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LncRNA SNHG5 upregulation induced by YY1 contributes to angiogenesis via miR-26b/CTGF/VEGFA axis in acute myelogenous leukemia
Acute myelogenous leukemia (AML) is the most common acute leukemia in adults. Despite great progress has been made in this field, the pathogenesis of AML is still not fully understood. We report here the biological role of lncRNA small nucleolar RNA host gene 5 (SNHG5) in the pathogenesis of AML and...
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| Published in: | Laboratory investigation 2021-03, Vol.101 (3), p.341-352 |
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| creator | Li, Zhen-Jiang Cheng, Jing Song, Yuan Li, Hui-Hui Zheng, Ji-Fu |
| description | Acute myelogenous leukemia (AML) is the most common acute leukemia in adults. Despite great progress has been made in this field, the pathogenesis of AML is still not fully understood. We report here the biological role of lncRNA small nucleolar RNA host gene 5 (SNHG5) in the pathogenesis of AML and the underlying mechanisms. The results showed that lncRNA SNHG5 was highly expressed in AML cancer cell lines. In vitro studies displayed that inhibition of SNHG5 with shRNA resulted in suppression of survival, cell cycle progression, migration/invasion of AML and capacity of adhesion and angiogenesis in human umbilical vein endothelial cells. Mechanistic studies revealed a SNHG5/miR-26b/connective tissue growth factor (CTGF)/vascular endothelial growth factor A (VEGFA) axis in the regulation of AML angiogenesis. Finally, Yin Yang 1 (YY1) was found to transactivate and interact with SNHG5 promoter, leading to the upregulation of SNHG5 in AML. Collectively, upregulation of lncRNA SNHG5 mediated by YY1, activates CTGF/VEGFA via targeting miR-26b to regulate angiogenesis of AML. Our work provides new insights into the molecular mechanisms of AML.
This study reveals that upregulation of lncRNA small nucleolar RNA host gene 5 (SNHG5), mediated by Yin Yang 1 (YY1), activates connective tissue growth factor (CTGF)/vascular endothelial growth factor (VEGFA) axis via targeting miR-26b to regulate angiogenesis of acute myelogenous leukemia (AML), providing new insights into mechanisms of AML. |
| doi_str_mv | 10.1038/s41374-020-00519-9 |
| format | article |
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This study reveals that upregulation of lncRNA small nucleolar RNA host gene 5 (SNHG5), mediated by Yin Yang 1 (YY1), activates connective tissue growth factor (CTGF)/vascular endothelial growth factor (VEGFA) axis via targeting miR-26b to regulate angiogenesis of acute myelogenous leukemia (AML), providing new insights into mechanisms of AML.</description><identifier>ISSN: 0023-6837</identifier><identifier>EISSN: 1530-0307</identifier><identifier>DOI: 10.1038/s41374-020-00519-9</identifier><identifier>PMID: 33318617</identifier><language>eng</language><publisher>New York: Elsevier Inc</publisher><subject>631/67/1990/283/1897 ; 692/699/67/1990/283/1897 ; Acute myeloid leukemia ; Adult ; Angiogenesis ; Cell cycle ; Cell Line, Tumor ; Cell migration ; Cell Survival ; Connective tissue ; Connective tissue growth factor ; Connective Tissue Growth Factor - genetics ; Connective Tissue Growth Factor - metabolism ; Connective tissues ; Endothelial cells ; Female ; Growth factors ; Humans ; Laboratory Medicine ; Leukemia ; Leukemia, Myeloid, Acute - genetics ; Leukemia, Myeloid, Acute - metabolism ; Male ; Medicine ; Medicine & Public Health ; MicroRNAs - genetics ; MicroRNAs - metabolism ; Molecular modelling ; Myeloid leukemia ; Neovascularization, Pathologic - genetics ; Nucleoli ; Pathogenesis ; Pathology ; Ribonucleic acid ; RNA ; RNA, Long Noncoding - genetics ; RNA, Long Noncoding - metabolism ; Signal Transduction - genetics ; snoRNA ; Tumor cell lines ; Umbilical vein ; Up-regulation ; Up-Regulation - genetics ; Vascular endothelial growth factor ; Vascular Endothelial Growth Factor A - genetics ; Vascular Endothelial Growth Factor A - metabolism ; YY1 protein ; YY1 Transcription Factor - genetics ; YY1 Transcription Factor - metabolism</subject><ispartof>Laboratory investigation, 2021-03, Vol.101 (3), p.341-352</ispartof><rights>2020 United States & Canadian Academy of Pathology</rights><rights>The Author(s), under exclusive licence to United States and Canadian Academy of Pathology 2020</rights><rights>The Author(s), under exclusive licence to United States and Canadian Academy of Pathology 2020.