High mobility group box 1-induced epithelial mesenchymal transition in human airway epithelial cells
Epithelial–mesenchymal transition (EMT) is implicated in bronchial remodeling and loss of lung function in chronic inflammatory airway diseases. Previous studies showed the involvement of the high mobility group box 1 (HMGB1) protein in the pathology of chronic pulmonary inflammatory diseases. Howev...
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| Veröffentlicht in: | Scientific reports 2016-01, Vol.6 (1), p.18815-18815, Article 18815 |
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| creator | Chen, Yu-Ching Statt, Sarah Wu, Reen Chang, Hao-Teng Liao, Jiunn-Wang Wang, Chien-Neng Shyu, Woei-Cherng Lee, Chen-Chen |
| description | Epithelial–mesenchymal transition (EMT) is implicated in bronchial remodeling and loss of lung function in chronic inflammatory airway diseases. Previous studies showed the involvement of the high mobility group box 1 (HMGB1) protein in the pathology of chronic pulmonary inflammatory diseases. However, the role of HMGB1 in EMT of human airway epithelial cells is still unclear. In this study, we used RNA sequencing to show that HMGB1 treatment regulated EMT-related gene expression in human primary-airway epithelial cells. The top five upregulated genes were
SNAI2
,
FGFBP1
,
VIM
,
SPARC (
osteonectin) and
SERPINE1
, while the downregulated genes included
OCLN
,
TJP1
(
ZO-1
),
FZD7
,
CDH1
(E-cadherin) and
LAMA5
. We found that HMGB1 induced downregulation of E-cadherin and ZO-1 and upregulation of vimentin mRNA transcription and protein translation in a dose-dependent manner. Additionally, we observed that HMGB1 induced AKT phosphorylation, resulting in GSK3β inactivation, cytoplasmic accumulation and nuclear translocation of β-catenin to induce EMT in human airway epithelial cells. Treatment with PI3K inhibitor (LY294006) and β-catenin shRNA reversed HMGB1-induced EMT. Moreover, HMGB1 induced expression of receptor for advanced glycation products (RAGE), but not that of Toll-like receptor (TLR) 2 or TLR4 and RAGE shRNA inhibited HMGB1-induced EMT in human airway epithelial cells. In conclusion, we found that HMGB1 induced EMT through RAGE and the PI3K/AKT/GSK3β/β-catenin signaling pathway. |
| doi_str_mv | 10.1038/srep18815 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4703978</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1899038090</sourcerecordid><originalsourceid>FETCH-LOGICAL-c504t-265a976feefac078838ddae4b353465cc6d983694130bd15046aae9276ccbbb63</originalsourceid><addsrcrecordid>eNplkU9r3DAQxUVJ6YZNDv0CRdBLUnCiP7YsXQIlpEkh0Et6FrI8u1awJVey0-y3j8Julm2qgzQwv3l6w0PoMyUXlHB5mSKMVEpafUDHjJRVwThjRwf1Ap2m9EjyqZgqqfqEFkzUXEklj1F759YdHkLjejdt8DqGecRNeMa0cL6dLbQYRjd10DvT4wESeNtthlxP0fjkJhc8dh5382A8Ni7-NZvDCQt9n07Qx5XpE5zu3iX6_ePm4fquuP91-_P6-31hK1JOBROVUbVYAayMJbWUXLatgbLhFS9FZa1oleQi78BJ09I8I4wBxWphbdM0gi_R1VZ3nJsBWgs-m-z1GN1g4kYH4_S_He86vQ5PuqwJV7XMAmc7gRj-zJAmPbj0uoLxEOakaS2IVKVkZUa_vkMfwxx9Xk9TqVROhuRric63lI0h5aRWezOU6Nf49D6-zH45dL8n38LKwLctkHLLryEefPmf2gv5R6YI</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1899038090</pqid></control><display><type>article</type><title>High mobility group box 1-induced epithelial mesenchymal transition in human airway epithelial cells</title><source>MEDLINE</source><source>DOAJ Directory of Open Access Journals</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Nature Free</source><source>PubMed Central</source><source>Springer Nature OA/Free Journals</source><source>Free Full-Text Journals in Chemistry</source><creator>Chen, Yu-Ching ; Statt, Sarah ; Wu, Reen ; Chang, Hao-Teng ; Liao, Jiunn-Wang ; Wang, Chien-Neng ; Shyu, Woei-Cherng ; Lee, Chen-Chen</creator><creatorcontrib>Chen, Yu-Ching ; Statt, Sarah ; Wu, Reen ; Chang, Hao-Teng ; Liao, Jiunn-Wang ; Wang, Chien-Neng ; Shyu, Woei-Cherng ; Lee, Chen-Chen</creatorcontrib><description>Epithelial–mesenchymal transition (EMT) is implicated in bronchial remodeling and loss of lung function in chronic inflammatory airway diseases. Previous studies showed the involvement of the high mobility group box 1 (HMGB1) protein in the pathology of chronic pulmonary inflammatory diseases. However, the role of HMGB1 in EMT of human airway epithelial cells is still unclear. In this study, we used RNA sequencing to show that HMGB1 treatment regulated EMT-related gene expression in human primary-airway epithelial cells. The top five upregulated genes were
SNAI2
,
FGFBP1
,
VIM
,
SPARC (
osteonectin) and
SERPINE1
, while the downregulated genes included
OCLN
,
TJP1
(
ZO-1
),
FZD7
,
CDH1
(E-cadherin) and
LAMA5
. We found that HMGB1 induced downregulation of E-cadherin and ZO-1 and upregulation of vimentin mRNA transcription and protein translation in a dose-dependent manner. Additionally, we observed that HMGB1 induced AKT phosphorylation, resulting in GSK3β inactivation, cytoplasmic accumulation and nuclear translocation of β-catenin to induce EMT in human airway epithelial cells. Treatment with PI3K inhibitor (LY294006) and β-catenin shRNA reversed HMGB1-induced EMT. Moreover, HMGB1 induced expression of receptor for advanced glycation products (RAGE), but not that of Toll-like receptor (TLR) 2 or TLR4 and RAGE shRNA inhibited HMGB1-induced EMT in human airway epithelial cells. In conclusion, we found that HMGB1 induced EMT through RAGE and the PI3K/AKT/GSK3β/β-catenin signaling pathway.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/srep18815</identifier><identifier>PMID: 26739898</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>1-Phosphatidylinositol 3-kinase ; 14/63 ; 38/77 ; 38/91 ; 42/89 ; 631/80/84/2176 ; 692/699/1785/31 ; 82/1 ; 82/80 ; 96 ; 96/109 ; 96/95 ; Advanced glycosylation end products ; AKT protein ; Antigens, Neoplasm - metabolism ; beta Catenin - metabolism ; Cell Line ; Cell Movement ; E-cadherin ; Epithelial cells ; Epithelial Cells - physiology ; Epithelial-Mesenchymal Transition ; Gene Expression ; Glycogen Synthase Kinase 3 beta - metabolism ; Glycosylation ; High mobility group proteins ; HMGB1 protein ; HMGB1 Protein - physiology ; Humanities and Social Sciences ; Humans ; Inflammatory diseases ; Lung diseases ; Mesenchyme ; Mitogen-Activated Protein Kinases - metabolism ; Mobility ; Mucous membrane ; multidisciplinary ; Nuclear transport ; Osteonectin ; Phosphorylation ; Proto-Oncogene Proteins c-akt - metabolism ; Respiratory function ; Respiratory Mucosa - cytology ; Respiratory tract diseases ; Science ; Signal Transduction ; Snail protein ; TLR4 protein ; Toll-like receptors ; Transcription ; Vimentin ; β-catenin</subject><ispartof>Scientific reports, 2016-01, Vol.6 (1), p.18815-18815, Article 18815</ispartof><rights>The Author(s) 2016</rights><rights>Copyright Nature Publishing Group Jan 2016</rights><rights>Copyright © 2016, Macmillan Publishers Limited 2016 Macmillan Publishers Limited</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c504t-265a976feefac078838ddae4b353465cc6d983694130bd15046aae9276ccbbb63</citedby><cites>FETCH-LOGICAL-c504t-265a976feefac078838ddae4b353465cc6d983694130bd15046aae9276ccbbb63</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/PMC4703978/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4703978/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,728,781,785,865,886,27929,27930,41125,42194,51581,53796,53798</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26739898$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chen, Yu-Ching</creatorcontrib><creatorcontrib>Statt, Sarah</creatorcontrib><creatorcontrib>Wu, Reen</creatorcontrib><creatorcontrib>Chang, Hao-Teng</creatorcontrib><creatorcontrib>Liao, Jiunn-Wang</creatorcontrib><creatorcontrib>Wang, Chien-Neng</creatorcontrib><creatorcontrib>Shyu, Woei-Cherng</creatorcontrib><creatorcontrib>Lee, Chen-Chen</creatorcontrib><title>High