A critical role for the long non-coding RNA GAS5 in proliferation and apoptosis in non-small-cell lung cancer
In more recent years, long non‐coding RNAs (lncRNAs) have been investigated as a new class of regulators of cellular processes, such as cell growth, apoptosis, and carcinogenesis. Although lncRNAs are dysregulated in numerous cancer types, limited data are available on the expression profile and fun...
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| Veröffentlicht in: | Molecular carcinogenesis 2015-06, Vol.54 (S1), p.E1-E12 |
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| creator | Shi, Xuefei Sun, Ming Liu, Hongbing Yao, Yanwen Kong, Rong Chen, Fangfang Song, Yong |
| description | In more recent years, long non‐coding RNAs (lncRNAs) have been investigated as a new class of regulators of cellular processes, such as cell growth, apoptosis, and carcinogenesis. Although lncRNAs are dysregulated in numerous cancer types, limited data are available on the expression profile and functional role of lncRNAs in non‐small cell lung cancer (NSCLC). In the present study, we determined the expression pattern of the growth arrest‐specific transcript 5 (GAS5) in 72 NSCLC specimens by qRT‐PCR and assess its biological functions in the development and progression of NSCLC. The results revealed that GAS5 expression was down‐regulated in cancerous tissues compared to adjacent noncancerous tissues (P |
| doi_str_mv | 10.1002/mc.22120 |
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Although lncRNAs are dysregulated in numerous cancer types, limited data are available on the expression profile and functional role of lncRNAs in non‐small cell lung cancer (NSCLC). In the present study, we determined the expression pattern of the growth arrest‐specific transcript 5 (GAS5) in 72 NSCLC specimens by qRT‐PCR and assess its biological functions in the development and progression of NSCLC. The results revealed that GAS5 expression was down‐regulated in cancerous tissues compared to adjacent noncancerous tissues (P < 0.05) and was highly related to tumor size and TNM stage (P < 0.05). This correlation between GAS5 and clinicopathological parameters indicates that GAS5 might function as a tumor suppressor. Furthermore, GAS5 overexpression increased tumor cell growth arrest and induced apoptosis in vitro and in vivo. Meanwhile, siRNA‐mediated knockdown of GAS5 promoted tumor cell growth. Importantly, through western blot analysis, we found that ectopic expression of GAS5 significantly up‐regulated p53 expression and down‐regulated transcription factor E2F1 expression. Taken together, these findings suggest that GAS5 is a tumor suppressor in NSCLC, and the action of GAS5 is mediated by p53‐dependent and p53‐independent pathways. GAS5 could serve as a potential diagnostic marker for NSCLC and may be a novel therapeutic target in patients with NSCLC. © 2013 Wiley Periodicals, Inc.</description><identifier>ISSN: 0899-1987</identifier><identifier>EISSN: 1098-2744</identifier><identifier>DOI: 10.1002/mc.22120</identifier><identifier>PMID: 24357161</identifier><language>eng</language><publisher>United States: Blackwell Publishing Ltd</publisher><subject>Aged ; Animals ; apoptosis ; Apoptosis - genetics ; Biomarkers, Tumor - genetics ; Biomarkers, Tumor - physiology ; Carcinoma, Non-Small-Cell Lung - genetics ; Carcinoma, Non-Small-Cell Lung - pathology ; Cell Line, Tumor ; Cell Proliferation - genetics ; Female ; GAS5 ; Gene Knockdown Techniques ; Humans ; long non-coding RNAs ; Lung Neoplasms - genetics ; Lung Neoplasms - pathology ; Male ; Mice ; Mice, Nude ; Middle Aged ; NSCLC ; proliferation ; RNA, Long Noncoding - genetics ; RNA, Long Noncoding - physiology</subject><ispartof>Molecular carcinogenesis, 2015-06, Vol.54 (S1), p.E1-E12</ispartof><rights>2013 Wiley Periodicals, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5280-50c42e5b14434fda56d3e440c8808619b764be12e6f7a30c7da66e8651b56a3c3</citedby><cites>FETCH-LOGICAL-c5280-50c42e5b14434fda56d3e440c8808619b764be12e6f7a30c7da66e8651b56a3c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fmc.22120$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fmc.22120$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24357161$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Shi, Xuefei</creatorcontrib><creatorcontrib>Sun, Ming</creatorcontrib><creatorcontrib>Liu, Hongbing</creatorcontrib><creatorcontrib>Yao, Yanwen</creatorcontrib><creatorcontrib>Kong, Rong</creatorcontrib><creatorcontrib>Chen, Fangfang</creatorcontrib><creatorcontrib>Song, Yong</creatorcontrib><title>A