Protein-Serine-Threonine Kinases - antagonists & inhibitors</subject><subject>Protein-Serine-Threonine Kinases - genetics</subject><subject>Protein-Serine-Threonine Kinases - metabolism</subject><subject>RNA Interference</subject><subject>RNA, Small Interfering - metabolism</subject><subject>siRNA</subject><subject>Transplantation, Heterologous</subject><subject>Tumor Suppressor Proteins - antagonists & inhibitors</subject><subject>Tumor Suppressor Proteins - genetics</subject><subject>Tumor Suppressor Proteins - metabolism</subject><subject>tumorigenesis</subject><issn>1538-4101</issn><issn>1551-4005</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>0YH</sourceid><sourceid>EIF</sourceid><recordid>eNplkFtLAzEQhYMoVqvgL5B99GVrJpe9vBSKeIOKoPU5ZLPZbWQ3qclW6b93a2tVhIGZw3ycGQ5CZ4BHDBK4VGpESJLiPXQEnEPMMOb765lmMQMMA3QcwivGJEtzOEQDQgGAZvkRGj-YpzinkbZzaZUOkbS1cbW2Opi1KKNWdzL01ctiFXXS17ozto6mk9kzOUEHlWyCPt32IXq5uZ5d3cXTx9v7q8k0Vv1_XUxkSsoi4UlVUZYyyTMMnGUcSF4khcYlg4opSQlQljHFMWUsTXOCU0olBk2HaLzxXSyLVpdK287LRiy8aaVfCSeN-LuxZi5q9y4o5ySHrDe42Bp497bUoROtCUo3jbTaLYMAQlOcE8LgB1XeheB1tTsDWKzjFkqJr7h79Pz3WzvwO98eoBvA2Mr5Vn4435Sik6vG-cr3iZsg6D_bT8Quieg</recordid><startdate>20121201</startdate><enddate>20121201</enddate><creator>Fang, Ling</creator><creator>Du, William W.</creator><creator>Yang, Weining</creator><creator>Rutnam, Zina Jeyapalan</creator><creator>Peng, Chun</creator><creator>Li, Haoran</creator><creator>O'Malley, Yunxia Q.</creator><creator>Askeland, Ryan W.</creator><creator>Sugg, Sonia</creator><creator>Liu, Mingyao</creator><creator>Mehta, Tanvi</creator><creator>Deng, Zhaoqun</creator><creator>Yang, Burton B.</creator><general>Taylor & Francis</general><general>Landes Bioscience</general><scope>0YH</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>20121201</creationdate><title>MiR-93 enhances angiogenesis and metastasis by targeting LATS2</title><author>Fang, Ling ; Du, William W. ; Yang, Weining ; Rutnam, Zina Jeyapalan ; Peng, Chun ; Li, Haoran ; O'Malley, Yunxia Q. ; Askeland, Ryan W. ; Sugg, Sonia ; Liu, Mingyao ; Mehta, Tanvi ; Deng, Zhaoqun ; Yang, Burton B.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c416t-2a72db656ff3474a58015485129b6be0d41f4ca3213484c5034477920733a01e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>angiogenesis</topic><topic>Animals</topic><topic>Base Sequence</topic><topic>Breast Neoplasms - blood supply</topic><topic>Breast Neoplasms - metabolism</topic><topic>Breast Neoplasms - pathology</topic><topic>Cell Line</topic><topic>Cell Movement</topic><topic>Cell Survival</topic><topic>Coculture Techniques</topic><topic>Disease Models, Animal</topic><topic>Endothelial Cells - cytology</topic><topic>Endothelial Cells - metabolism</topic><topic>Female</topic><topic>Humans</topic><topic>KPM</topic><topic>Lung Neoplasms - pathology</topic><topic>Lung Neoplasms - secondary</topic><topic>Mice</topic><topic>Mice, Nude</topic><topic>Mice, SCID</topic><topic>microRNA</topic><topic>MicroRNAs - metabolism</topic><topic>Neovascularization, Pathologic</topic><topic>Protein-Serine-Threonine Kinases - antagonists & inhibitors</topic><topic>Protein-Serine-Threonine Kinases - genetics</topic><topic>Protein-Serine-Threonine Kinases - metabolism</topic><topic>RNA Interference</topic><topic>RNA, Small Interfering - metabolism</topic><topic>siRNA</topic><topic>Transplantation, Heterologous</topic><topic>Tumor Suppressor Proteins - antagonists & inhibitors</topic><topic>Tumor Suppressor Proteins - genetics</topic><topic>Tumor Suppressor Proteins - metabolism</topic><topic>tumorigenesis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Fang, Ling</creatorcontrib><creatorcontrib>Du, William W.