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c472t-993ec44b7b95a5105c70ed6f3cf55fbb8adb4ddfbd321950042b630069a43e3</citedby><cites>FETCH-LOGICAL-c472t-993ec44b7b95a5105c70ed6f3cf55fbb8adb4ddfbd321950042b630069a43e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33318617$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Zhen-Jiang</creatorcontrib><creatorcontrib>Cheng, Jing</creatorcontrib><creatorcontrib>Song, Yuan</creatorcontrib><creatorcontrib>Li, Hui-Hui</creatorcontrib><creatorcontrib>Zheng, Ji-Fu</creatorcontrib><title>LncRNA SNHG5 upregulation induced by YY1 contributes to angiogenesis via miR-26b/CTGF/VEGFA axis in acute myelogenous leukemia</title><title>Laboratory investigation</title><addtitle>Lab Invest</addtitle><addtitle>Lab Invest</addtitle><description>Acute myelogenous leukemia (AML) is the most common acute leukemia in adults. Despite great progress has been made in this field, the pathogenesis of AML is still not fully understood. We report here the biological role of lncRNA small nucleolar RNA host gene 5 (SNHG5) in the pathogenesis of AML and the underlying mechanisms. The results showed that lncRNA SNHG5 was highly expressed in AML cancer cell lines. In vitro studies displayed that inhibition of SNHG5 with shRNA resulted in suppression of survival, cell cycle progression, migration/invasion of AML and capacity of adhesion and angiogenesis in human umbilical vein endothelial cells. Mechanistic studies revealed a SNHG5/miR-26b/connective tissue growth factor (CTGF)/vascular endothelial growth factor A (VEGFA) axis in the regulation of AML angiogenesis. Finally, Yin Yang 1 (YY1) was found to transactivate and interact with SNHG5 promoter, leading to the upregulation of SNHG5 in AML. Collectively, upregulation of lncRNA SNHG5 mediated by YY1, activates CTGF/VEGFA via targeting miR-26b to regulate angiogenesis of AML. Our work provides new insights into the molecular mechanisms of AML.
This study reveals that upregulation of lncRNA small nucleolar RNA host gene 5 (SNHG5), mediated by Yin Yang 1 (YY1), activates connective tissue growth factor (CTGF)/vascular endothelial growth factor (VEGFA) axis via targeting miR-26b to regulate angiogenesis of acute myelogenous leukemia (AML), providing new insights into mechanisms of AML.</description><subject>631/67/1990/283/1897</subject><subject>692/699/67/1990/283/1897</subject><subject>Acute myeloid leukemia</subject><subject>Adult</subject><subject>Angiogenesis</subject><subject>Cell cycle</subject><subject>Cell Line, Tumor</subject><subject>Cell migration</subject><subject>Cell Survival</subject><subject>Connective tissue</subject><subject>Connective tissue growth factor</subject><subject>Connective Tissue Growth Factor - genetics</subject><subject>Connective Tissue Growth Factor - metabolism</subject><subject>Connective tissues</subject><subject>Endothelial cells</subject><subject>Female</subject><subject>Growth factors</subject><subject>Humans</subject><subject>Laboratory Medicine</subject><subject>Leukemia</subject><subject>Leukemia, Myeloid, Acute - 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genetics</topic><topic>Connective Tissue Growth Factor - metabolism</topic><topic>Connective tissues</topic><topic>Endothelial cells</topic><topic>Female</topic><topic>Growth factors</topic><topic>Humans</topic><topic>Laboratory Medicine</topic><topic>Leukemia</topic><topic>Leukemia, Myeloid, Acute - genetics</topic><topic>Leukemia, Myeloid, Acute - metabolism</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>Molecular modelling</topic><topic>Myeloid leukemia</topic><topic>Neovascularization, Pathologic - genetics</topic><topic>Nucleoli</topic><topic>Pathogenesis</topic><topic>Pathology</topic><topic>Ribonucleic acid</topic><topic>RNA</topic><topic>RNA, Long Noncoding - genetics</topic><topic>RNA, Long Noncoding - metabolism</topic><topic>Signal Transduction - genetics</topic><topic>snoRNA</topic><topic>Tumor cell lines</topic><topic>Umbilical vein</topic><topic>Up-regulation</topic><topic>Up-Regulation - genetics</topic><topic>Vascular endothelial growth factor</topic><topic>Vascular Endothelial Growth Factor A - genetics</topic><topic>Vascular Endothelial Growth