High ECT2 expression is an independent prognostic factor for poor overall survival and recurrence-free survival in non-small cell lung adenocarcinoma
Different subtypes of non-small cell lung cancer (NSCLC) have distinct sites of origin, histologies, genetic and epigenetic changes. In this study, we explored the mechanisms of ECT2 dysregulation and compared its prognostic value in lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC)...
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| creator | Zhou, Shijie Wang, Ping Su, Xiaolan Chen, Jingxia Chen, Hongfen Yang, Hanbing Fang, Aiping Xie, Linshen Yao, Yuqin Yang, Jinliang |
| description | Different subtypes of non-small cell lung cancer (NSCLC) have distinct sites of origin, histologies, genetic and epigenetic changes. In this study, we explored the mechanisms of ECT2 dysregulation and compared its prognostic value in lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC). In addition, we also investigated the enrichment of ECT2 co-expressed genes in KEGG pathways in LUAD and LUSC. Bioinformatic analysis was performed based on data from the Cancer Genome Atlas (TCGA)-LUAD and TCGA-LUSC. Results showed that ECT2 expression was significantly upregulated in both LUAD and LUSC compared with normal lung tissues. ECT2 expression was considerably higher in LUSC than in LUAD. The level of ECT2 DNA methylation was significantly lower in LUSC than in LUAD. ECT2 mutation was observed in 5% of LUAD and in 51% of LUSC cases. Amplification was the predominant alteration. LUAD patients with ECT2 amplification had significantly worse disease-free survival (p = 0.022). High ECT2 expression was associated with unfavorable overall survival (OS) (p |
| doi_str_mv | 10.1371/journal.pone.0187356 |
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In this study, we explored the mechanisms of ECT2 dysregulation and compared its prognostic value in lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC). In addition, we also investigated the enrichment of ECT2 co-expressed genes in KEGG pathways in LUAD and LUSC. Bioinformatic analysis was performed based on data from the Cancer Genome Atlas (TCGA)-LUAD and TCGA-LUSC. Results showed that ECT2 expression was significantly upregulated in both LUAD and LUSC compared with normal lung tissues. ECT2 expression was considerably higher in LUSC than in LUAD. The level of ECT2 DNA methylation was significantly lower in LUSC than in LUAD. ECT2 mutation was observed in 5% of LUAD and in 51% of LUSC cases. Amplification was the predominant alteration. LUAD patients with ECT2 amplification had significantly worse disease-free survival (p = 0.022). High ECT2 expression was associated with unfavorable overall survival (OS) (p<0.0001) and recurrence-free survival (RFS) (p = 0.001) in LUAD patients. Nevertheless, these associations were not observed in patients with LUSC. The following univariate and multivariate analysis showed that the high ECT2 expression was an independent prognostic factor for poor OS (HR: 2.039, 95%CI: 1.457-2.852, p<0.001) and RFS (HR: 1.715, 95%CI: 1.210-2.432, p = 0.002) in LUAD patients, but not in LUSC patients. Among 518 genes co-expressed with ECT2 in LUAD and 386 genes co-expressed with ECT2 in LUSC, there were only 98 genes in the overlapping cluster. Some of the genes related KEGG pathways in LUAD were not observed in LUSC. These differences might help to explain the different prognostic value of ECT2 in LUAD and LUSC, which are also worthy of further studies.