Epithelial-mesenchymal transition and cancer stem cells, mediated by a long non-coding RNA, HOTAIR, are involved in cell malignant transformation induced by cigarette smoke extract
The incidence of lung diseases, including cancer, caused by cigarette smoke is increasing, but the molecular mechanisms of gene regulation induced by cigarette smoke remain unclear. This report describes a long noncoding RNA (lncRNA) that is induced by cigarette smoke extract (CSE) and experiments u...
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| creator | Liu, Yi Luo, Fei Xu, Yuan Wang, Bairu Zhao, Yue Xu, Wenchao Shi, Le Lu, Xiaolin Liu, Qizhan |
| description | The incidence of lung diseases, including cancer, caused by cigarette smoke is increasing, but the molecular mechanisms of gene regulation induced by cigarette smoke remain unclear. This report describes a long noncoding RNA (lncRNA) that is induced by cigarette smoke extract (CSE) and experiments utilizing lncRNAs to integrate inflammation with the epithelial-mesenchymal transition (EMT) in human bronchial epithelial (HBE) cells. The present study shows that, induced by CSE, IL-6, a pro-inflammatory cytokine, leads to activation of STAT3, a transcription activator. A ChIP assay determined that the interaction of STAT3 with the promoter regions of HOX transcript antisense RNA (HOTAIR) increased levels of HOTAIR. Blocking of IL-6 with anti-IL-6 antibody, decreasing STAT3, and inhibiting STAT3 activation reduced HOTAIR expression. Moreover, for HBE cells cultured in the presence of HOTAIR siRNA for 24h, the CSE-induced EMT, formation of cancer stem cells (CSCs), and malignant transformation were reversed. Thus, IL-6, acting on STAT3 signaling, which up-regulates HOTAIR in an autocrine manner, contributes to the EMT and to CSCs induced by CSE. These data define a link between inflammation and EMT, processes involved in the malignant transformation of cells caused by CSE. This link, mediated through lncRNAs, establishes a mechanism for CSE-induced lung carcinogenesis.
•STAT3 directly regulates the levels of LncRNA HOTAIR.•LncRNA HOTAIR mediates the link between inflammation and EMT.•LncRNA HOTAIR is involved in the malignant transformation of cells caused by CSE. |
| doi_str_mv | 10.1016/j.taap.2014.10.022 |
| format | Article |
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•STAT3 directly regulates the levels of LncRNA HOTAIR.•LncRNA HOTAIR mediates the link between inflammation and EMT.•LncRNA HOTAIR is involved in the malignant transformation of cells caused by CSE.</description><identifier>ISSN: 0041-008X</identifier><identifier>EISSN: 1096-0333</identifier><identifier>DOI: 10.1016/j.taap.2014.10.022</identifier><identifier>PMID: 25447409</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>60 APPLIED LIFE SCIENCES ; Animals ; ANTIBODIES ; Autocrine Communication - drug effects ; Cancer stem cells (CSCs) ; CARCINOGENESIS ; CELL CULTURES ; Cell Line, Transformed ; Cell Transformation, Neoplastic - genetics ; Cell Transformation, Neoplastic - metabolism ; Cell Transformation, Neoplastic - pathology ; Cigarette smoke extract (CSE) ; Dose-Response Relationship, Drug ; Epithelial Cells - drug effects ; Epithelial Cells - metabolism ; Epithelial Cells - pathology ; Epithelial-mesenchymal transition (EMT) ; Epithelial-Mesenchymal Transition - drug effects ; Female ; Gene Expression Regulation, Neoplastic ; GENE REGULATION ; Humans ; INFLAMMATION ; Interleukin-6 - metabolism ; lncRNAs ; Lung - drug effects ; Lung - metabolism ; Lung - pathology ; Lung Neoplasms - etiology ; Lung Neoplasms - genetics ; Lung Neoplasms - metabolism ; Lung Neoplasms - pathology ; LUNGS ; Mice ; Mice, Nude ; NEOPLASMS ; Neoplastic Stem Cells - drug effects ; Neoplastic Stem Cells - metabolism ; Neoplastic Stem Cells - pathology ; RNA ; RNA Interference ; RNA, Long Noncoding - genetics ; RNA, Long Noncoding - metabolism ; Signal Transduction - drug effects ; Smoke - adverse effects ; Smoking - adverse effects ; STAT3 Transcription Factor - metabolism ; STEM CELLS ; Time Factors ; TOBACCO SMOKES ; Transfection ; Up-Regulation</subject><ispartof>Toxicology and applied pharmacology, 2015-01, Vol.282 (1), p.9-19</ispartof><rights>2014 Elsevier Inc.</rights><rights>Copyright © 2014 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c417t-5994d5c2410fbc93674d33fc5f79fc0f49ce88019c941d5e7f407f990138b1e33</citedby><cites>FETCH-LOGICAL-c417t-5994d5c2410fbc93674d33fc5f79fc0f49ce88019c941d5e7f407f990138b1e33</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.taap.2014.10.022$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,780,784,885,3548,27923,27924,45994</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25447409$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://www.osti.gov/biblio/22439937$$D View this record in Osti.gov$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, Yi</creatorcontrib><creatorcontrib>Luo, Fei</creatorcontrib><creatorcontrib>Xu, Yuan</creatorcontrib><creatorcontrib>Wang, Bairu</creatorcontrib><creatorcontrib>Zhao, Yue</creatorcontrib><creatorcontrib>Xu, Wenchao</creatorcontrib><creatorcontrib>Shi, Le</creatorcontrib><creatorcontrib>Lu, Xiaolin</creatorcontrib><creatorcontrib>Liu, Qizhan</creatorcontrib><title>Epithelial-mesenchymal transition and cancer stem cells, mediated by a long non-coding RNA, HOTAIR, are involved in cell malignant transformation induced by cigarette smoke extract</title><title>Toxicology and applied pharmacology</title><addtitle>Toxicol Appl Pharmacol</addtitle><description>The incidence of lung diseases, including cancer, caused by cigarette smoke is increasing, but the molecular mechanisms of gene regulation induced by cigarette smoke remain unclear. This report describes a long noncoding RNA (lncRNA) that is induced by cigarette smoke extract (CSE) and experiments utilizing lncRNAs to integrate inflammation with the epithelial-mesenchymal transition (EMT) in human bronchial epithelial (HBE) cells. The present study shows that, induced by CSE, IL-6, a pro-inflammatory cytokine, leads to activation of STAT3, a transcription activator. A ChIP assay determined that the interaction of STAT3 with the promoter regions of HOX transcript antisense RNA (HOTAIR) increased levels of HOTAIR. Blocking of IL-6 with anti-IL-6 antibody, decreasing STAT3, and inhibiting STAT3 activation reduced HOTAIR expression. Moreover, for HBE cells cultured in the presence of HOTAIR siRNA for 24h, the CSE-induced EMT, formation of cancer stem cells (CSCs), and malignant transformation were reversed. Thus, IL-6, acting on STAT3 signaling, which up-regulates HOTAIR in an autocrine manner, contributes to the EMT and to CSCs induced by CSE. These data define a link between inflammation and EMT, processes involved in the malignant transformation of cells caused by CSE. This link, mediated through lncRNAs, establishes a mechanism for CSE-induced lung carcinogenesis.