Factor A - metabolism</topic><topic>YY1 protein</topic><topic>YY1 Transcription Factor - genetics</topic><topic>YY1 Transcription Factor - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Zhen-Jiang</creatorcontrib><creatorcontrib>Cheng, Jing</creatorcontrib><creatorcontrib>Song, Yuan</creatorcontrib><creatorcontrib>Li, Hui-Hui</creatorcontrib><creatorcontrib>Zheng, Ji-Fu</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect: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>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>ProQuest Health and Medical</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection (Proquest) (PQ_SDU_P3)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>ProQuest Biological Science Journals</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Laboratory investigation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Zhen-Jiang</au><au>Cheng, Jing</au><au>Song, Yuan</au><au>Li, Hui-Hui</au><au>Zheng, Ji-Fu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>LncRNA SNHG5 upregulation induced by YY1 contributes to angiogenesis via miR-26b/CTGF/VEGFA axis in acute myelogenous leukemia</atitle><jtitle>Laboratory investigation</jtitle><stitle>Lab Invest</stitle><addtitle>Lab Invest</addtitle><date>2021-03-01</date><risdate>2021</risdate><volume>101</volume><issue>3</issue><spage>341</spage><epage>352</epage><pages>341-352</pages><issn>0023-6837</issn><eissn>1530-0307</eissn><abstract>Acute myelogenous leukemia (AML) is the most common acute leukemia in adults. Despite great progress has been made in this field, the pathogenesis of AML is still not fully understood. We report here the biological role of lncRNA small nucleolar RNA host gene 5 (SNHG5) in the pathogenesis of AML and the underlying mechanisms. The results showed that lncRNA SNHG5 was highly expressed in AML cancer cell lines. In vitro studies displayed that inhibition of SNHG5 with shRNA resulted in suppression of survival, cell cycle progression, migration/invasion of AML and capacity of adhesion and angiogenesis in human umbilical vein endothelial cells. Mechanistic studies revealed a SNHG5/miR-26b/connective tissue growth factor (CTGF)/vascular endothelial growth factor A (VEGFA) axis in the regulation of AML angiogenesis. Finally, Yin Yang 1 (YY1) was found to transactivate and interact with SNHG5 promoter, leading to the upregulation of SNHG5 in AML. Collectively, upregulation of lncRNA SNHG5 mediated by YY1, activates CTGF/VEGFA via targeting miR-26b to regulate angiogenesis of AML. Our work provides new insights into the molecular mechanisms of AML.
This study reveals that upregulation of lncRNA small nucleolar RNA host gene 5 (SNHG5), mediated by Yin Yang 1 (YY1), activates connective tissue growth factor (CTGF)/vascular endothelial growth factor (VEGFA) axis via targeting miR-26b to regulate angiogenesis of acute myelogenous leukemia (AML), providing new insights into mechanisms of AML.</abstract><cop>New York</cop><pub>Elsevier Inc</pub><pmid>33318617</pmid><doi>10.1038/s41374-020-00519-9</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 631/67/1990/283/1897 692/699/67/1990/283/1897 Acute myeloid leukemia Adult Angiogenesis Cell cycle Cell Line, Tumor Cell migration Cell Survival Connective tissue Connective tissue growth factor Connective Tissue Growth Factor - genetics Connective Tissue Growth Factor - metabolism Connective tissues Endothelial cells Female Growth factors Humans Laboratory Medicine Leukemia Leukemia, Myeloid, Acute - genetics Leukemia, Myeloid, Acute - metabolism Male Medicine Medicine & Public Health MicroRNAs - genetics MicroRNAs - metabolism Molecular modelling Myeloid leukemia Neovascularization, Pathologic - genetics Nucleoli Pathogenesis Pathology Ribonucleic acid RNA RNA, Long Noncoding - genetics RNA, Long Noncoding - metabolism Signal Transduction - genetics snoRNA Tumor cell lines Umbilical vein Up-regulation Up-Regulation - genetics Vascular endothelial growth factor Vascular Endothelial Growth Factor A - genetics Vascular Endothelial Growth Factor A - metabolism YY1 protein YY1 Transcription Factor - genetics YY1 Transcription Factor - metabolism |
| title | LncRNA SNHG5 upregulation induced by YY1 contributes to angiogenesis via miR-26b/CTGF/VEGFA axis in acute myelogenous leukemia |
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