mobility group box 1-induced epithelial mesenchymal transition in human airway epithelial cells</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><addtitle>Sci Rep</addtitle><description>Epithelial–mesenchymal transition (EMT) is implicated in bronchial remodeling and loss of lung function in chronic inflammatory airway diseases. Previous studies showed the involvement of the high mobility group box 1 (HMGB1) protein in the pathology of chronic pulmonary inflammatory diseases. However, the role of HMGB1 in EMT of human airway epithelial cells is still unclear. In this study, we used RNA sequencing to show that HMGB1 treatment regulated EMT-related gene expression in human primary-airway epithelial cells. The top five upregulated genes were
SNAI2
,
FGFBP1
,
VIM
,
SPARC (
osteonectin) and
SERPINE1
, while the downregulated genes included
OCLN
,
TJP1
(
ZO-1
),
FZD7
,
CDH1
(E-cadherin) and
LAMA5
. We found that HMGB1 induced downregulation of E-cadherin and ZO-1 and upregulation of vimentin mRNA transcription and protein translation in a dose-dependent manner. Additionally, we observed that HMGB1 induced AKT phosphorylation, resulting in GSK3β inactivation, cytoplasmic accumulation and nuclear translocation of β-catenin to induce EMT in human airway epithelial cells. Treatment with PI3K inhibitor (LY294006) and β-catenin shRNA reversed HMGB1-induced EMT. Moreover, HMGB1 induced expression of receptor for advanced glycation products (RAGE), but not that of Toll-like receptor (TLR) 2 or TLR4 and RAGE shRNA inhibited HMGB1-induced EMT in human airway epithelial cells. In conclusion, we found that HMGB1 induced EMT through RAGE and the PI3K/AKT/GSK3β/β-catenin signaling pathway.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>14/63</subject><subject>38/77</subject><subject>38/91</subject><subject>42/89</subject><subject>631/80/84/2176</subject><subject>692/699/1785/31</subject><subject>82/1</subject><subject>82/80</subject><subject>96</subject><subject>96/109</subject><subject>96/95</subject><subject>Advanced glycosylation end products</subject><subject>AKT protein</subject><subject>Antigens, Neoplasm - metabolism</subject><subject>beta Catenin - metabolism</subject><subject>Cell Line</subject><subject>Cell Movement</subject><subject>E-cadherin</subject><subject>Epithelial cells</subject><subject>Epithelial Cells - physiology</subject><subject>Epithelial-Mesenchymal Transition</subject><subject>Gene Expression</subject><subject>Glycogen Synthase Kinase 3 beta - metabolism</subject><subject>Glycosylation</subject><subject>High mobility group proteins</subject><subject>HMGB1 protein</subject><subject>HMGB1 Protein - physiology</subject><subject>Humanities and Social Sciences</subject><subject>Humans</subject><subject>Inflammatory diseases</subject><subject>Lung diseases</subject><subject>Mesenchyme</subject><subject>Mitogen-Activated Protein Kinases - metabolism</subject><subject>Mobility</subject><subject>Mucous membrane</subject><subject>multidisciplinary</subject><subject>Nuclear transport</subject><subject>Osteonectin</subject><subject>Phosphorylation</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Respiratory function</subject><subject>Respiratory Mucosa - cytology</subject><subject>Respiratory tract diseases</subject><subject>Science</subject><subject>Signal Transduction</subject><subject>Snail protein</subject><subject>TLR4 protein</subject><subject>Toll-like