•STAT3 directly regulates the levels of LncRNA HOTAIR.•LncRNA HOTAIR mediates the link between inflammation and EMT.•LncRNA HOTAIR is involved in the malignant transformation of cells caused by CSE.</description><subject>60 APPLIED LIFE SCIENCES</subject><subject>Animals</subject><subject>ANTIBODIES</subject><subject>Autocrine Communication - drug effects</subject><subject>Cancer stem cells (CSCs)</subject><subject>CARCINOGENESIS</subject><subject>CELL CULTURES</subject><subject>Cell Line, Transformed</subject><subject>Cell Transformation, Neoplastic - genetics</subject><subject>Cell Transformation, Neoplastic - metabolism</subject><subject>Cell Transformation, Neoplastic - pathology</subject><subject>Cigarette smoke extract (CSE)</subject><subject>Dose-Response Relationship, Drug</subject><subject>Epithelial Cells - drug effects</subject><subject>Epithelial Cells - metabolism</subject><subject>Epithelial Cells - pathology</subject><subject>Epithelial-mesenchymal transition (EMT)</subject><subject>Epithelial-Mesenchymal Transition - drug effects</subject><subject>Female</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>GENE REGULATION</subject><subject>Humans</subject><subject>INFLAMMATION</subject><subject>Interleukin-6 - metabolism</subject><subject>lncRNAs</subject><subject>Lung - drug effects</subject><subject>Lung - metabolism</subject><subject>Lung - pathology</subject><subject>Lung Neoplasms - etiology</subject><subject>Lung Neoplasms - genetics</subject><subject>Lung Neoplasms - metabolism</subject><subject>Lung Neoplasms - pathology</subject><subject>LUNGS</subject><subject>Mice</subject><subject>Mice, Nude</subject><subject>NEOPLASMS</subject><subject>Neoplastic Stem Cells - drug effects</subject><subject>Neoplastic Stem Cells - metabolism</subject><subject>Neoplastic Stem Cells - pathology</subject><subject>RNA</subject><subject>RNA Interference</subject><subject>RNA, Long Noncoding - genetics</subject><subject>RNA, Long Noncoding - metabolism</subject><subject>Signal Transduction - drug effects</subject><subject>Smoke - adverse effects</subject><subject>Smoking - adverse effects</subject><subject>STAT3 Transcription Factor - metabolism</subject><subject>STEM CELLS</subject><subject>Time Factors</subject><subject>TOBACCO SMOKES</subject><subject>Transfection</subject><subject>Up-Regulation</subject><issn>0041-008X</issn><issn>1096-0333</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kcFuEzEQhi0EomnhBTggS1w4ZMN47d2NJS5RVWilikpVkbitHO84cdi1g-1E5L14wHq7hSMnW9Y3_4znI-QdgwUDVn_aLZJS-0UJTOSHBZTlCzJjIOsCOOcvyQxAsAJg-eOMnMe4AwApBHtNzspKiEaAnJE_V3ubtthb1RcDRnR6expUT1NQLtpkvaPKdVQrpzHQmHCgGvs-zumAnVUJO7o-UUV77zbUeVdo39l8vf-2mtPru4fVzf2cqoDUuqPvjxm37imB5i5245RLUy_jw6Ce-lnXHfSUq-0m16aENA7-J1L8nVmd3pBXRvUR3z6fF-T7l6uHy-vi9u7rzeXqttCCNamopBRdpUvBwKy15HUjOs6NrkwjjQYjpMblEpjUUrCuwsYIaIyUwPhyzZDzC_JhyvUx2TZqm1BvtXcOdWrLUnApeZOpjxO1D_7XAWNqBxvHLyqH_hBbVleiXtYlrzJaTqgOPsaApt0HO6hwahm0o9N2145O29Hp-Jad5qL3z_mHdV76v5K_EjPweQIw7-JoMYyjZpNZUBgn7bz9X_4joQe0cQ</recordid><startdate>20150101</startdate><enddate>20150101</enddate><creator>Liu, Yi</creator><creator>Luo, Fei</creator><creator>Xu, Yuan</creator><creator>Wang, Bairu</creator><creator>Zhao, Yue</creator><creator>Xu, Wenchao</creator><creator>Shi, Le</creator><creator>Lu, Xiaolin</creator><creator>Liu, Qizhan</creator><general>Elsevier Inc</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>7TM</scope><scope>7U7</scope><scope>C1K</scope><scope>OTOTI</scope></search><sort><creationdate>20150101</creationdate><title>Epithelial-mesenchymal transition and cancer stem cells, mediated