Suppressed expression of long non-coding RNA HOTAIR inhibits proliferation and tumourigenicity of renal carcinoma cells
Although long non-coding RNAs (lncRNAs) are known to play an important role in cell regulation in several cancers, the regulatory mechanisms in renal carcinoma cells remain unclear. HOX transcript antisense RNA (HOTAIR), an lncRNA, coordinates with chromatin-modifying enzymes to regulate gene silenc...
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| Veröffentlicht in: | Tumor biology 2014-12, Vol.35 (12), p.11887-11894 |
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| creator | Wu, Yuanhao Liu, Junfeng Zheng, Yin You, Li Kuang, Dingwei Liu, Te |
| description | Although long non-coding RNAs (lncRNAs) are known to play an important role in cell regulation in several cancers, the regulatory mechanisms in renal carcinoma cells remain unclear. HOX transcript antisense RNA (HOTAIR), an lncRNA, coordinates with chromatin-modifying enzymes to regulate gene silencing. HOTAIR is over-expressed in several types of carcinoma cells. Thus, we hypothesised that lncRNA HOTAIR is crucial for cell proliferation and invasion and that its knockdown induces apoptosis in renal carcinoma cells. lncRNA HOTAIR expression was found to be elevated in renal carcinoma cells. Additionally, lncRNA HOTAIR knockdown by RNA interference with siRNA was found to significantly affect the cell cycle in the G0/G1 phase and weaken the abilities of cell proliferation and invasion in vitro. Xenograft experiments confirmed that the growth of xenograft tumours formed by renal carcinoma cells was suppressed after silencing lncRNA HOTAIR expression. Moreover, chromatin immunoprecipitation (ChIP) and RNA-binding protein immunoprecipitation (RIP) assays revealed that knockdown of lncRNA HOTAIR led to the weakening of the recruitment and binding abilities of EZH2 and H3K27me3 locus with lncRNA HOTAIR. Furthermore, the cell cycle-related gene locus was in an active transcriptional state by the silencing of lncRNA HOTAIR expression and modulation of covalent histones. |
| doi_str_mv | 10.1007/s13277-014-2453-4 |
| format | Article |
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HOX transcript antisense RNA (HOTAIR), an lncRNA, coordinates with chromatin-modifying enzymes to regulate gene silencing. HOTAIR is over-expressed in several types of carcinoma cells. Thus, we hypothesised that lncRNA HOTAIR is crucial for cell proliferation and invasion and that its knockdown induces apoptosis in renal carcinoma cells. lncRNA HOTAIR expression was found to be elevated in renal carcinoma cells. Additionally, lncRNA HOTAIR knockdown by RNA interference with siRNA was found to significantly affect the cell cycle in the G0/G1 phase and weaken the abilities of cell proliferation and invasion in vitro. Xenograft experiments confirmed that the growth of xenograft tumours formed by renal carcinoma cells was suppressed after silencing lncRNA HOTAIR expression. Moreover, chromatin immunoprecipitation (ChIP) and RNA-binding protein immunoprecipitation (RIP) assays revealed that knockdown of lncRNA HOTAIR led to the weakening of the recruitment and binding abilities of EZH2 and H3K27me3 locus with lncRNA HOTAIR. Furthermore, the cell cycle-related gene locus was in an active transcriptional state by the silencing of lncRNA HOTAIR expression and modulation of covalent histones.</description><identifier>ISSN: 1010-4283</identifier><identifier>EISSN: 1423-0380</identifier><identifier>DOI: 10.1007/s13277-014-2453-4</identifier><identifier>PMID: 25149152</identifier><language>eng</language><publisher>Dordrecht: Springer Netherlands</publisher><subject>Animals ; Biomedicine ; Cancer Research ; Carcinoma, Renal Cell - genetics ; Carcinoma, Renal Cell - metabolism ; Carcinoma, Renal Cell - pathology ; Cell Cycle - genetics ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Cell Transformation, Neoplastic - genetics ; Cellular biology ; Disease Models, Animal ; Epigenesis, Genetic ; Gene Expression Regulation, Neoplastic ; Gene Knockdown Techniques ; Gene Silencing ; Heterografts ; Histones - metabolism ; Humans ; Kidney cancer ; Kidney Neoplasms - genetics ; Kidney Neoplasms - metabolism ; Kidney Neoplasms - pathology ; Methylation ; Mice ; Research Article ; Ribonucleic acid ; RNA ; RNA, Long Noncoding - genetics ; RNA, Small Interfering - genetics ; Tumor Burden ; Tumorigenesis</subject><ispartof>Tumor biology, 2014-12, Vol.35 (12), p.11887-11894</ispartof><rights>International Society of Oncology and BioMarkers (ISOBM) 