receptors</subject><subject>Transcription</subject><subject>Vimentin</subject><subject>β-catenin</subject><issn>2045-2322</issn><issn>2045-2322</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNplkU9r3DAQxUVJ6YZNDv0CRdBLUnCiP7YsXQIlpEkh0Et6FrI8u1awJVey0-y3j8Julm2qgzQwv3l6w0PoMyUXlHB5mSKMVEpafUDHjJRVwThjRwf1Ap2m9EjyqZgqqfqEFkzUXEklj1F759YdHkLjejdt8DqGecRNeMa0cL6dLbQYRjd10DvT4wESeNtthlxP0fjkJhc8dh5382A8Ni7-NZvDCQt9n07Qx5XpE5zu3iX6_ePm4fquuP91-_P6-31hK1JOBROVUbVYAayMJbWUXLatgbLhFS9FZa1oleQi78BJ09I8I4wBxWphbdM0gi_R1VZ3nJsBWgs-m-z1GN1g4kYH4_S_He86vQ5PuqwJV7XMAmc7gRj-zJAmPbj0uoLxEOakaS2IVKVkZUa_vkMfwxx9Xk9TqVROhuRric63lI0h5aRWezOU6Nf49D6-zH45dL8n38LKwLctkHLLryEefPmf2gv5R6YI</recordid><startdate>20160107</startdate><enddate>20160107</enddate><creator>Chen, Yu-Ching</creator><creator>Statt, Sarah</creator><creator>Wu, Reen</creator><creator>Chang, Hao-Teng</creator><creator>Liao, Jiunn-Wang</creator><creator>Wang, Chien-Neng</creator><creator>Shyu, Woei-Cherng</creator><creator>Lee, Chen-Chen</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>C6C</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>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20160107</creationdate><title>High mobility group box 1-induced epithelial mesenchymal transition in human airway epithelial cells</title><author>Chen, Yu-Ching ; Statt, Sarah ; Wu, Reen ; Chang, Hao-Teng ; Liao, Jiunn-Wang ; Wang, Chien-Neng ; Shyu, Woei-Cherng ; Lee, Chen-Chen</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c504t-265a976feefac078838ddae4b353465cc6d983694130bd15046aae9276ccbbb63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>1-Phosphatidylinositol 3-kinase</topic><topic>14/63</topic><topic>38/77</topic><topic>38/91</topic><topic>42/89</topic><topic>631/80/84/2176</topic><topic>692/699/1785/31</topic><topic>82/1</topic><topic>82/80</topic><topic>96</topic><topic>96/109</topic><topic>96/95</topic><topic>Advanced glycosylation end products</topic><topic>AKT protein</topic><topic>Antigens, Neoplasm - metabolism</topic><topic>beta Catenin - metabolism</topic><topic>Cell Line</topic><topic>Cell Movement</topic><topic>E-cadherin</topic><topic>Epithelial cells</topic><topic>Epithelial Cells - physiology</topic><topic>Epithelial-Mesenchymal Transition</topic><topic>Gene Expression</topic><topic>Glycogen Synthase Kinase 3 beta - metabolism</topic><topic>Glycosylation</topic><topic>High mobility group proteins</topic><topic>HMGB1 protein</topic><topic>HMGB1 Protein - physiology</topic><topic>Humanities and Social Sciences</topic><topic>Humans</topic><topic>Inflammatory diseases</topic><topic>Lung diseases</topic><topic>Mesenchyme</topic><topic>Mitogen-Activated Protein Kinases - metabolism</topic><topic>Mobility</topic><topic>Mucous membrane</topic><topic>multidisciplinary</topic><topic>Nuclear transport</topic><topic>Osteonectin</topic><topic>Phosphorylation</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Respiratory function</topic><topic>Respiratory Mucosa - cytology</topic><topic>Respiratory tract diseases</topic><topic>Science</topic><topic>Signal Transduction</topic><topic>Snail protein</topic><topic>TLR4 protein</topic><topic>Toll-like receptors</topic><topic>Transcription</topic><topic>Vimentin</topic><topic>β-catenin</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chen, Yu-Ching</creatorcontrib><creatorcontrib>Statt, Sarah</creatorcontrib><creatorcontrib>Wu, Reen</creatorcontrib><creatorcontrib>Chang, Hao-Teng</creatorcontrib><creatorcontrib>Liao, Jiunn-Wang</creatorcontrib><creatorcontrib>Wang, Chien-Neng</creatorcontrib><creatorcontrib>Shyu, Woei-Cherng</creatorcontrib><creatorcontrib>Lee, Chen-Chen</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 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>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 