Comprehensive analysis of the long noncoding RNA HOXA11-AS gene interaction regulatory network in NSCLC cells
Long noncoding RNAs (lncRNAs) are related to different biological processes in non-small cell lung cancer (NSCLC). However, the possible molecular mechanisms underlying the effects of the long noncoding RNA HOXA11-AS (HOXA11 antisense RNA) in NSCLC are unknown. HOXA11-AS was knocked down in the NSCL...
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| Veröffentlicht in: | Cancer Cell International 2016-12, Vol.16 (1), p.89-89, Article 89 |
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| creator | Zhang, Yu He, Rong-Quan Dang, Yi-Wu Zhang, Xiu-Ling Wang, Xiao Huang, Su-Ning Huang, Wen-Ting Jiang, Meng-Tong Gan, Xiao-Ning Xie, You Li, Ping Luo, Dian-Zhong Chen, Gang Gan, Ting-Qing |
| description | Long noncoding RNAs (lncRNAs) are related to different biological processes in non-small cell lung cancer (NSCLC). However, the possible molecular mechanisms underlying the effects of the long noncoding RNA HOXA11-AS (HOXA11 antisense RNA) in NSCLC are unknown.
HOXA11-AS was knocked down in the NSCLC A549 cell line and a high throughput microarray assay was applied to detect changes in the gene profiles of the A549 cells. Bioinformatics analyses (gene ontology (GO), pathway, Kyoto Encyclopedia of Genes and Genomes (KEGG), and network analyses) were performed to investigate the potential pathways and networks of the differentially expressed genes. The molecular signatures database (MSigDB) was used to display the expression profiles of these differentially expressed genes. Furthermore, the relationships between the HOXA11-AS, de-regulated genes and clinical NSCLC parameters were verified by using NSCLC patient information from The Cancer Genome Atlas (TCGA) database. In addition, the relationship between HOXA11-AS expression and clinical diagnostic value was analyzed by receiver operating characteristic (ROC) curve.
Among the differentially expressed genes, 277 and 80 genes were upregulated and downregulated in NSCLC, respectively (fold change ≥2.0, P |
| doi_str_mv | 10.1186/s12935-016-0366-6 |
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HOXA11-AS was knocked down in the NSCLC A549 cell line and a high throughput microarray assay was applied to detect changes in the gene profiles of the A549 cells. Bioinformatics analyses (gene ontology (GO), pathway, Kyoto Encyclopedia of Genes and Genomes (KEGG), and network analyses) were performed to investigate the potential pathways and networks of the differentially expressed genes. The molecular signatures database (MSigDB) was used to display the expression profiles of these differentially expressed genes. Furthermore, the relationships between the HOXA11-AS, de-regulated genes and clinical NSCLC parameters were verified by using NSCLC patient information from The Cancer Genome Atlas (TCGA) database. In addition, the relationship between HOXA11-AS expression and clinical diagnostic value was analyzed by receiver operating characteristic (ROC) curve.
Among the differentially expressed genes, 277 and 80 genes were upregulated and downregulated in NSCLC, respectively (fold change ≥2.0, P < 0.05 and false discovery rate (FDR) < 0.05). According to the degree of the fold change, six upregulated and three downregulated genes were selected for further investigation. Only four genes (RSPO3, ADAMTS8, DMBT1, and DOCK8) were reported to be related with the development or progression of NSCLC based on a PubMed search. Among all possible pathways, three pathways (the PI3K-Akt, TGF-beta and Hippo signaling pathways) were the most likely to be involved in NSCLC development and progression. Furthermore, we found that HOXA11-AS was highly expressed in both lung adenocarcinoma and squamous cell carcinoma based on TCGA database. The ROC curve showed that the area under curve (AUC) of HOXA11-AS was 0.727 (95% CI 0.663-0.790) for lung adenocarcinoma and 0.933 (95% CI 0.906-0.960) for squamous cell carcinoma patients. Additionally, the original data from TCGA verified that ADAMTS8, DMBT1 and DOCK8 were downregulated in both lung adenocarcinoma and squamous cell carcinoma, whereas RSPO3 expression was upregulated in lung adenocarcinoma and downregulated in lung squamous cell carcinoma. For the other five genes (STMN2, SPINK6, TUSC3, LOC100128054, and C8orf22), we found that STMN2, TUSC3 and C8orf22 were upregulated in squamous cell carcinoma and that STMN2 and USC3 were upregulated in lung adenocarcinoma. Furthermore, we compared the correlation between HOXA11-AS and de-regulated genes in NSCLC based on TCGA. The results showed that the HOXA11-AS expression was negatively correlated with DOCK8 in squamous cell carcinoma (r = -0.124, P = 0.048) and lung adenocarcinoma (r = -0.176, P = 0.005). In addition, RSPO3, ADAMTS8 and DOCK8 were related to overall survival and disease-free survival (all P < 0.05) of lung adenocarcinoma patients in TCGA.