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0187356</identifier><identifier>PMID: 29088286</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Adenocarcinoma ; Adenocarcinoma - pathology ; Amplification ; Biology and life sciences ; Cancer ; Cell survival ; Chromosomes ; Deoxyribonucleic acid ; Disease-Free Survival ; DNA ; DNA Methylation ; Emergency medical care ; Epigenetic inheritance ; Gene expression ; Genes ; Genetic aspects ; Genomes ; Genomics ; Humans ; Kinases ; Lung cancer ; Lung carcinoma ; Lung diseases ; Lung Neoplasms - pathology ; Medical prognosis ; Medicine and Health Sciences ; Methylation ; Multivariate analysis ; Mutation ; Non-small cell lung cancer ; Non-small cell lung carcinoma ; Pathways ; Patient outcomes ; Patients ; Physical Sciences ; Preventive medicine ; Prognosis ; Proto-Oncogene Proteins - genetics ; Research and Analysis Methods ; Small cell lung carcinoma ; Squamous cell carcinoma ; Survival ; Survival Analysis ; Tissues</subject><ispartof>PloS one, 2017-10, Vol.12 (10), p.e0187356-e0187356</ispartof><rights>COPYRIGHT 2017 Public Library of Science</rights><rights>2017 Zhou et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2017 Zhou et al 2017 Zhou et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-3f14a7362821c959c86c45aecaa3e23d20af9563acdcf1a96cfd174b69b2ddae3</citedby><cites>FETCH-LOGICAL-c692t-3f14a7362821c959c86c45aecaa3e23d20af9563acdcf1a96cfd174b69b2ddae3</cites><orcidid>0000-0002-7787-8722</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5663495/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5663495/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,725,778,782,862,883,2098,2917,23849,27907,27908,53774,53776,79351,79352</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29088286$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Ahmad, Aamir</contributor><creatorcontrib>Zhou, Shijie</creatorcontrib><creatorcontrib>Wang, Ping</creatorcontrib><creatorcontrib>Su, Xiaolan</creatorcontrib><creatorcontrib>Chen, Jingxia</creatorcontrib><creatorcontrib>Chen, Hongfen</creatorcontrib><creatorcontrib>Yang, Hanbing</creatorcontrib><creatorcontrib>Fang, Aiping</creatorcontrib><creatorcontrib>Xie, Linshen</creatorcontrib><creatorcontrib>Yao, Yuqin</creatorcontrib><creatorcontrib>Yang, Jinliang</creatorcontrib><title>High ECT2 expression is an independent prognostic factor for poor overall survival and recurrence-free survival in non-small cell lung adenocarcinoma</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Different subtypes of non-small cell lung cancer (NSCLC) have distinct sites of origin, histologies, genetic and epigenetic changes. In this study, we explored the mechanisms of ECT2 dysregulation and compared its prognostic value in lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC). In addition, we also investigated the enrichment of ECT2 co-expressed genes in KEGG pathways in LUAD and LUSC. Bioinformatic analysis was performed based on data from the Cancer Genome Atlas (TCGA)-LUAD and TCGA-LUSC. Results showed that ECT2 expression was significantly upregulated in both LUAD and LUSC compared with normal lung tissues. ECT2 expression was considerably higher in LUSC than in LUAD. The level of ECT2 DNA methylation was significantly lower in LUSC than in LUAD. ECT2 mutation was observed in 5% of LUAD and in 51% of LUSC cases. Amplification was the predominant alteration. LUAD patients with ECT2 amplification had significantly worse disease-free survival (p = 0.022). High ECT2 expression was associated with unfavorable overall survival (OS) (p<0.0001) and recurrence-free survival (RFS) (p = 0.001) in LUAD patients. Nevertheless, these associations were not observed in patients with LUSC. The following univariate and multivariate analysis showed that the high ECT2 expression was an independent prognostic factor for poor OS (HR: 2.039, 95%CI: 1.457-2.852, p<0.001) and RFS (HR: 1.715, 95%CI: 1.210-2.432, p = 0.002) in LUAD patients, but not in LUSC patients. Among 518 genes co-expressed with ECT2 in LUAD and 386 genes co-expressed with ECT2 in LUSC, there were only 98 genes in the overlapping cluster. Some of the genes related KEGG pathways in LUAD were not observed in LUSC. These differences might help to explain the different prognostic value of ECT2 in LUAD and LUSC, which are also worthy of further studies.