2014</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c541t-20285fa6264c2735cfc46a6a6115bd58eb0f44289f53f7824cea982cff6f965e3</citedby><cites>FETCH-LOGICAL-c541t-20285fa6264c2735cfc46a6a6115bd58eb0f44289f53f7824cea982cff6f965e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s13277-014-2453-4$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s13277-014-2453-4$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25149152$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wu, Yuanhao</creatorcontrib><creatorcontrib>Liu, Junfeng</creatorcontrib><creatorcontrib>Zheng, Yin</creatorcontrib><creatorcontrib>You, Li</creatorcontrib><creatorcontrib>Kuang, Dingwei</creatorcontrib><creatorcontrib>Liu, Te</creatorcontrib><title>Suppressed expression of long non-coding RNA HOTAIR inhibits proliferation and tumourigenicity of renal carcinoma cells</title><title>Tumor biology</title><addtitle>Tumor Biol</addtitle><addtitle>Tumour Biol</addtitle><description>Although long non-coding RNAs (lncRNAs) are known to play an important role in cell regulation in several cancers, the regulatory mechanisms in renal carcinoma cells remain unclear. HOX transcript antisense RNA (HOTAIR), an lncRNA, coordinates with chromatin-modifying enzymes to regulate gene silencing. HOTAIR is over-expressed in several types of carcinoma cells. Thus, we hypothesised that lncRNA HOTAIR is crucial for cell proliferation and invasion and that its knockdown induces apoptosis in renal carcinoma cells. lncRNA HOTAIR expression was found to be elevated in renal carcinoma cells. Additionally, lncRNA HOTAIR knockdown by RNA interference with siRNA was found to significantly affect the cell cycle in the G0/G1 phase and weaken the abilities of cell proliferation and invasion in vitro. Xenograft experiments confirmed that the growth of xenograft tumours formed by renal carcinoma cells was suppressed after silencing lncRNA HOTAIR expression. Moreover, chromatin immunoprecipitation (ChIP) and RNA-binding protein immunoprecipitation (RIP) assays revealed that knockdown of lncRNA HOTAIR led to the weakening of the recruitment and binding abilities of EZH2 and H3K27me3 locus with lncRNA HOTAIR. Furthermore, the cell cycle-related gene locus was in an active transcriptional state by the silencing of lncRNA HOTAIR expression and modulation of covalent histones.</description><subject>Animals</subject><subject>Biomedicine</subject><subject>Cancer Research</subject><subject>Carcinoma, Renal Cell - genetics</subject><subject>Carcinoma, Renal Cell - metabolism</subject><subject>Carcinoma, Renal Cell - pathology</subject><subject>Cell Cycle - genetics</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement</subject><subject>Cell Proliferation</subject><subject>Cell Transformation, Neoplastic - genetics</subject><subject>Cellular biology</subject><subject>Disease Models, Animal</subject><subject>Epigenesis, Genetic</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Gene Knockdown Techniques</subject><subject>Gene Silencing</subject><subject>Heterografts</subject><subject>Histones - metabolism</subject><subject>Humans</subject><subject>Kidney cancer</subject><subject>Kidney Neoplasms - genetics</subject><subject>Kidney Neoplasms - metabolism</subject><subject>Kidney Neoplasms - pathology</subject><subject>Methylation</subject><subject>Mice</subject><subject>Research Article</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>RNA, Long Noncoding - genetics</subject><subject>RNA, Small Interfering - genetics</subject><subject>Tumor Burden</subject><subject>Tumorigenesis</subject><issn>1010-4283</issn><issn>1423-0380</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp1kV1LHDEYhYMoald_QG8k4E1vUvM9mctFahWkwqrXIZtJtpGZZJvMUP33zXS1SEFykRfynJPzcgD4TPBXgnFzUQijTYMw4YhywRDfA8eEU4YwU3i_zphgxKliR-BTKU8YE9G28hAcUUF4SwQ9Br_vp-02u1JcB93z3ymkCJOHfYobGFNENnWhjqsfS3h997C8WcEQf4Z1GAvc5tQH77IZZ5GJHRynIU05bFwMNowvs1F20fTQmmxDTIOB1vV9OQEH3vTFnb7eC_B49e3h8hrd3n2_uVzeIis4GRHFVAlvJJXc0oYJ6y2Xph5CxLoTyq2x53XD1gvmG0W5daZV1HovfSuFYwvwZedbo_6aXBn1EMqcwESXpqKJFFwqShpc0fP_0Ke6Ss0-U6xVjeSNqhTZUTanUrLzepvDYPKLJljPrehdK7q2oudWNK-as1fnaT247p_irYYK0B1Q6lPcuPzu6w9d_wCdSZgW</recordid><startdate>20141201</startdate><enddate>20141201</enddate><creator>Wu, Yuanhao</creator><creator>Liu, Junfeng</creator><creator>Zheng, Yin</creator><creator>You, Li</creator><creator>Kuang, Dingwei</creator><creator>Liu, Te</creator><general>Springer Netherlands</general><general>Springer Nature B.V</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>3V.