Our results showed that the gene profiles were significantly changed after HOXA11-AS knock-down in NSCLC cells. We speculated that HOXA11-AS may play an important role in NSCLC development and progression by regulating the expression of various pathways and genes, especially DOCK8 and TGF-beta pathway. However, the exact mechanism should be verified by functional experiments.</description><identifier>ISSN: 1475-2867</identifier><identifier>EISSN: 1475-2867</identifier><identifier>DOI: 10.1186/s12935-016-0366-6</identifier><identifier>PMID: 27980454</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Analysis ; Care and treatment ; Complications and side effects ; Hypothesis ; Influence ; Lung cancer, Non-small cell ; Patient education ; Transforming growth factors</subject><ispartof>Cancer Cell International, 2016-12, Vol.16 (1), p.89-89, Article 89</ispartof><rights>COPYRIGHT 2016 BioMed Central Ltd.</rights><rights>Copyright BioMed Central 2016</rights><rights>The Author(s) 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c594t-cdb75c600a58127a9bbaec9d6a66f2b249f1b9aee44835a11a10f2ff512e37b43</citedby><cites>FETCH-LOGICAL-c594t-cdb75c600a58127a9bbaec9d6a66f2b249f1b9aee44835a11a10f2ff512e37b43</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/PMC5133743/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5133743/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27980454$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Yu</creatorcontrib><creatorcontrib>He, Rong-Quan</creatorcontrib><creatorcontrib>Dang, Yi-Wu</creatorcontrib><creatorcontrib>Zhang, Xiu-Ling</creatorcontrib><creatorcontrib>Wang, Xiao</creatorcontrib><creatorcontrib>Huang, Su-Ning</creatorcontrib><creatorcontrib>Huang, Wen-Ting</creatorcontrib><creatorcontrib>Jiang, Meng-Tong</creatorcontrib><creatorcontrib>Gan, Xiao-Ning</creatorcontrib><creatorcontrib>Xie, You</creatorcontrib><creatorcontrib>Li, Ping</creatorcontrib><creatorcontrib>Luo, Dian-Zhong</creatorcontrib><creatorcontrib>Chen, Gang</creatorcontrib><creatorcontrib>Gan, Ting-Qing</creatorcontrib><title>Comprehensive analysis of the long noncoding RNA HOXA11-AS gene interaction regulatory network in NSCLC cells</title><title>Cancer Cell International</title><addtitle>Cancer Cell Int</addtitle><description>Long noncoding RNAs (lncRNAs) are related to different biological processes in non-small cell lung cancer (NSCLC). However, the possible molecular mechanisms underlying the effects of the long noncoding RNA HOXA11-AS (HOXA11 antisense RNA) in NSCLC are unknown.