</description><subject>Adenocarcinoma</subject><subject>Adenocarcinoma - pathology</subject><subject>Amplification</subject><subject>Biology and life sciences</subject><subject>Cancer</subject><subject>Cell survival</subject><subject>Chromosomes</subject><subject>Deoxyribonucleic acid</subject><subject>Disease-Free Survival</subject><subject>DNA</subject><subject>DNA Methylation</subject><subject>Emergency medical care</subject><subject>Epigenetic inheritance</subject><subject>Gene expression</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>Genomes</subject><subject>Genomics</subject><subject>Humans</subject><subject>Kinases</subject><subject>Lung cancer</subject><subject>Lung carcinoma</subject><subject>Lung diseases</subject><subject>Lung Neoplasms - pathology</subject><subject>Medical prognosis</subject><subject>Medicine and Health Sciences</subject><subject>Methylation</subject><subject>Multivariate analysis</subject><subject>Mutation</subject><subject>Non-small cell lung cancer</subject><subject>Non-small cell lung carcinoma</subject><subject>Pathways</subject><subject>Patient outcomes</subject><subject>Patients</subject><subject>Physical Sciences</subject><subject>Preventive medicine</subject><subject>Prognosis</subject><subject>Proto-Oncogene Proteins - genetics</subject><subject>Research and Analysis Methods</subject><subject>Small cell lung carcinoma</subject><subject>Squamous cell carcinoma</subject><subject>Survival</subject><subject>Survival Analysis</subject><subject>Tissues</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNk99u0zAUxiMEYmPwBggiISG4aPGf2I1vkKZqsEqTJsHg1jpxTlJXqR3spBoPwvvi0m60aBcoyklk_77P8RefLHtJyZTyGf2w8mNw0E1773BKaDnjQj7KTqnibCIZ4Y8P3k-yZzGuCBG8lPJpdsIUKUtWytPs16Vtl_nF_IbleNsHjNF6l9uYQ6quxh5TcUPeB986Hwdr8gbM4EPepLv3qfgNBui6PI5hYzfQJWmdBzRjCOgMTpqA-HfSutx5N4nrrcRgKt3o2hzSKt5AMNb5NTzPnjTQRXyxf55l3z5d3MwvJ1fXnxfz86uJkYoNE97QAmZcspJRo4QypTSFADQAHBmvGYFGCcnB1KahoKRpajorKqkqVteA_Cx7vfPtOx_1PtGoqRIlK0pCZCIWO6L2sNJ9sGsIP7UHq_8M-NBqCCmVDvWsYCCwUoopLCTlFVZ1JTmhEoSQauv1cb_aWK2xNinXFNyR6fGMs0vd-o0WUvJCiWTwbm8Q_I8R46DXNm4zBId-3H23KKgkKqFv_kEf3t2eaiFtwLrGp3XN1lSfC8oKJaUgiZo-QKWrxrU16fg1No0fCd4fCRIz4O3QwhijXnz98v_s9fdj9u0Bu0TohmX03TikMxuPwWIHmuBjDNjch0yJ3nbPXRp62z163z1J9urwB92L7tqF_wbMRhfO</recordid><startdate>20171031</startdate><enddate>20171031</enddate><creator>Zhou, Shijie</creator><creator>Wang, Ping</creator><creator>Su, Xiaolan</creator><creator>Chen, Jingxia</creator><creator>Chen, Hongfen</creator><creator>Yang, Hanbing</creator><creator>Fang, Aiping</creator><creator>Xie, Linshen</creator><creator>Yao, Yuqin</creator><creator>Yang, Jinliang</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0002-7787-8722</orcidid></search><sort><creationdate>20171031</creationdate><title>High ECT2 expression is an independent prognostic factor for poor overall survival and recurrence-free survival in non-small cell lung adenocarcinoma</title><author>Zhou, Shijie ; Wang, Ping ; Su, Xiaolan ; Chen, Jingxia ; Chen, Hongfen ; Yang, Hanbing ; Fang, Aiping ; Xie, Linshen ; Yao, Yuqin ; Yang, Jinliang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c692t-3f14a7362821c959c86c45aecaa3e23d20af9563acdcf1a96cfd174b69b2ddae3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Adenocarcinoma</topic><topic>Adenocarcinoma - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhou, Shijie</au><au>Wang, Ping</au><au>Su, Xiaolan</au><au>Chen, Jingxia</au><au>Chen, Hongfen</au><au>Yang, Hanbing</au><au>Fang, Aiping</au><au>Xie, Linshen</au><au>Yao, Yuqin</au><au>Yang, Jinliang</au><au>Ahmad, Aamir</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>High ECT2 expression is an independent prognostic factor for poor overall survival and recurrence-free survival in non-small cell lung adenocarcinoma</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2017-10-31</date><risdate>2017</risdate><volume>12</volume><issue>10</issue><spage>e0187356</spage><epage>e0187356</epage><pages>e0187356-e0187356</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Different