LncRNA TUG1 contributes to the tumorigenesis of lung adenocarcinoma by regulating miR-138-5p-HIF1A axis
Introduction: Increasing evidence indicates that lncRNA TUG1 represents an oncogenic factor in cancer. But, the mechanisms by which lncRNA TUG1 contributes to lung adenocarcinoma (LAC) remain undocumented. Methods: The relationship between lncRNA TUG1/miR-138-5p expression and clinical outcomes in p...
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| Veröffentlicht in: | International journal of immunopathology and pharmacology 2021, Vol.35, p.20587384211048265, Article 20587384211048265 |
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| creator | Li, Ke Niu, Huatao Wang, Ying Li, Ruilei Zhao, Yuan Liu, Chao Cao, Honghua Chen, Haitao Xie, Ran Zhuang, Li |
| description | Introduction: Increasing evidence indicates that lncRNA TUG1 represents an oncogenic factor in cancer. But, the mechanisms by which lncRNA TUG1 contributes to lung adenocarcinoma (LAC) remain undocumented. Methods: The relationship between lncRNA TUG1/miR-138-5p expression and clinical outcomes in patients with LAC was indicated by qPCR, FISH, and TCGA cohort. Gain- or loss-of-function experiments and in vivo tumorigenesis were used to assess the role of lncRNA TUG1 in LAC. The interplay between TUG1 and miR-138-5p was validated by luciferase gene report and RIP assays. qPCR and Western blot analyses were used to investigate the effects of TUG1 on miR-138-5p/HIF1A axis in LAC cells. Results: We found that upregulation of TUG1 or downregulation of miR-138-5p was associated with lymph node or distant metastasis and indicated a poor survival in LAC. Reduced expression of TUG1 restrained the growth of LAC cells, while restored expression of TUG1 had the opposite effects. TUG1 was identified to negatively regulate miR-138-5p expression, and miR-138-5p reversed TUG1-induced cell proliferation by targeting HIF1A. Elevated expression of HIF1A predicted a poor survival in LAC. Conclusion: Our findings demonstrate that lncRNA TUG1 promotes the growth of LAC by regulating miR-138-5p-HIF1A axis. |
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But, the mechanisms by which lncRNA TUG1 contributes to lung adenocarcinoma (LAC) remain undocumented. Methods: The relationship between lncRNA TUG1/miR-138-5p expression and clinical outcomes in patients with LAC was indicated by qPCR, FISH, and TCGA cohort. Gain- or loss-of-function experiments and in vivo tumorigenesis were used to assess the role of lncRNA TUG1 in LAC. The interplay between TUG1 and miR-138-5p was validated by luciferase gene report and RIP assays. qPCR and Western blot analyses were used to investigate the effects of TUG1 on miR-138-5p/HIF1A axis in LAC cells. Results: We found that upregulation of TUG1 or downregulation of miR-138-5p was associated with lymph node or distant metastasis and indicated a poor survival in LAC. Reduced expression of TUG1 restrained the growth of LAC cells, while restored expression of TUG1 had the opposite effects. TUG1 was identified to negatively regulate miR-138-5p expression, and miR-138-5p reversed TUG1-induced cell proliferation by targeting HIF1A. Elevated expression of HIF1A predicted a poor survival in LAC. Conclusion: Our findings demonstrate that lncRNA TUG1 promotes the growth of LAC by regulating miR-138-5p-HIF1A axis.</description><identifier>ISSN: 2058-7384</identifier><identifier>ISSN: 0394-6320</identifier><identifier>EISSN: 2058-7384</identifier><identifier>DOI: 10.1177/20587384211048265</identifier><identifier>PMID: 34608813</identifier><language>eng</language><publisher>London, England: SAGE Publications</publisher><subject>Adenocarcinoma ; Adenocarcinoma of Lung - genetics ; Adenocarcinoma of Lung - mortality ; Adenocarcinoma of Lung - pathology ; Animals ; Cancer ; Carcinogenesis ; Cell Line, Tumor ; Cell proliferation ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit - genetics ; Immunology ; Kaplan-Meier Estimate ; Life Sciences & Biomedicine ; Lung cancer ; Lung Neoplasms - genetics ; Lung Neoplasms - mortality ; Lung Neoplasms - pathology ; Lymph nodes ; Lymphatic Metastasis - genetics ; Metastases ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; MicroRNAs ; Non-coding RNA ; Original ; Pathology ; Pharmacology & Pharmacy ; RNA, Long Noncoding ; Science & Technology ; Tumorigenesis</subject><ispartof>International journal of immunopathology and pharmacology, 2021, Vol.35, p.20587384211048265, Article 20587384211048265</ispartof><rights>The Author(s) 2021</rights><rights>The Author(s) 2021. This work is licensed under the Creative Commons Attribution – Non-Commercial License https://creativecommons.org/licenses/by-nc/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>The Author(s) 2021 2021 SAGE Publications Ltd unless otherwise noted. Manuscript content on this site is licensed under Creative Commons Licenses</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>true</woscitedreferencessubscribed><woscitedreferencescount>5</woscitedreferencescount><woscitedreferencesoriginalsourcerecordid>wos000705916400001</woscitedreferencesoriginalsourcerecordid><citedby>FETCH-LOGICAL-c466t-e66376a819454a95d2b3b3183f5bc46e56c9dab182795a794711b3d8509a612d3</citedby><cites>FETCH-LOGICAL-c466t-e66376a819454a95d2b3b3183f5bc46e56c9dab182795a794711b3d8509a612d3</cites><orcidid>0000-0002-2487-463X</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/PMC8495526/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8495526/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,728,781,785,886,4025,21971,27858,27928,27929,27930,39263,44950,45338,53796,53798</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34608813$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Ke</creatorcontrib><creatorcontrib>Niu, Huatao</creatorcontrib><creatorcontrib>Wang, Ying</creatorcontrib><creatorcontrib>Li, Ruilei</creatorcontrib><creatorcontrib>Zhao, Yuan</creatorcontrib><creatorcontrib>Liu, Chao</creatorcontrib><creatorcontrib>Cao, Honghua</creatorcontrib><creatorcontrib>Chen, Haitao</creatorcontrib><creatorcontrib>Xie, Ran</creatorcontrib><creatorcontrib>Zhuang, Li</creatorcontrib><title>LncRNA TUG1 contributes to the tumorigenesis of lung adenocarcinoma by regulating miR-138-5p-HIF1A axis</title><title>International journal of immunopathology and pharmacology</title><addtitle>INT J IMMUNOPATH PH</addtitle><addtitle>Int J Immunopathol Pharmacol</addtitle><description>Introduction: Increasing evidence indicates that lncRNA TUG1 represents an oncogenic factor in cancer. But, the mechanisms by which lncRNA TUG1 contributes to lung adenocarcinoma (LAC) remain undocumented. Methods: The relationship between lncRNA TUG1/miR-138-5p expression and clinical outcomes in patients with LAC was indicated by qPCR, FISH, and TCGA cohort. Gain- or loss-of-function experiments and in vivo tumorigenesis were used to assess the role of lncRNA TUG1 in LAC. The interplay between TUG1 and miR-138-5p was validated by luciferase gene report and RIP assays. qPCR and Western blot analyses were used to investigate the effects of TUG1 on miR-138-5p/HIF1A axis in LAC cells. Results: We found that upregulation of TUG1 or downregulation of miR-138-5p was associated with lymph node or distant metastasis and indicated a poor survival in LAC. Reduced expression of TUG1 restrained the growth of LAC cells, while restored expression of TUG1 had the opposite effects. TUG1 was identified to negatively regulate miR-138-5p expression, and miR-138-5p reversed TUG1-induced cell proliferation by targeting HIF1A. Elevated expression of HIF1A predicted a poor survival in LAC. Conclusion: Our findings demonstrate that lncRNA TUG1 promotes the growth of LAC by regulating miR-138-5p-HIF1A axis.