by a long non-coding RNA, HOTAIR, are involved in cell malignant transformation induced by cigarette smoke extract</title><author>Liu, Yi ; Luo, Fei ; Xu, Yuan ; Wang, Bairu ; Zhao, Yue ; Xu, Wenchao ; Shi, Le ; Lu, Xiaolin ; Liu, Qizhan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c417t-5994d5c2410fbc93674d33fc5f79fc0f49ce88019c941d5e7f407f990138b1e33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>60 APPLIED LIFE SCIENCES</topic><topic>Animals</topic><topic>ANTIBODIES</topic><topic>Autocrine Communication - drug effects</topic><topic>Cancer stem cells (CSCs)</topic><topic>CARCINOGENESIS</topic><topic>CELL CULTURES</topic><topic>Cell Line, Transformed</topic><topic>Cell Transformation, Neoplastic - genetics</topic><topic>Cell Transformation, Neoplastic - metabolism</topic><topic>Cell Transformation, Neoplastic - pathology</topic><topic>Cigarette smoke extract (CSE)</topic><topic>Dose-Response Relationship, Drug</topic><topic>Epithelial Cells - drug effects</topic><topic>Epithelial Cells - metabolism</topic><topic>Epithelial Cells - pathology</topic><topic>Epithelial-mesenchymal transition (EMT)</topic><topic>Epithelial-Mesenchymal Transition - drug effects</topic><topic>Female</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>GENE REGULATION</topic><topic>Humans</topic><topic>INFLAMMATION</topic><topic>Interleukin-6 - metabolism</topic><topic>lncRNAs</topic><topic>Lung - drug effects</topic><topic>Lung - metabolism</topic><topic>Lung - pathology</topic><topic>Lung Neoplasms - etiology</topic><topic>Lung Neoplasms - genetics</topic><topic>Lung Neoplasms - metabolism</topic><topic>Lung Neoplasms - pathology</topic><topic>LUNGS</topic><topic>Mice</topic><topic>Mice, Nude</topic><topic>NEOPLASMS</topic><topic>Neoplastic Stem Cells - drug effects</topic><topic>Neoplastic Stem Cells - metabolism</topic><topic>Neoplastic Stem Cells - pathology</topic><topic>RNA</topic><topic>RNA Interference</topic><topic>RNA, Long Noncoding - genetics</topic><topic>RNA, Long Noncoding - metabolism</topic><topic>Signal Transduction - drug effects</topic><topic>Smoke - adverse effects</topic><topic>Smoking - adverse effects</topic><topic>STAT3 Transcription Factor - metabolism</topic><topic>STEM CELLS</topic><topic>Time Factors</topic><topic>TOBACCO SMOKES</topic><topic>Transfection</topic><topic>Up-Regulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, Yi</creatorcontrib><creatorcontrib>Luo, Fei</creatorcontrib><creatorcontrib>Xu, Yuan</creatorcontrib><creatorcontrib>Wang, Bairu</creatorcontrib><creatorcontrib>Zhao, Yue</creatorcontrib><creatorcontrib>Xu, Wenchao</creatorcontrib><creatorcontrib>Shi, Le</creatorcontrib><creatorcontrib>Lu, Xiaolin</creatorcontrib><creatorcontrib>Liu, Qizhan</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Nucleic Acids Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>OSTI.GOV</collection><jtitle>Toxicology and applied pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, Yi</au><au>Luo, Fei</au><au>Xu, Yuan</au><au>Wang, Bairu</au><au>Zhao, Yue</au><au>Xu, Wenchao</au><au>Shi, Le</au><au>Lu, Xiaolin</au><au>Liu, Qizhan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Epithelial-mesenchymal transition and cancer stem cells, mediated by a long non-coding RNA, HOTAIR, are involved in cell malignant transformation induced by cigarette smoke extract</atitle><jtitle>Toxicology and applied pharmacology</jtitle><addtitle>Toxicol Appl Pharmacol</addtitle><date>2015-01-01</date><risdate>2015</risdate><volume>282</volume><issue>1</issue><spage>9</spage><epage>19</epage><pages>9-19</pages><issn>0041-008X</issn><eissn>1096-0333</eissn><abstract>The