HOXA11-AS was knocked down in the NSCLC A549 cell line and a high throughput microarray assay was applied to detect changes in the gene profiles of the A549 cells. Bioinformatics analyses (gene ontology (GO), pathway, Kyoto Encyclopedia of Genes and Genomes (KEGG), and network analyses) were performed to investigate the potential pathways and networks of the differentially expressed genes. The molecular signatures database (MSigDB) was used to display the expression profiles of these differentially expressed genes. Furthermore, the relationships between the HOXA11-AS, de-regulated genes and clinical NSCLC parameters were verified by using NSCLC patient information from The Cancer Genome Atlas (TCGA) database. In addition, the relationship between HOXA11-AS expression and clinical diagnostic value was analyzed by receiver operating characteristic (ROC) curve.
Among the differentially expressed genes, 277 and 80 genes were upregulated and downregulated in NSCLC, respectively (fold change ≥2.0, P < 0.05 and false discovery rate (FDR) < 0.05). According to the degree of the fold change, six upregulated and three downregulated genes were selected for further investigation. Only four genes (RSPO3, ADAMTS8, DMBT1, and DOCK8) were reported to be related with the development or progression of NSCLC based on a PubMed search. Among all possible pathways, three pathways (the PI3K-Akt, TGF-beta and Hippo signaling pathways) were the most likely to be involved in NSCLC development and progression. Furthermore, we found that HOXA11-AS was highly expressed in both lung adenocarcinoma and squamous cell carcinoma based on TCGA database. The ROC curve showed that the area under curve (AUC) of HOXA11-AS was 0.727 (95% CI 0.663-0.790) for lung adenocarcinoma and 0.933 (95% CI 0.906-0.960) for squamous cell carcinoma patients. Additionally, the original data from TCGA verified that ADAMTS8, DMBT1 and DOCK8 were downregulated in both lung adenocarcinoma and squamous cell carcinoma, whereas RSPO3 expression was upregulated in lung adenocarcinoma and downregulated in lung squamous cell carcinoma. For the other five genes (STMN2, SPINK6, TUSC3, LOC100128054, and C8orf22), we found that STMN2, TUSC3 and C8orf22 were upregulated in squamous cell carcinoma and that STMN2 and USC3 were upregulated in lung adenocarcinoma. Furthermore, we compared the correlation between HOXA11-AS and de-regulated genes in NSCLC based on TCGA. The results showed that the HOXA11-AS expression was negatively correlated with DOCK8 in squamous cell carcinoma (r = -0.124, P = 0.048) and lung adenocarcinoma (r = -0.176, P = 0.005). In addition, RSPO3, ADAMTS8 and DOCK8 were related to overall survival and disease-free survival (all P < 0.05) of lung adenocarcinoma patients in TCGA.
Our results showed that the gene profiles were significantly changed after HOXA11-AS knock-down in NSCLC cells. We speculated that HOXA11-AS may play an important role in NSCLC development and progression by regulating the expression of various pathways and genes, especially DOCK8 and TGF-beta pathway. However, the exact mechanism should be verified by functional experiments.</description><subject>Analysis</subject><subject>Care and treatment</subject><subject>Complications and side effects</subject><subject>Hypothesis</subject><subject>Influence</subject><subject>Lung cancer, Non-small cell</subject><subject>Patient education</subject><subject>Transforming growth