Long intergenic non-coding RNA 00152 promotes tumor cell cycle progression by binding to EZH2 and repressing p15 and p21 in gastric cancer
Long noncoding RNAs (lncRNAs) play important regulatory roles in several human cancers. Integrated analysis revealed that expression of long intergenic non-coding RNA 152 (LINC00152) was significantly upregulated in gastric cancer (GC). Further analysis in a cohort of 97 GC patients revealed that LI...
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| Veröffentlicht in: | Oncotarget 2016-03, Vol.7 (9), p.9773-9787 |
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| creator | Chen, Wen-ming Huang, Ming-de Sun, Dao-ping Kong, Rong Xu, Tong-peng Xia, Rui Zhang, Er-bao Shu, Yong-qian |
| description | Long noncoding RNAs (lncRNAs) play important regulatory roles in several human cancers. Integrated analysis revealed that expression of long intergenic non-coding RNA 152 (LINC00152) was significantly upregulated in gastric cancer (GC). Further analysis in a cohort of 97 GC patients revealed that LINC00152 expression was positively correlated with tumor invasion depth, lymph node metastasis, higher TNM stage, and poor survival. Gene set enrichment analysis revealed that cell proliferation and cell cycle progression were increased in patients with high LINC00152 expression. In both GC cell lines and xenograft systems, LINC00152 overexpression facilitated GC cell proliferation by accelerating the cell cycle, whereas LINC00152 knockdown had the opposite effect. Moreover, by binding to enhancer of zeste homolog 2 (EZH2), LINC00152 promotes GC tumor cell cycle progression by silencing the expression of p15 and p21. These findings suggest that LINC00152 may play contribute to the progression of GC and may be an effective therapeutic target. |
| doi_str_mv | 10.18632/oncotarget.6949 |
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Integrated analysis revealed that expression of long intergenic non-coding RNA 152 (LINC00152) was significantly upregulated in gastric cancer (GC). Further analysis in a cohort of 97 GC patients revealed that LINC00152 expression was positively correlated with tumor invasion depth, lymph node metastasis, higher TNM stage, and poor survival. Gene set enrichment analysis revealed that cell proliferation and cell cycle progression were increased in patients with high LINC00152 expression. In both GC cell lines and xenograft systems, LINC00152 overexpression facilitated GC cell proliferation by accelerating the cell cycle, whereas LINC00152 knockdown had the opposite effect. Moreover, by binding to enhancer of zeste homolog 2 (EZH2), LINC00152 promotes GC tumor cell cycle progression by silencing the expression of p15 and p21. These findings suggest that LINC00152 may play contribute to the progression of GC and may be an effective therapeutic target.</description><identifier>ISSN: 1949-2553</identifier><identifier>EISSN: 1949-2553</identifier><identifier>DOI: 10.18632/oncotarget.6949</identifier><identifier>PMID: 26799422</identifier><language>eng</language><publisher>United States: Impact Journals LLC</publisher><subject>Cell Cycle - genetics ; Cell Line, Tumor ; Cell Proliferation - genetics ; Cyclin-Dependent Kinase Inhibitor p15 - antagonists & inhibitors ; Cyclin-Dependent Kinase Inhibitor p15 - genetics ; Cyclin-Dependent Kinase Inhibitor p21 - antagonists & inhibitors ; Cyclin-Dependent Kinase Inhibitor p21 - genetics ; Enhancer of Zeste Homolog 2 Protein - metabolism ; Female ; Humans ; Lymphatic Metastasis - genetics ; Male ; Middle Aged ; Neoplasm Staging ; Research Paper ; RNA, Long Noncoding - genetics ; RNA, Long Noncoding - metabolism ; RNA-Binding Proteins - metabolism ; Stomach Neoplasms - genetics ; Stomach Neoplasms - mortality ; Stomach Neoplasms - pathology</subject><ispartof>Oncotarget, 2016-03, Vol.7 (9), p.9773-9787</ispartof><rights>Copyright: © 2016 Chen et al. 