</creatorcontrib><creatorcontrib>Yang, Weining</creatorcontrib><creatorcontrib>Rutnam, Zina Jeyapalan</creatorcontrib><creatorcontrib>Peng, Chun</creatorcontrib><creatorcontrib>Li, Haoran</creatorcontrib><creatorcontrib>O'Malley, Yunxia Q.</creatorcontrib><creatorcontrib>Askeland, Ryan W.</creatorcontrib><creatorcontrib>Sugg, Sonia</creatorcontrib><creatorcontrib>Liu, Mingyao</creatorcontrib><creatorcontrib>Mehta, Tanvi</creatorcontrib><creatorcontrib>Deng, Zhaoqun</creatorcontrib><creatorcontrib>Yang, Burton B.</creatorcontrib><collection>Taylor & Francis Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cell cycle (Georgetown, Tex.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Fang, Ling</au><au>Du, William W.</au><au>Yang, Weining</au><au>Rutnam, Zina Jeyapalan</au><au>Peng, Chun</au><au>Li, Haoran</au><au>O'Malley, Yunxia Q.</au><au>Askeland, Ryan W.</au><au>Sugg, Sonia</au><au>Liu, Mingyao</au><au>Mehta, Tanvi</au><au>Deng, Zhaoqun</au><au>Yang, Burton B.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>MiR-93 enhances angiogenesis and metastasis by targeting LATS2</atitle><jtitle>Cell cycle (Georgetown, Tex.)</jtitle><addtitle>Cell Cycle</addtitle><date>2012-12-01</date><risdate>2012</risdate><volume>11</volume><issue>23</issue><spage>4352</spage><epage>4365</epage><pages>4352-4365</pages><issn>1538-4101</issn><eissn>1551-4005</eissn><abstract>Here we report that miR-93, a miRNA in the miR-106B~25 cluster, a paralog of the miR-17-92 cluster, was significantly upregulated in human breast carcinoma tissues. We stably expressed miR-93 in the MT-1 human breast carcinoma cell line and found that tumors formed by the miR-93 cells contained more blood vessels than those formed by the control cells. Co-culture experiments indicated that the MT-1 cells displayed a high activity of adhesion with endothelial cells and could form larger and more tube-like structures with endothelial cells. Lung metastasis assays were performed in a mouse metastatic model, and it was found that expression of miR-93 promoted tumor cell metastasis to lung tissue. In cell culture, expression of miR-93 enhanced cell survival and invasion. We examined the potential target that mediated miR-93's effects and found that the large tumor suppressor, homology 2 (LATS2) was a target of miR-93. Higher levels of LATS2 were associated with cell death in the tumor mass. Silencing LATS2 expression promoted cell survival, tube formation and invasion, while ectopic expression of LATS2 decreased cell survival and invasion. These findings demonstrated that miR-93 promoted tumor angiogenesis and metastasis by suppressing LATS2 expression. Our results suggest that the inhibition of miR-93 function may be a feasible approach to repress tumor metastasis.</abstract><cop>United States</cop><pub>Taylor & Francis</pub><pmid>23111389</pmid><doi>10.4161/cc.22670</doi><tpages>14</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | angiogenesis Animals Base Sequence Breast Neoplasms - blood supply Breast Neoplasms - metabolism Breast Neoplasms - pathology Cell Line Cell Movement Cell Survival Coculture Techniques Disease Models, Animal Endothelial Cells - cytology Endothelial Cells - metabolism Female Humans KPM Lung Neoplasms - pathology Lung Neoplasms - secondary Mice Mice, Nude Mice, SCID microRNA MicroRNAs - metabolism Neovascularization, Pathologic Protein-Serine-Threonine Kinases - antagonists & inhibitors Protein-Serine-Threonine Kinases - genetics Protein-Serine-Threonine Kinases - metabolism RNA Interference RNA, Small Interfering - metabolism siRNA Transplantation, Heterologous Tumor Suppressor Proteins - antagonists & inhibitors Tumor Suppressor Proteins - genetics Tumor Suppressor Proteins - metabolism tumorigenesis |
| title | MiR-93 enhances angiogenesis and metastasis by targeting LATS2 |
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