</scope><scope>7T5</scope><scope>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7TM</scope></search><sort><creationdate>20141201</creationdate><title>Suppressed expression of long non-coding RNA HOTAIR inhibits proliferation and tumourigenicity of renal carcinoma cells</title><author>Wu, Yuanhao ; Liu, Junfeng ; Zheng, Yin ; You, Li ; Kuang, Dingwei ; Liu, Te</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c541t-20285fa6264c2735cfc46a6a6115bd58eb0f44289f53f7824cea982cff6f965e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Animals</topic><topic>Biomedicine</topic><topic>Cancer Research</topic><topic>Carcinoma, Renal Cell - genetics</topic><topic>Carcinoma, Renal Cell - metabolism</topic><topic>Carcinoma, Renal Cell - pathology</topic><topic>Cell Cycle - genetics</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement</topic><topic>Cell Proliferation</topic><topic>Cell Transformation, Neoplastic - genetics</topic><topic>Cellular biology</topic><topic>Disease Models, Animal</topic><topic>Epigenesis, Genetic</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Gene Knockdown Techniques</topic><topic>Gene Silencing</topic><topic>Heterografts</topic><topic>Histones - metabolism</topic><topic>Humans</topic><topic>Kidney cancer</topic><topic>Kidney Neoplasms - genetics</topic><topic>Kidney Neoplasms - metabolism</topic><topic>Kidney Neoplasms - pathology</topic><topic>Methylation</topic><topic>Mice</topic><topic>Research Article</topic><topic>Ribonucleic acid</topic><topic>RNA</topic><topic>RNA, Long Noncoding - genetics</topic><topic>RNA, Small Interfering - genetics</topic><topic>Tumor Burden</topic><topic>Tumorigenesis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wu, Yuanhao</creatorcontrib><creatorcontrib>Liu, Junfeng</creatorcontrib><creatorcontrib>Zheng, Yin</creatorcontrib><creatorcontrib>You, Li</creatorcontrib><creatorcontrib>Kuang, Dingwei</creatorcontrib><creatorcontrib>Liu, Te</creatorcontrib><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>Immunology Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health 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>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Publicly Available Content Database</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>ProQuest Central Basic</collection><collection>Nucleic Acids Abstracts</collection><jtitle>Tumor biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wu, Yuanhao</au><au>Liu, Junfeng</au><au>Zheng, Yin</au><au>You, Li</au><au>Kuang, Dingwei</au><au>Liu, Te</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Suppressed expression of long non-coding RNA HOTAIR inhibits proliferation and tumourigenicity of renal carcinoma cells</atitle><jtitle>Tumor biology</jtitle><stitle>Tumor Biol</stitle><addtitle>Tumour Biol</addtitle><date>2014-12-01</date><risdate>2014</risdate><volume>35</volume><issue>12</issue><spage>11887</spage><epage>11894</epage><pages>11887-11894</pages><issn>1010-4283</issn><eissn>1423-0380</eissn><abstract>Although long non-coding RNAs (lncRNAs) are known to play an important role in cell regulation in several cancers, the regulatory mechanisms in renal carcinoma cells remain unclear. HOX transcript antisense RNA (HOTAIR), an lncRNA, coordinates with chromatin-modifying enzymes to regulate gene silencing. HOTAIR is over-expressed in several types of carcinoma cells. Thus, we hypothesised that lncRNA HOTAIR is crucial for cell proliferation and invasion and that its knockdown induces apoptosis in renal carcinoma cells. lncRNA HOTAIR expression was found to be elevated in renal carcinoma cells. Additionally, lncRNA HOTAIR knockdown by RNA interference with siRNA was found to significantly affect the cell cycle in the G0/G1 phase and weaken the abilities of cell proliferation and invasion in vitro. Xenograft experiments confirmed that the growth of xenograft tumours formed by renal carcinoma cells was suppressed after silencing lncRNA HOTAIR expression. Moreover, chromatin immunoprecipitation (ChIP) and RNA-binding protein immunoprecipitation (RIP) assays revealed that knockdown of lncRNA HOTAIR led to the weakening of the recruitment and binding abilities of EZH2 and H3K27me3 locus with lncRNA HOTAIR. Furthermore, the cell cycle-related gene locus was in an active transcriptional state by the silencing of lncRNA HOTAIR expression and modulation of covalent histones.</abstract><cop>Dordrecht</cop><pub>Springer Netherlands</pub><pmid>25149152</pmid><doi>10.1007/s13277-014-2453-4</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Biomedicine Cancer Research Carcinoma, Renal Cell - genetics Carcinoma, Renal Cell - metabolism Carcinoma, Renal Cell - pathology Cell Cycle - genetics Cell Line, Tumor Cell Movement Cell Proliferation Cell Transformation, Neoplastic - genetics Cellular biology Disease Models, Animal Epigenesis, Genetic Gene Expression Regulation, Neoplastic Gene Knockdown Techniques Gene Silencing Heterografts Histones - metabolism Humans Kidney cancer Kidney Neoplasms - genetics Kidney Neoplasms - metabolism Kidney Neoplasms - pathology Methylation Mice Research Article Ribonucleic acid RNA RNA, Long Noncoding - genetics RNA, Small Interfering - genetics Tumor Burden Tumorigenesis |
| title | Suppressed expression of long non-coding RNA HOTAIR inhibits proliferation and tumourigenicity of renal carcinoma cells |
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