Basic</collection><collection>MEDLINE - Academic</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>Chen, Yu-Ching</au><au>Statt, Sarah</au><au>Wu, Reen</au><au>Chang, Hao-Teng</au><au>Liao, Jiunn-Wang</au><au>Wang, Chien-Neng</au><au>Shyu, Woei-Cherng</au><au>Lee, Chen-Chen</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>High mobility group box 1-induced epithelial mesenchymal transition in human airway epithelial cells</atitle><jtitle>Scientific reports</jtitle><stitle>Sci Rep</stitle><addtitle>Sci Rep</addtitle><date>2016-01-07</date><risdate>2016</risdate><volume>6</volume><issue>1</issue><spage>18815</spage><epage>18815</epage><pages>18815-18815</pages><artnum>18815</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>Epithelial–mesenchymal transition (EMT) is implicated in bronchial remodeling and loss of lung function in chronic inflammatory airway diseases. Previous studies showed the involvement of the high mobility group box 1 (HMGB1) protein in the pathology of chronic pulmonary inflammatory diseases. However, the role of HMGB1 in EMT of human airway epithelial cells is still unclear. In this study, we used RNA sequencing to show that HMGB1 treatment regulated EMT-related gene expression in human primary-airway epithelial cells. The top five upregulated genes were
SNAI2
,
FGFBP1
,
VIM
,
SPARC (
osteonectin) and
SERPINE1
, while the downregulated genes included
OCLN
,
TJP1
(
ZO-1
),
FZD7
,
CDH1
(E-cadherin) and
LAMA5
. We found that HMGB1 induced downregulation of E-cadherin and ZO-1 and upregulation of vimentin mRNA transcription and protein translation in a dose-dependent manner. Additionally, we observed that HMGB1 induced AKT phosphorylation, resulting in GSK3β inactivation, cytoplasmic accumulation and nuclear translocation of β-catenin to induce EMT in human airway epithelial cells. Treatment with PI3K inhibitor (LY294006) and β-catenin shRNA reversed HMGB1-induced EMT. Moreover, HMGB1 induced expression of receptor for advanced glycation products (RAGE), but not that of Toll-like receptor (TLR) 2 or TLR4 and RAGE shRNA inhibited HMGB1-induced EMT in human airway epithelial cells. In conclusion, we found that HMGB1 induced EMT through RAGE and the PI3K/AKT/GSK3β/β-catenin signaling pathway.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>26739898</pmid><doi>10.1038/srep18815</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| language | eng |
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| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Nature Free; PubMed Central; Springer Nature OA/Free Journals; Free Full-Text Journals in Chemistry |
| subjects | 1-Phosphatidylinositol 3-kinase 14/63 38/77 38/91 42/89 631/80/84/2176 692/699/1785/31 82/1 82/80 96 96/109 96/95 Advanced glycosylation end products AKT protein Antigens, Neoplasm - metabolism beta Catenin - metabolism Cell Line Cell Movement E-cadherin Epithelial cells Epithelial Cells - physiology Epithelial-Mesenchymal Transition Gene Expression Glycogen Synthase Kinase 3 beta - metabolism Glycosylation High mobility group proteins HMGB1 protein HMGB1 Protein - physiology Humanities and Social Sciences Humans Inflammatory diseases Lung diseases Mesenchyme Mitogen-Activated Protein Kinases - metabolism Mobility Mucous membrane multidisciplinary Nuclear transport Osteonectin Phosphorylation Proto-Oncogene Proteins c-akt - metabolism Respiratory function Respiratory Mucosa - cytology Respiratory tract diseases Science Signal Transduction Snail protein TLR4 protein Toll-like receptors Transcription Vimentin β-catenin |
| title | High mobility group box 1-induced epithelial mesenchymal transition in human airway epithelial cells |
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