2016</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c396t-be27dd078d244b957753ec27af6de2fb71551a5a84564a30b44193d1abac986e3</citedby><cites>FETCH-LOGICAL-c396t-be27dd078d244b957753ec27af6de2fb71551a5a84564a30b44193d1abac986e3</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/PMC4891083/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4891083/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27903,27904,53770,53772</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26799422$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chen, Wen-ming</creatorcontrib><creatorcontrib>Huang, Ming-de</creatorcontrib><creatorcontrib>Sun, Dao-ping</creatorcontrib><creatorcontrib>Kong, Rong</creatorcontrib><creatorcontrib>Xu, Tong-peng</creatorcontrib><creatorcontrib>Xia, Rui</creatorcontrib><creatorcontrib>Zhang, Er-bao</creatorcontrib><creatorcontrib>Shu, Yong-qian</creatorcontrib><title>Long intergenic non-coding RNA 00152 promotes tumor cell cycle progression by binding to EZH2 and repressing p15 and p21 in gastric cancer</title><title>Oncotarget</title><addtitle>Oncotarget</addtitle><description>Long noncoding RNAs (lncRNAs) play important regulatory roles in several human cancers. Integrated analysis revealed that expression of long intergenic non-coding RNA 152 (LINC00152) was significantly upregulated in gastric cancer (GC). Further analysis in a cohort of 97 GC patients revealed that LINC00152 expression was positively correlated with tumor invasion depth, lymph node metastasis, higher TNM stage, and poor survival. Gene set enrichment analysis revealed that cell proliferation and cell cycle progression were increased in patients with high LINC00152 expression. In both GC cell lines and xenograft systems, LINC00152 overexpression facilitated GC cell proliferation by accelerating the cell cycle, whereas LINC00152 knockdown had the opposite effect. Moreover, by binding to enhancer of zeste homolog 2 (EZH2), LINC00152 promotes GC tumor cell cycle progression by silencing the expression of p15 and p21. These findings suggest that LINC00152 may play contribute to the progression of GC and may be an effective therapeutic target.</description><subject>Cell Cycle - genetics</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation - genetics</subject><subject>Cyclin-Dependent Kinase Inhibitor p15 - antagonists & inhibitors</subject><subject>Cyclin-Dependent Kinase Inhibitor p15 - genetics</subject><subject>Cyclin-Dependent Kinase Inhibitor p21 - antagonists & inhibitors</subject><subject>Cyclin-Dependent Kinase Inhibitor p21 - genetics</subject><subject>Enhancer of Zeste Homolog 2 Protein - metabolism</subject><subject>Female</subject><subject>Humans</subject><subject>Lymphatic Metastasis - genetics</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Neoplasm Staging</subject><subject>Research Paper</subject><subject>RNA, Long Noncoding - genetics</subject><subject>RNA, Long Noncoding - metabolism</subject><subject>RNA-Binding Proteins - metabolism</subject><subject>Stomach Neoplasms - genetics</subject><subject>Stomach Neoplasms - mortality</subject><subject>Stomach Neoplasms - pathology</subject><issn>1949-2553</issn><issn>1949-2553</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVUU1rFTEUDaLYUrt3JVm6mZrPSbIRSqlWeFQQ3bgJmcx9Y2QmGZM84f0Ff7V5r7Wt2dxw7vkIOQi9puSC6p6zdyn6VF2eoF70Rphn6JS20TEp-fMn9xN0XspP0o4USjPzEp2wXhkjGDtFfzYpTjjECs0nBo9jip1PY2jol9tLTAiVDK85LalCwXW3pIw9zDP2ez_DYTNlKCWkiIc9HkI8SmvC199vGHZxxBnWI6PBK5VHaGW0ZeLJlZpbpnfRQ36FXmzdXOD8fp6hbx-uv17ddJvPHz9dXW46z01fuwGYGkei9MiEGIxUSnLwTLltPwLbDopKSZ10WsheOE4GIajhI3WD80b3wM_Q-zvfdTcsMHqINbvZrjksLu9tcsH-v4nhh53Sbyu0oUTzZvD23iCnXzso1S6hHP7ERUi7YqnSVHKpiWhUckf1OZWSYfsQQ4k9tmgfW7SHFpvkzdPnPQj-dcb_AitOnFc</recordid><startdate>20160301</startdate><enddate>20160301</enddate><creator>Chen, Wen-ming</creator><creator>Huang, Ming-de</creator><creator>Sun, Dao-ping</creator><creator>Kong, Rong</creator><creator>Xu, Tong-peng</creator><creator>Xia, Rui</creator><creator>Zhang, Er-bao</creator><creator>Shu, Yong-qian</creator><general>Impact Journals LLC</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>7X8</scope><scope>5PM</scope></search><sort><creationdate>20160301</creationdate><title>Long intergenic non-coding RNA 00152 promotes tumor cell cycle progression by binding to EZH2 and repressing p15 and p21 in gastric cancer</title><author>Chen, Wen-ming ; Huang, Ming-de ; Sun, Dao-ping ; Kong, Rong ; Xu, Tong-peng ; Xia, Rui ; Zhang, Er-bao ; Shu, Yong-qian</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c396t-be27dd078d244b957753ec27af6de2fb71551a5a84564a30b44193d1abac986e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Cell Cycle - genetics</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation - genetics</topic><topic>Cyclin-Dependent Kinase Inhibitor p15 - antagonists & inhibitors</topic><topic>Cyclin-Dependent Kinase Inhibitor p15 - genetics</topic><topic>Cyclin-Dependent Kinase Inhibitor p21 - antagonists & inhibitors</topic><topic>Cyclin-Dependent Kinase Inhibitor p21 - genetics</topic><topic>Enhancer of Zeste Homolog 2 Protein - metabolism</topic><topic>Female</topic><topic>Humans</topic><topic>Lymphatic Metastasis - genetics</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Neoplasm Staging</topic><topic>Research Paper</topic><topic>RNA, Long Noncoding - genetics</topic><topic>RNA, Long Noncoding - metabolism</topic><topic>RNA-Binding Proteins - metabolism</topic><topic>Stomach Neoplasms - genetics</topic><topic>Stomach Neoplasms - mortality</topic><topic>Stomach Neoplasms - pathology</topic><toplevel>online_resources</toplevel><creatorcontrib>Chen, Wen-ming</creatorcontrib><creatorcontrib>Huang, Ming-de</creatorcontrib><creatorcontrib>Sun, Dao-ping</creatorcontrib><creatorcontrib>Kong, Rong</creatorcontrib><creatorcontrib>Xu, Tong-peng</creatorcontrib><creatorcontrib>Xia, Rui</creatorcontrib><creatorcontrib>Zhang, Er-bao</creatorcontrib><creatorcontrib>Shu, Yong-qian</creatorcontrib><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>Oncotarget</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chen, Wen-ming</au><au>Huang, Ming-de</au><au>Sun, Dao-ping</au><au>Kong, Rong</au><au>Xu, Tong-peng</au><au>Xia, Rui</au><au>Zhang, Er-bao</au><au>Shu, Yong-qian</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Long intergenic non-coding RNA 00152 promotes tumor cell cycle progression by binding to EZH2 and repressing p15 and p21 in gastric cancer</atitle><jtitle>Oncotarget</jtitle><addtitle>Oncotarget</addtitle><date>2016-03-01</date><risdate>2016</risdate><volume>7</volume><issue>9</issue><spage>9773</spage><epage>9787</epage><pages>9773-9787</pages><issn>1949-2553</issn><eissn>1949-2553</eissn><abstract>Long noncoding RNAs (lncRNAs) play important regulatory roles in several human cancers. Integrated analysis revealed that expression of long intergenic non-coding RNA 152 (LINC00152) was significantly upregulated in gastric cancer (GC). Further analysis in a cohort of 97 GC patients revealed that LINC00152 expression was positively correlated with tumor invasion depth, lymph node metastasis, higher TNM stage, and poor survival. Gene set enrichment analysis revealed that cell proliferation and cell cycle progression were increased in patients with high LINC00152 expression. In both GC cell lines and xenograft systems, LINC00152 overexpression facilitated GC cell proliferation by accelerating the cell cycle, whereas LINC00152 knockdown had the opposite effect. Moreover, by binding to enhancer of zeste homolog 2 (EZH2), LINC00152 promotes GC tumor cell cycle progression by silencing the expression of p15 and p21. These findings suggest that LINC00152 may play contribute to the progression of GC and may be an effective therapeutic target.</abstract><cop>United States</cop><pub>Impact Journals LLC</pub><pmid>26799422</pmid><doi>10.18632/oncotarget.6949</doi><tpages>15</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Cell Cycle - genetics Cell Line, Tumor Cell Proliferation - genetics Cyclin-Dependent Kinase Inhibitor p15 - antagonists & inhibitors Cyclin-Dependent Kinase Inhibitor p15 - genetics Cyclin-Dependent Kinase Inhibitor p21 - antagonists & inhibitors Cyclin-Dependent Kinase Inhibitor p21 - genetics Enhancer of Zeste Homolog 2 Protein - metabolism Female Humans Lymphatic Metastasis - genetics Male Middle Aged Neoplasm Staging Research Paper RNA, Long Noncoding - genetics RNA, Long Noncoding - metabolism RNA-Binding Proteins - metabolism Stomach Neoplasms - genetics Stomach Neoplasms - mortality Stomach Neoplasms - pathology |
| title | Long intergenic non-coding RNA 00152 promotes tumor cell cycle progression by binding to EZH2 and repressing p15 and p21 in gastric cancer |
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