subtypes of non-small cell lung cancer (NSCLC) have distinct sites of origin, histologies, genetic and epigenetic changes. In this study, we explored the mechanisms of ECT2 dysregulation and compared its prognostic value in lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC). In addition, we also investigated the enrichment of ECT2 co-expressed genes in KEGG pathways in LUAD and LUSC. Bioinformatic analysis was performed based on data from the Cancer Genome Atlas (TCGA)-LUAD and TCGA-LUSC. Results showed that ECT2 expression was significantly upregulated in both LUAD and LUSC compared with normal lung tissues. ECT2 expression was considerably higher in LUSC than in LUAD. The level of ECT2 DNA methylation was significantly lower in LUSC than in LUAD. ECT2 mutation was observed in 5% of LUAD and in 51% of LUSC cases. Amplification was the predominant alteration. LUAD patients with ECT2 amplification had significantly worse disease-free survival (p = 0.022). High ECT2 expression was associated with unfavorable overall survival (OS) (p<0.0001) and recurrence-free survival (RFS) (p = 0.001) in LUAD patients. Nevertheless, these associations were not observed in patients with LUSC. The following univariate and multivariate analysis showed that the high ECT2 expression was an independent prognostic factor for poor OS (HR: 2.039, 95%CI: 1.457-2.852, p<0.001) and RFS (HR: 1.715, 95%CI: 1.210-2.432, p = 0.002) in LUAD patients, but not in LUSC patients. Among 518 genes co-expressed with ECT2 in LUAD and 386 genes co-expressed with ECT2 in LUSC, there were only 98 genes in the overlapping cluster. Some of the genes related KEGG pathways in LUAD were not observed in LUSC. These differences might help to explain the different prognostic value of ECT2 in LUAD and LUSC, which are also worthy of further studies.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>29088286</pmid><doi>10.1371/journal.pone.0187356</doi><tpages>e0187356</tpages><orcidid>https://orcid.org/0000-0002-7787-8722</orcidid><oa>free_for_read</oa></addata></record> |
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| language | eng |
| recordid | cdi_plos_journals_1958248006 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Public Library of Science (PLoS); PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Adenocarcinoma Adenocarcinoma - pathology Amplification Biology and life sciences Cancer Cell survival Chromosomes Deoxyribonucleic acid Disease-Free Survival DNA DNA Methylation Emergency medical care Epigenetic inheritance Gene expression Genes Genetic aspects Genomes Genomics Humans Kinases Lung cancer Lung carcinoma Lung diseases Lung Neoplasms - pathology Medical prognosis Medicine and Health Sciences Methylation Multivariate analysis Mutation Non-small cell lung cancer Non-small cell lung carcinoma Pathways Patient outcomes Patients Physical Sciences Preventive medicine Prognosis Proto-Oncogene Proteins - genetics Research and Analysis Methods Small cell lung carcinoma Squamous cell carcinoma Survival Survival Analysis Tissues |
| title | High ECT2 expression is an independent prognostic factor for poor overall survival and recurrence-free survival in non-small cell lung adenocarcinoma |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-16T11%3A01%3A26IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=High%20ECT2%20expression%20is%20an%20independent%20prognostic%20factor%20for%20poor%20overall%20survival%20and%20recurrence-free%20survival%20in%20non-small%20cell%20lung%20adenocarcinoma&rft.jtitle=PloS%20one&rft.au=Zhou,%20Shijie&rft.date=2017-10-31&rft.volume=12&rft.issue=10&rft.spage=e0187356&rft.epage=e0187356&rft.pages=e0187356-e0187356&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0187356&rft_dat=%3Cgale_plos_%3EA512496650%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1958248006&rft_id=info:pmid/29088286&rft_galeid=A512496650&rft_doaj_id=oai_doaj_org_article_742a5eb9929e4613bebdb63016a55696&rfr_iscdi=true |