</description><subject>Adenocarcinoma</subject><subject>Adenocarcinoma of Lung - genetics</subject><subject>Adenocarcinoma of Lung - mortality</subject><subject>Adenocarcinoma of Lung - pathology</subject><subject>Animals</subject><subject>Cancer</subject><subject>Carcinogenesis</subject><subject>Cell Line, Tumor</subject><subject>Cell proliferation</subject><subject>Humans</subject><subject>Hypoxia-Inducible Factor 1, alpha Subunit - genetics</subject><subject>Immunology</subject><subject>Kaplan-Meier Estimate</subject><subject>Life Sciences & Biomedicine</subject><subject>Lung cancer</subject><subject>Lung Neoplasms - genetics</subject><subject>Lung Neoplasms - mortality</subject><subject>Lung Neoplasms - pathology</subject><subject>Lymph nodes</subject><subject>Lymphatic Metastasis - genetics</subject><subject>Metastases</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Nude</subject><subject>MicroRNAs</subject><subject>Non-coding RNA</subject><subject>Original</subject><subject>Pathology</subject><subject>Pharmacology & Pharmacy</subject><subject>RNA, Long Noncoding</subject><subject>Science & Technology</subject><subject>Tumorigenesis</subject><issn>2058-7384</issn><issn>0394-6320</issn><issn>2058-7384</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>AFRWT</sourceid><sourceid>HGBXW</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><recordid>eNqNkVtr3DAQhUVpaUKaH5CXIuhjcarRzfJLYVlyg6WFkDwbWZYdhbW0leSk-ffVsuk2pRTyJDHznZkzHIROgJwC1PUXSoSqmeIUgHBFpXiDDre1alt8--J_gI5TuieEAGFcKHiPDhiXRClgh2hceXP9bYFvbi8Am-BzdN2cbcI54HxncZ6nEN1ovU0u4TDg9exHrHvrg9HROB8mjbsnHO04r3V2pTm56wqYqsSmurw6hwXWP136gN4Nep3s8fN7hG7Pz26Wl9Xq-8XVcrGqDJcyV1ZKVkutoOGC60b0tGMdA8UG0RXCCmmaXnegaN0IXTe8BuhYrwRptATasyP0dTd3M3eT7Y0tF-l1u4lu0vGpDdq1f3e8u2vH8NAq3ghBZRnw6XlADD9mm3J7H-boi-eWSmBUSUVUoWBHmRhSinbYbwDSbuNp_4mnaD6-tLZX_A6jAJ93wKPtwpCMs97YPVYCrIloQHKyzbLQ6vX00uUSTvDLMPtcpKc7adKj_XPf_63_AhODtpA</recordid><startdate>2021</startdate><enddate>2021</enddate><creator>Li, Ke</creator><creator>Niu, Huatao</creator><creator>Wang, Ying</creator><creator>Li, Ruilei</creator><creator>Zhao, Yuan</creator><creator>Liu, Chao</creator><creator>Cao, Honghua</creator><creator>Chen, Haitao</creator><creator>Xie, Ran</creator><creator>Zhuang, Li</creator><general>SAGE Publications</general><general>Sage</general><general>Sage Publications Ltd</general><scope>AFRWT</scope><scope>BLEPL</scope><scope>DTL</scope><scope>HGBXW</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>3V.</scope><scope>7T5</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>5PM</scope><orcidid>https://orcid.org/0000-0002-2487-463X</orcidid></search><sort><creationdate>2021</creationdate><title>LncRNA TUG1 contributes to the tumorigenesis of lung adenocarcinoma by regulating miR-138-5p-HIF1A axis</title><author>Li, Ke ; Niu, Huatao ; Wang, Ying ; Li, Ruilei ; Zhao, Yuan ; Liu, Chao ; Cao, Honghua ; Chen, Haitao ; Xie, Ran ; Zhuang, Li</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c466t-e66376a819454a95d2b3b3183f5bc46e56c9dab182795a794711b3d8509a612d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Adenocarcinoma</topic><topic>Adenocarcinoma of Lung - genetics</topic><topic>Adenocarcinoma of Lung - mortality</topic><topic>Adenocarcinoma of Lung - pathology</topic><topic>Animals</topic><topic>Cancer</topic><topic>Carcinogenesis</topic><topic>Cell Line, Tumor</topic><topic>Cell proliferation</topic><topic>Humans</topic><topic>Hypoxia-Inducible Factor 1, alpha Subunit - genetics</topic><topic>Immunology</topic><topic>Kaplan-Meier Estimate</topic><topic>Life Sciences & Biomedicine</topic><topic>Lung cancer</topic><topic>Lung Neoplasms - genetics</topic><topic>Lung Neoplasms - mortality</topic><topic>Lung Neoplasms - pathology</topic><topic>Lymph nodes</topic><topic>Lymphatic Metastasis - genetics</topic><topic>Metastases</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Nude</topic><topic>MicroRNAs</topic><topic>Non-coding RNA</topic><topic>Original</topic><topic>Pathology</topic><topic>Pharmacology & Pharmacy</topic><topic>RNA, Long Noncoding</topic><topic>Science & Technology</topic><topic>Tumorigenesis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Ke</creatorcontrib><creatorcontrib>Niu, Huatao</creatorcontrib><creatorcontrib>Wang, Ying</creatorcontrib><creatorcontrib>Li, Ruilei</creatorcontrib><creatorcontrib>Zhao, Yuan</creatorcontrib><creatorcontrib>Liu, Chao</creatorcontrib><creatorcontrib>Cao, Honghua</creatorcontrib><creatorcontrib>Chen, Haitao</creatorcontrib><creatorcontrib>Xie, Ran</creatorcontrib><creatorcontrib>Zhuang, Li</creatorcontrib><collection>Sage Journals GOLD Open Access 2024</collection><collection>Web of Science Core Collection</collection><collection>Science Citation Index Expanded</collection><collection>Web of Science - Science Citation Index Expanded - 2021</collection><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>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>Access via ProQuest (Open Access)</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>PubMed Central (Full Participant titles)</collection><jtitle>International journal of immunopathology and pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Ke</au><au>Niu, Huatao</au><au>Wang, Ying</au><au>Li, Ruilei</au><au>Zhao, Yuan</au><au>Liu, Chao</au><au>Cao, Honghua</au><au>Chen, Haitao</au><au>Xie, Ran</au><au>Zhuang, Li</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>LncRNA TUG1 contributes to the tumorigenesis of lung adenocarcinoma by regulating miR-138-5p-HIF1A axis</atitle><jtitle>International journal of immunopathology and pharmacology</jtitle><stitle>INT J IMMUNOPATH PH</stitle><addtitle>Int J Immunopathol Pharmacol</addtitle><date>2021</date><risdate>2021</risdate><volume>35</volume><spage>20587384211048265</spage><pages>20587384211048265-</pages><artnum>20587384211048265</artnum><issn>2058-7384</issn><issn>0394-6320</issn><eissn>2058-7384</eissn><abstract>Introduction: Increasing evidence indicates that lncRNA TUG1 represents an oncogenic factor in cancer. But, the mechanisms by which lncRNA TUG1 contributes to lung adenocarcinoma (LAC) remain undocumented. Methods: The relationship between lncRNA TUG1/miR-138-5p expression and clinical outcomes in patients with LAC was indicated by qPCR, FISH, and TCGA cohort. Gain- or loss-of-function experiments and in vivo tumorigenesis were used to assess the role of lncRNA TUG1 in LAC. The interplay between TUG1 and miR-138-5p was validated by luciferase gene report and RIP assays. qPCR and Western blot analyses were used to investigate the effects of TUG1 on miR-138-5p/HIF1A axis in LAC cells. Results: We found that upregulation of TUG1 or downregulation of miR-138-5p was associated with lymph node or distant metastasis and indicated a poor survival in LAC. Reduced expression of TUG1 restrained the growth of LAC cells, while restored expression of TUG1 had the opposite effects. TUG1 was identified to negatively regulate miR-138-5p expression, and miR-138-5p reversed TUG1-induced cell proliferation by targeting HIF1A. Elevated expression of HIF1A predicted a poor survival in LAC. Conclusion: Our findings demonstrate that lncRNA TUG1 promotes the growth of LAC by regulating miR-138-5p-HIF1A axis.</abstract><cop>London, England</cop><pub>SAGE Publications</pub><pmid>34608813</pmid><doi>10.1177/20587384211048265</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0002-2487-463X</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Adenocarcinoma Adenocarcinoma of Lung - genetics Adenocarcinoma of Lung - mortality Adenocarcinoma of Lung - pathology Animals Cancer Carcinogenesis Cell Line, Tumor Cell proliferation Humans Hypoxia-Inducible Factor 1, alpha Subunit - genetics Immunology Kaplan-Meier Estimate Life Sciences & Biomedicine Lung cancer Lung Neoplasms - genetics Lung Neoplasms - mortality Lung Neoplasms - pathology Lymph nodes Lymphatic Metastasis - genetics Metastases Mice Mice, Inbred BALB C Mice, Nude MicroRNAs Non-coding RNA Original Pathology Pharmacology & Pharmacy RNA, Long Noncoding Science & Technology Tumorigenesis |
| title | LncRNA TUG1 contributes to the tumorigenesis of lung adenocarcinoma by regulating miR-138-5p-HIF1A axis |
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