critical role for the long non-coding RNA GAS5 in proliferation and apoptosis in non-small-cell lung cancer</title><title>Molecular carcinogenesis</title><addtitle>Mol. Carcinog</addtitle><description>In more recent years, long non‐coding RNAs (lncRNAs) have been investigated as a new class of regulators of cellular processes, such as cell growth, apoptosis, and carcinogenesis. Although lncRNAs are dysregulated in numerous cancer types, limited data are available on the expression profile and functional role of lncRNAs in non‐small cell lung cancer (NSCLC). In the present study, we determined the expression pattern of the growth arrest‐specific transcript 5 (GAS5) in 72 NSCLC specimens by qRT‐PCR and assess its biological functions in the development and progression of NSCLC. The results revealed that GAS5 expression was down‐regulated in cancerous tissues compared to adjacent noncancerous tissues (P < 0.05) and was highly related to tumor size and TNM stage (P < 0.05). This correlation between GAS5 and clinicopathological parameters indicates that GAS5 might function as a tumor suppressor. Furthermore, GAS5 overexpression increased tumor cell growth arrest and induced apoptosis in vitro and in vivo. Meanwhile, siRNA‐mediated knockdown of GAS5 promoted tumor cell growth. Importantly, through western blot analysis, we found that ectopic expression of GAS5 significantly up‐regulated p53 expression and down‐regulated transcription factor E2F1 expression. Taken together, these findings suggest that GAS5 is a tumor suppressor in NSCLC, and the action of GAS5 is mediated by p53‐dependent and p53‐independent pathways. GAS5 could serve as a potential diagnostic marker for NSCLC and may be a novel therapeutic target in patients with NSCLC. © 2013 Wiley Periodicals, Inc.</description><subject>Aged</subject><subject>Animals</subject><subject>apoptosis</subject><subject>Apoptosis - genetics</subject><subject>Biomarkers, Tumor - genetics</subject><subject>Biomarkers, Tumor - physiology</subject><subject>Carcinoma, Non-Small-Cell Lung - genetics</subject><subject>Carcinoma, Non-Small-Cell Lung - pathology</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation - genetics</subject><subject>Female</subject><subject>GAS5</subject><subject>Gene Knockdown Techniques</subject><subject>Humans</subject><subject>long non-coding RNAs</subject><subject>Lung Neoplasms - genetics</subject><subject>Lung Neoplasms - pathology</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Nude</subject><subject>Middle Aged</subject><subject>NSCLC</subject><subject>proliferation</subject><subject>RNA, Long Noncoding - genetics</subject><subject>RNA, Long Noncoding - physiology</subject><issn>0899-1987</issn><issn>1098-2744</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqF0U1P3DAQBmALFcEWKvELKh97CfW3neNqVbaUj0rQit4sx5lQt0682FkV_j3ZssCp6skj-ZlXoxmEjig5poSwj70_ZowysoNmlNSmYlqIN2hGTF1XtDZ6H70t5RchlGpJ9tA-E1xqqugM9XPscxiDdxHnFAF3KePxJ-CYhls8pKHyqQ1TeXU5x8v5tcRhwKtJhg6yG0MasBta7FZpNaYSyuZ701V6F2PlIUYc11O7d4OHfIh2OxcLvNu-B-j7yadvi8_V-dfl6WJ-XnnJDKkk8YKBbKgQXHStk6rlIATxxhCjaN1oJRqgDFSnHSdet04pMErSRirHPT9AH55yp0nv1lBG24eyGcYNkNbFUk1qaoTi7P9U1WRaLavlK_U5lZKhs6scepcfLCV2cwfbe_v3DhN9v01dNz20L_B58ROonsCfEOHhn0H2YvEcuPWhjHD_4l3-bZXmWtqby6X9Qs9-3JwJZq_5I_17nbY</recordid><startdate>20150601</startdate><enddate>20150601</enddate><creator>Shi, Xuefei</creator><creator>Sun, Ming</creator><creator>Liu, Hongbing</creator><creator>Yao, Yanwen</creator><creator>Kong, Rong</creator><creator>Chen, Fangfang</creator><creator>Song, Yong</creator><general>Blackwell Publishing Ltd</general><scope>BSCLL</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>7TM</scope></search><sort><creationdate>20150601</creationdate><title>A critical role for the long non-coding RNA GAS5 in proliferation and apoptosis in non-small-cell lung cancer</title><author>Shi, Xuefei ; Sun, Ming ; Liu, Hongbing ; Yao, Yanwen ; Kong, Rong ; Chen, Fangfang ; Song, Yong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5280-50c42e5b14434fda56d3e440c8808619b764be12e6f7a30c7da66e8651b56a3c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Aged</topic><topic>Animals</topic><topic>apoptosis</topic><topic>Apoptosis - genetics</topic><topic>Biomarkers, Tumor - genetics</topic><topic>Biomarkers, Tumor - physiology</topic><topic>Carcinoma, Non-Small-Cell Lung - genetics</topic><topic>Carcinoma, Non-Small-Cell Lung - pathology</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation - genetics</topic><topic>Female</topic><topic>GAS5</topic><topic>Gene Knockdown Techniques</topic><topic>Humans</topic><topic>long non-coding RNAs</topic><topic>Lung Neoplasms - genetics</topic><topic>Lung Neoplasms - pathology</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Nude</topic><topic>Middle Aged</topic><topic>NSCLC</topic><topic>proliferation</topic><topic>RNA, Long Noncoding - genetics</topic><topic>RNA, Long Noncoding - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Shi, Xuefei</creatorcontrib><creatorcontrib>Sun, Ming</creatorcontrib><creatorcontrib>Liu, Hongbing</creatorcontrib><creatorcontrib>Yao, Yanwen</creatorcontrib><creatorcontrib>Kong, Rong</creatorcontrib><creatorcontrib>Chen, Fangfang</creatorcontrib><creatorcontrib>Song, Yong</creatorcontrib><collection>Istex</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>Nucleic Acids Abstracts</collection><jtitle>Molecular carcinogenesis</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Shi, Xuefei</au><au>Sun, Ming</au><au>Liu, Hongbing</au><au>Yao, Yanwen</au><au>Kong, Rong</au><au>Chen, Fangfang</au><au>Song, Yong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A critical role for the long non-coding RNA GAS5 in proliferation and apoptosis in non-small-cell lung cancer</atitle><jtitle>Molecular carcinogenesis</jtitle><addtitle>Mol. Carcinog</addtitle><date>2015-06-01</date><risdate>2015</risdate><volume>54</volume><issue>S1</issue><spage>E1</spage><epage>E12</epage><pages>E1-E12</pages><issn>0899-1987</issn><eissn>1098-2744</eissn><abstract>In more recent years, long non‐coding RNAs (lncRNAs) have been investigated as a new class of regulators of cellular processes, such as cell growth, apoptosis, and carcinogenesis. Although lncRNAs are dysregulated in numerous cancer types, limited data are available on the expression profile and functional role of lncRNAs in non‐small cell lung cancer (NSCLC). In the present study, we determined the expression pattern of the growth arrest‐specific transcript 5 (GAS5) in 72 NSCLC specimens by qRT‐PCR and assess its biological functions in the development and progression of NSCLC. The results revealed that GAS5 expression was down‐regulated in cancerous tissues compared to adjacent noncancerous tissues (P < 0.05) and was highly related to tumor size and TNM stage (P < 0.05). This correlation between GAS5 and clinicopathological parameters indicates that GAS5 might function as a tumor suppressor. Furthermore, GAS5 overexpression increased tumor cell growth arrest and induced apoptosis in vitro and in vivo. Meanwhile, siRNA‐mediated knockdown of GAS5 promoted tumor cell growth. Importantly, through western blot analysis, we found that ectopic expression of GAS5 significantly up‐regulated p53 expression and down‐regulated transcription factor E2F1 expression. Taken together, these findings suggest that GAS5 is a tumor suppressor in NSCLC, and the action of GAS5 is mediated by p53‐dependent and p53‐independent pathways. GAS5 could serve as a potential diagnostic marker for NSCLC and may be a novel therapeutic target in patients with NSCLC. © 2013 Wiley Periodicals, Inc.</abstract><cop>United States</cop><pub>Blackwell Publishing Ltd</pub><pmid>24357161</pmid><doi>10.1002/mc.22120</doi><tpages>12</tpages></addata></record> |
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| subjects | Aged Animals apoptosis Apoptosis - genetics Biomarkers, Tumor - genetics Biomarkers, Tumor - physiology Carcinoma, Non-Small-Cell Lung - genetics Carcinoma, Non-Small-Cell Lung - pathology Cell Line, Tumor Cell Proliferation - genetics Female GAS5 Gene Knockdown Techniques Humans long non-coding RNAs Lung Neoplasms - genetics Lung Neoplasms - pathology Male Mice Mice, Nude Middle Aged NSCLC proliferation RNA, Long Noncoding - genetics RNA, Long Noncoding - physiology |
| title | A critical role for the long non-coding RNA GAS5 in proliferation and apoptosis in non-small-cell lung cancer |
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