Upregulation of microRNA-4417 and Its Target Genes Contribute to Nickel Chloride-promoted Lung Epithelial Cell Fibrogenesis and Tumorigenesis
Nickel compounds have been classified as carcinogens and shown to be associated with induction of epithelial-mesenchymal transition (EMT) in fibrogenesis and tumorigenesis, as well as the crucial role of microRNAs (miRNAs) and their related genes in controlling EMT and cancer metastasis. Thus, the m...
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| description | Nickel compounds have been classified as carcinogens and shown to be associated with induction of epithelial-mesenchymal transition (EMT) in fibrogenesis and tumorigenesis, as well as the crucial role of microRNAs (miRNAs) and their related genes in controlling EMT and cancer metastasis. Thus, the mechanisms involved in the regulation of EMT in nickel-treated cells are of potential interest in understanding lung fibrosis and tumor progression. We investigated the miRNA-dependent mechanisms involved in nickel-induced EMT in lung epithelial cells. Nickel increased miR-4417 expression and decreased its target gene TAB2 expression. Treatment of cells with TGF-β inhibitor SB525334 significantly blocked NiCl
2
and TGF-β-induced EMT. The expression of miR-4417 was abolished by SB525334 in TGF-β-treated cells, but not in nickel-treated cells. Both overexpression of miR-4417 and silencing of TAB2 induced fibronectin expression, but did not reduce E-cadherin expression. Moreover, oral administration of nickel promoted lung tumor growth in nude mice that had received BEAS-2B transformed cells by intravenous injection. The induction of EMT by nickel is mediated through multiple pathways. Induction of abundant miR-4417 and reduction of TAB2 expression following nickel exposure and may be involved in nickel-induced fibronectin. These findings provide novel insight into the roles of nickel in fibrogenesis and tumor progression. |
| doi_str_mv | 10.1038/s41598-017-14610-7 |
| format | Article |
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2
and TGF-β-induced EMT. The expression of miR-4417 was abolished by SB525334 in TGF-β-treated cells, but not in nickel-treated cells. Both overexpression of miR-4417 and silencing of TAB2 induced fibronectin expression, but did not reduce E-cadherin expression. Moreover, oral administration of nickel promoted lung tumor growth in nude mice that had received BEAS-2B transformed cells by intravenous injection. The induction of EMT by nickel is mediated through multiple pathways. Induction of abundant miR-4417 and reduction of TAB2 expression following nickel exposure and may be involved in nickel-induced fibronectin. These findings provide novel insight into the roles of nickel in fibrogenesis and tumor progression.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/s41598-017-14610-7</identifier><identifier>PMID: 29127306</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/109 ; 13/51 ; 38/61 ; 38/90 ; 631/67/69 ; 631/80/84/2176 ; 64/60 ; 82/80 ; Cancer ; Carcinogens ; Cell Line, Transformed ; Cell Transformation, Neoplastic - chemically induced ; Cell Transformation, Neoplastic - metabolism ; Cell Transformation, Neoplastic - pathology ; E-cadherin ; Epithelial cells ; Epithelial Cells - metabolism ; Epithelial Cells - pathology ; Fibronectin ; Fibrosis ; Humanities and Social Sciences ; Humans ; Intravenous administration ; Lung - metabolism ; Lung - pathology ; Lung cancer ; Lung Neoplasms - chemically induced ; Lung Neoplasms - metabolism ; Lung Neoplasms - pathology ; Lungs ; Mesenchyme ; Metastases ; MicroRNAs - metabolism ; miRNA ; multidisciplinary ; Nickel ; Nickel - toxicity ; Nickel chloride ; Oral administration ; Pulmonary Fibrosis - chemically induced ; Pulmonary Fibrosis - metabolism ; Pulmonary Fibrosis - pathology ; Respiratory Mucosa - metabolism ; Respiratory Mucosa - pathology ; RNA, Neoplasm - metabolism ; Science ; Science (multidisciplinary) ; Transformed cells ; Tumorigenesis</subject><ispartof>Scientific reports, 2017-11, Vol.7 (1), p.15320-13, Article 15320</ispartof><rights>The Author(s) 2017</rights><rights>2017. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c474t-eade65098653423b05c4138892623fe78d400de5e3821a5b80b7f00c62c595503</citedby><cites>FETCH-LOGICAL-c474t-eade65098653423b05c4138892623fe78d400de5e3821a5b80b7f00c62c595503</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/PMC5681645/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5681645/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27901,27902,41096,42165,51551,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29127306$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wu, Chih-Hsien</creatorcontrib><creatorcontrib>Hsiao, Yi-Min</creatorcontrib><creatorcontrib>Yeh, Kun-Tu</creatorcontrib><creatorcontrib>Tsou, Tsui-Chun</creatorcontrib><creatorcontrib>Chen, Chih-Yi</creatorcontrib><creatorcontrib>Wu, Ming-Fang</creatorcontrib><creatorcontrib>Ko, Jiunn-Liang</creatorcontrib><title>Upregulation of microRNA-4417 and Its Target Genes Contribute to Nickel Chloride-promoted Lung Epithelial Cell Fibrogenesis and Tumorigenesis</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><addtitle>Sci Rep</addtitle><description>Nickel compounds have been classified as carcinogens and shown to be associated with induction of epithelial-mesenchymal transition (EMT) in fibrogenesis and tumorigenesis, as well as the crucial role of microRNAs (miRNAs) and their related genes in controlling EMT and cancer metastasis. Thus, the mechanisms involved in the regulation of EMT in nickel-treated cells are of potential interest in understanding lung fibrosis and tumor progression. We investigated the miRNA-dependent mechanisms involved in nickel-induced EMT in lung epithelial cells. Nickel increased miR-4417 expression and decreased its target gene TAB2 expression. Treatment of cells with TGF-β inhibitor SB525334 significantly blocked NiCl
2
and TGF-β-induced EMT. The expression of miR-4417 was abolished by SB525334 in TGF-β-treated cells, but not in nickel-treated cells. Both overexpression of miR-4417 and silencing of TAB2 induced fibronectin expression, but did not reduce E-cadherin expression. Moreover, oral administration of nickel promoted lung tumor growth in nude mice that had received BEAS-2B transformed cells by intravenous injection. The induction of EMT by nickel is mediated through multiple pathways. Induction of abundant miR-4417 and reduction of TAB2 expression following nickel exposure and may be involved in nickel-induced fibronectin. These findings provide novel insight into the roles of nickel in fibrogenesis and tumor progression.</description><subject>13/109</subject><subject>13/51</subject><subject>38/61</subject><subject>38/90</subject><subject>631/67/69</subject><subject>631/80/84/2176</subject><subject>64/60</subject><subject>82/80</subject><subject>Cancer</subject><subject>Carcinogens</subject><subject>Cell Line, Transformed</subject><subject>Cell Transformation, Neoplastic - chemically induced</subject><subject>Cell Transformation, Neoplastic - metabolism</subject><subject>Cell Transformation, Neoplastic - pathology</subject><subject>E-cadherin</subject><subject>Epithelial cells</subject><subject>Epithelial Cells - metabolism</subject><subject>Epithelial Cells - pathology</subject><subject>Fibronectin</subject><subject>Fibrosis</subject><subject>Humanities and Social Sciences</subject><subject>Humans</subject><subject>Intravenous administration</subject><subject>Lung - metabolism</subject><subject>Lung - pathology</subject><subject>Lung cancer</subject><subject>Lung Neoplasms - 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metabolism</topic><topic>Pulmonary Fibrosis - pathology</topic><topic>Respiratory Mucosa - metabolism</topic><topic>Respiratory Mucosa - pathology</topic><topic>RNA, Neoplasm - metabolism</topic><topic>Science</topic><topic>Science (multidisciplinary)</topic><topic>Transformed cells</topic><topic>Tumorigenesis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wu, Chih-Hsien</creatorcontrib><creatorcontrib>Hsiao, Yi-Min</creatorcontrib><creatorcontrib>Yeh, Kun-Tu</creatorcontrib><creatorcontrib>Tsou, Tsui-Chun</creatorcontrib><creatorcontrib>Chen, Chih-Yi</creatorcontrib><creatorcontrib>Wu, Ming-Fang</creatorcontrib><creatorcontrib>Ko, Jiunn-Liang</creatorcontrib><collection>Springer