incidence of lung diseases, including cancer, caused by cigarette smoke is increasing, but the molecular mechanisms of gene regulation induced by cigarette smoke remain unclear. This report describes a long noncoding RNA (lncRNA) that is induced by cigarette smoke extract (CSE) and experiments utilizing lncRNAs to integrate inflammation with the epithelial-mesenchymal transition (EMT) in human bronchial epithelial (HBE) cells. The present study shows that, induced by CSE, IL-6, a pro-inflammatory cytokine, leads to activation of STAT3, a transcription activator. A ChIP assay determined that the interaction of STAT3 with the promoter regions of HOX transcript antisense RNA (HOTAIR) increased levels of HOTAIR. Blocking of IL-6 with anti-IL-6 antibody, decreasing STAT3, and inhibiting STAT3 activation reduced HOTAIR expression. Moreover, for HBE cells cultured in the presence of HOTAIR siRNA for 24h, the CSE-induced EMT, formation of cancer stem cells (CSCs), and malignant transformation were reversed. Thus, IL-6, acting on STAT3 signaling, which up-regulates HOTAIR in an autocrine manner, contributes to the EMT and to CSCs induced by CSE. These data define a link between inflammation and EMT, processes involved in the malignant transformation of cells caused by CSE. This link, mediated through lncRNAs, establishes a mechanism for CSE-induced lung carcinogenesis.
•STAT3 directly regulates the levels of LncRNA HOTAIR.•LncRNA HOTAIR mediates the link between inflammation and EMT.•LncRNA HOTAIR is involved in the malignant transformation of cells caused by CSE.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>25447409</pmid><doi>10.1016/j.taap.2014.10.022</doi><tpages>11</tpages></addata></record> |
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| ispartof | Toxicology and applied pharmacology, 2015-01, Vol.282 (1), p.9-19 |
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| language | eng |
| recordid | cdi_osti_scitechconnect_22439937 |
| source | MEDLINE; ScienceDirect Journals (5 years ago - present) |
| subjects | 60 APPLIED LIFE SCIENCES Animals ANTIBODIES Autocrine Communication - drug effects Cancer stem cells (CSCs) CARCINOGENESIS CELL CULTURES Cell Line, Transformed Cell Transformation, Neoplastic - genetics Cell Transformation, Neoplastic - metabolism Cell Transformation, Neoplastic - pathology Cigarette smoke extract (CSE) Dose-Response Relationship, Drug Epithelial Cells - drug effects Epithelial Cells - metabolism Epithelial Cells - pathology Epithelial-mesenchymal transition (EMT) Epithelial-Mesenchymal Transition - drug effects Female Gene Expression Regulation, Neoplastic GENE REGULATION Humans INFLAMMATION Interleukin-6 - metabolism lncRNAs Lung - drug effects Lung - metabolism Lung - pathology Lung Neoplasms - etiology Lung Neoplasms - genetics Lung Neoplasms - metabolism Lung Neoplasms - pathology LUNGS Mice Mice, Nude NEOPLASMS Neoplastic Stem Cells - drug effects Neoplastic Stem Cells - metabolism Neoplastic Stem Cells - pathology RNA RNA Interference RNA, Long Noncoding - genetics RNA, Long Noncoding - metabolism Signal Transduction - drug effects Smoke - adverse effects Smoking - adverse effects STAT3 Transcription Factor - metabolism STEM CELLS Time Factors TOBACCO SMOKES Transfection Up-Regulation |
| title | Epithelial-mesenchymal transition and cancer stem cells, mediated by a long non-coding RNA, HOTAIR, are involved in cell malignant transformation induced by cigarette smoke extract |
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