factors</subject><issn>1475-2867</issn><issn>1475-2867</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>BENPR</sourceid><recordid>eNpdUU1v1DAUjBCIloUfwAVZ4sIlxXb8kVyQoggo0qqVKEjcLMd53nVJ7MVOivbf42hLVZAPfvKbN-N5UxSvCb4gpBbvE6FNxUtMRIkrIUrxpDgnTPKS1kI-fVSfFS9SusWYyFrg58UZlU2NGWfnxdSF6RBhDz65O0Da6_GYXELBonkPaAx-h3zwJgwuV1-vWnR5_aMlpGxv0A48IOdniNrMLngUYbeMeg7xiDzMv0P8mdvo6qbbdsjAOKaXxTOrxwSv7u9N8f3Tx2_dZbm9_vyla7el4Q2bSzP0khuBseY1oVI3fa_BNIPQQljaU9ZY0jcagLG64poQTbCl1nJCoZI9qzbFhxPvYeknGAz4OepRHaKbdDyqoJ36t-PdXu3CneKkqiSrMsG7e4IYfi2QZjW5tFrQHsKSFKmzVkMJXaFv_4PehiXmPa6ovGOGGyYy6uKE2ukRlPM2ZF2TzwCTM8GDdfm9ZZJyKutsa1OQ04CJIaUI9uH3BKs1fXVKX-X01Zq-WkXePLb9MPE37uoP8TarBg</recordid><startdate>20161201</startdate><enddate>20161201</enddate><creator>Zhang, Yu</creator><creator>He, Rong-Quan</creator><creator>Dang, Yi-Wu</creator><creator>Zhang, Xiu-Ling</creator><creator>Wang, Xiao</creator><creator>Huang, Su-Ning</creator><creator>Huang, Wen-Ting</creator><creator>Jiang, Meng-Tong</creator><creator>Gan, Xiao-Ning</creator><creator>Xie, You</creator><creator>Li, Ping</creator><creator>Luo, Dian-Zhong</creator><creator>Chen, Gang</creator><creator>Gan, Ting-Qing</creator><general>BioMed Central Ltd</general><general>BioMed Central</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>IAO</scope><scope>3V.</scope><scope>7TM</scope><scope>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20161201</creationdate><title>Comprehensive analysis of the long noncoding RNA HOXA11-AS gene interaction regulatory network in NSCLC cells</title><author>Zhang, Yu ; He, Rong-Quan ; Dang, Yi-Wu ; Zhang, Xiu-Ling ; Wang, Xiao ; Huang, Su-Ning ; Huang, Wen-Ting ; Jiang, Meng-Tong ; Gan, Xiao-Ning ; Xie, You ; Li, Ping ; Luo, Dian-Zhong ; Chen, Gang ; Gan, Ting-Qing</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c594t-cdb75c600a58127a9bbaec9d6a66f2b249f1b9aee44835a11a10f2ff512e37b43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Analysis</topic><topic>Care and treatment</topic><topic>Complications and side effects</topic><topic>Hypothesis</topic><topic>Influence</topic><topic>Lung cancer, Non-small cell</topic><topic>Patient education</topic><topic>Transforming growth factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Yu</creatorcontrib><creatorcontrib>He, Rong-Quan</creatorcontrib><creatorcontrib>Dang, Yi-Wu</creatorcontrib><creatorcontrib>Zhang, Xiu-Ling</creatorcontrib><creatorcontrib>Wang, Xiao</creatorcontrib><creatorcontrib>Huang, Su-Ning</creatorcontrib><creatorcontrib>Huang, Wen-Ting</creatorcontrib><creatorcontrib>Jiang, Meng-Tong</creatorcontrib><creatorcontrib>Gan, Xiao-Ning</creatorcontrib><creatorcontrib>Xie, You</creatorcontrib><creatorcontrib>Li, Ping</creatorcontrib><creatorcontrib>Luo, Dian-Zhong</creatorcontrib><creatorcontrib>Chen, Gang</creatorcontrib><creatorcontrib>Gan, Ting-Qing</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale Academic OneFile</collection><collection>ProQuest Central (Corporate)</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</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 Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</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>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cancer Cell International</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Yu</au><au>He, Rong-Quan</au><au>Dang, Yi-Wu</au><au>Zhang, Xiu-Ling</au><au>Wang, Xiao</au><au>Huang, Su-Ning</au><au>Huang, Wen-Ting</au><au>Jiang, Meng-Tong</au><au>Gan, Xiao-Ning</au><au>Xie, You</au><au>Li, Ping</au><au>Luo, Dian-Zhong</au><au>Chen, Gang</au><au>Gan, Ting-Qing</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Comprehensive analysis of the long noncoding RNA HOXA11-AS gene interaction regulatory network in NSCLC cells</atitle><jtitle>Cancer Cell International</jtitle><addtitle>Cancer Cell Int</addtitle><date>2016-12-01</date><risdate>2016</risdate><volume>16</volume><issue>1</issue><spage>89</spage><epage>89</epage><pages>89-89</pages><artnum>89</artnum><issn>1475-2867</issn><eissn>1475-2867</eissn><abstract>Long noncoding RNAs (lncRNAs) are related to different biological processes in non-small cell lung cancer (NSCLC). However, the possible molecular mechanisms underlying the effects of the long noncoding RNA HOXA11-AS (HOXA11 antisense RNA) in NSCLC are unknown.