Nature OA Free Journals</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>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</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 One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</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>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</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 Basic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Scientific reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wu, Chih-Hsien</au><au>Hsiao, Yi-Min</au><au>Yeh, Kun-Tu</au><au>Tsou, Tsui-Chun</au><au>Chen, Chih-Yi</au><au>Wu, Ming-Fang</au><au>Ko, Jiunn-Liang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Upregulation of microRNA-4417 and Its Target Genes Contribute to Nickel Chloride-promoted Lung Epithelial Cell Fibrogenesis and Tumorigenesis</atitle><jtitle>Scientific reports</jtitle><stitle>Sci Rep</stitle><addtitle>Sci Rep</addtitle><date>2017-11-10</date><risdate>2017</risdate><volume>7</volume><issue>1</issue><spage>15320</spage><epage>13</epage><pages>15320-13</pages><artnum>15320</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>Nickel compounds have been classified as carcinogens and shown to be associated with induction of epithelial-mesenchymal transition (EMT) in fibrogenesis and tumorigenesis, as well as the crucial role of microRNAs (miRNAs) and their related genes in controlling EMT and cancer metastasis. Thus, the mechanisms involved in the regulation of EMT in nickel-treated cells are of potential interest in understanding lung fibrosis and tumor progression. We investigated the miRNA-dependent mechanisms involved in nickel-induced EMT in lung epithelial cells. Nickel increased miR-4417 expression and decreased its target gene TAB2 expression. Treatment of cells with TGF-β inhibitor SB525334 significantly blocked NiCl
2
and TGF-β-induced EMT. The expression of miR-4417 was abolished by SB525334 in TGF-β-treated cells, but not in nickel-treated cells. Both overexpression of miR-4417 and silencing of TAB2 induced fibronectin expression, but did not reduce E-cadherin expression. Moreover, oral administration of nickel promoted lung tumor growth in nude mice that had received BEAS-2B transformed cells by intravenous injection. The induction of EMT by nickel is mediated through multiple pathways. Induction of abundant miR-4417 and reduction of TAB2 expression following nickel exposure and may be involved in nickel-induced fibronectin. These findings provide novel insight into the roles of nickel in fibrogenesis and tumor progression.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>29127306</pmid><doi>10.1038/s41598-017-14610-7</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 13/109 13/51 38/61 38/90 631/67/69 631/80/84/2176 64/60 82/80 Cancer Carcinogens Cell Line, Transformed Cell Transformation, Neoplastic - chemically induced Cell Transformation, Neoplastic - metabolism Cell Transformation, Neoplastic - pathology E-cadherin Epithelial cells Epithelial Cells - metabolism Epithelial Cells - pathology Fibronectin Fibrosis Humanities and Social Sciences Humans Intravenous administration Lung - metabolism Lung - pathology Lung cancer Lung Neoplasms - chemically induced Lung Neoplasms - metabolism Lung Neoplasms - pathology Lungs Mesenchyme Metastases MicroRNAs - metabolism miRNA multidisciplinary Nickel Nickel - toxicity Nickel chloride Oral administration Pulmonary Fibrosis - chemically induced Pulmonary Fibrosis - metabolism Pulmonary Fibrosis - pathology Respiratory Mucosa - metabolism Respiratory Mucosa - pathology RNA, Neoplasm - metabolism Science Science (multidisciplinary) Transformed cells Tumorigenesis |
| title | Upregulation of microRNA-4417 and Its Target Genes Contribute to Nickel Chloride-promoted Lung Epithelial Cell Fibrogenesis and Tumorigenesis |
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