HOXA11-AS was knocked down in the NSCLC A549 cell line and a high throughput microarray assay was applied to detect changes in the gene profiles of the A549 cells. Bioinformatics analyses (gene ontology (GO), pathway, Kyoto Encyclopedia of Genes and Genomes (KEGG), and network analyses) were performed to investigate the potential pathways and networks of the differentially expressed genes. The molecular signatures database (MSigDB) was used to display the expression profiles of these differentially expressed genes. Furthermore, the relationships between the HOXA11-AS, de-regulated genes and clinical NSCLC parameters were verified by using NSCLC patient information from The Cancer Genome Atlas (TCGA) database. In addition, the relationship between HOXA11-AS expression and clinical diagnostic value was analyzed by receiver operating characteristic (ROC) curve.
Among the differentially expressed genes, 277 and 80 genes were upregulated and downregulated in NSCLC, respectively (fold change ≥2.0, P < 0.05 and false discovery rate (FDR) < 0.05). According to the degree of the fold change, six upregulated and three downregulated genes were selected for further investigation. Only four genes (RSPO3, ADAMTS8, DMBT1, and DOCK8) were reported to be related with the development or progression of NSCLC based on a PubMed search. Among all possible pathways, three pathways (the PI3K-Akt, TGF-beta and Hippo signaling pathways) were the most likely to be involved in NSCLC development and progression. Furthermore, we found that HOXA11-AS was highly expressed in both lung adenocarcinoma and squamous cell carcinoma based on TCGA database. The ROC curve showed that the area under curve (AUC) of HOXA11-AS was 0.727 (95% CI 0.663-0.790) for lung adenocarcinoma and 0.933 (95% CI 0.906-0.960) for squamous cell carcinoma patients. Additionally, the original data from TCGA verified that ADAMTS8, DMBT1 and DOCK8 were downregulated in both lung adenocarcinoma and squamous cell carcinoma, whereas RSPO3 expression was upregulated in lung adenocarcinoma and downregulated in lung squamous cell carcinoma. For the other five genes (STMN2, SPINK6, TUSC3, LOC100128054, and C8orf22), we found that STMN2, TUSC3 and C8orf22 were upregulated in squamous cell carcinoma and that STMN2 and USC3 were upregulated in lung adenocarcinoma. Furthermore, we compared the correlation between HOXA11-AS and de-regulated genes in NSCLC based on TCGA. The results showed that the HOXA11-AS expression was negatively correlated with DOCK8 in squamous cell carcinoma (r = -0.124, P = 0.048) and lung adenocarcinoma (r = -0.176, P = 0.005). In addition, RSPO3, ADAMTS8 and DOCK8 were related to overall survival and disease-free survival (all P < 0.05) of lung adenocarcinoma patients in TCGA.
Our results showed that the gene profiles were significantly changed after HOXA11-AS knock-down in NSCLC cells. We speculated that HOXA11-AS may play an important role in NSCLC development and progression by regulating the expression of various pathways and genes, especially DOCK8 and TGF-beta pathway. However, the exact mechanism should be verified by functional experiments.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>27980454</pmid><doi>10.1186/s12935-016-0366-6</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Analysis Care and treatment Complications and side effects Hypothesis Influence Lung cancer, Non-small cell Patient education Transforming growth factors |
| title | Comprehensive analysis of the long noncoding RNA HOXA11-AS gene interaction regulatory network in NSCLC cells |
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