Involvement of Intracellular and Extracellular High-Mobility Group Box-1 in the Progression of Esophageal Squamous Cell Carcinoma
Background High-mobility group box-1 (HMGB1) is involved in a broad range of inflammatory responses and the progression of various types of malignancy. However, the roles of HMGB1 in the progression of esophageal squamous cell carcinoma (ESCC) are unclear. The aim of this study was to investigate th...
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| Veröffentlicht in: | Annals of surgical oncology 2020-09, Vol.27 (9), p.3233-3244 |
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| creator | Matsubara, Daiki Konishi, Hirotaka Arita, Tomohiro Shoda, Katsutoshi Fujita, Yuji Ogino, Shinpei Takao, Koji Nanishi, Kenji Kosuga, Toshiyuki Komatsu, Shuhei Shiozaki, Atsushi Fujiwara, Hitoshi Okamoto, Kazuma Otsuji, Eigo |
| description | Background
High-mobility group box-1 (HMGB1) is involved in a broad range of inflammatory responses and the progression of various types of malignancy. However, the roles of HMGB1 in the progression of esophageal squamous cell carcinoma (ESCC) are unclear. The aim of this study was to investigate the significance of intracellular and extracellular HMGB1 in ESCC.
Methods
HMGB1 levels were measured in the tissue and plasma of patients with ESCC, or in ESCC cell lines and their conditioned medium. The effects of downregulation of intracellular HMGB1 or upregulation of extracellular HMGB1 on proliferation, cell migration, and invasion were evaluated using proliferation, transwell, and wound healing assays.
Results
Downregulation of HMGB1 expression inhibited cell proliferation, migration, and invasion. On the other hand, upregulation of extracellular HMGB1 level by addition of recombinant HMGB1 promoted the migratory and invasive abilities of ESCC cells through increases of phosphorylation of the signal-regulated kinase 1/2 and NF-κBp65 proteins. These effects of extracellular HMGB1 were attenuated by treatment with recombinant soluble thrombomodulin, which adsorbs HMGB1. The expression of HMGB1 was significantly higher in tumor tissue (
p
= 0.008), and the concentration of HMGB1 in the plasma was significantly higher in patients with ESCC than in healthy volunteers (
p
= 0.04). Cancer-specific survival was worse in patients with high concentration of plasma HMGB1 (
p
= 0.01).
Conclusion
Increase of HMGB1 levels in tumor cells or plasma plays a crucial role in the malignant potential of ESCC. Intracellular and extracellular HMGB1 may be a therapeutic target in ESCC. |
| doi_str_mv | 10.1245/s10434-020-08363-3 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2384204667</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2384204667</sourcerecordid><originalsourceid>FETCH-LOGICAL-c441t-5b4539db05aef7dae70b1ddd9e2156baef9a7d2a8721926bb891ed6fc9382cde3</originalsourceid><addsrcrecordid>eNp9kctO5DAQRS3EaHjM_AALZIkNG4OfeSyh1UBLoEFiZm05caU7KLEbO2nBkj_HTTOAWLBy6frUrSpdhA4YPWFcqtPIqBSSUE4JLUQmiNhCu0wlSWYF2041zQpS8kztoL0Y7ylluaDqJ9oRnPNUy130PHMr362gBzdg3-CZG4KpoevGzgRsnMXTx8_KVTtfkBtftV07POHL4MclPvePhOHW4WEB-Db4eYAYW-_WftPolwszB9Phu4fR9H6MeJLM8MSEunW-N7_Qj8Z0EX6_vfvo38X07-SKXP-5nE3OrkktJRuIqqQSpa2oMtDk1kBOK2atLYEzlVVJLE1uuSlyztLJVVWUDGzW1KUoeG1B7KPjje8y-IcR4qD7Nq7vMg7SVpqLQnIqsyxP6NEX9N6PwaXtNJeCFixXiieKb6g6-BgDNHoZ2t6EJ82oXgekNwHpFJB-DUiL1HT4Zj1WPdj3lv-JJEBsgJi-3BzCx-xvbF8A5LidBA</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2430817552</pqid></control><display><type>article</type><title>Involvement of Intracellular and Extracellular High-Mobility Group Box-1 in the Progression of Esophageal Squamous Cell Carcinoma</title><source>MEDLINE</source><source>SpringerLink Journals - AutoHoldings</source><creator>Matsubara, Daiki ; Konishi, Hirotaka ; Arita, Tomohiro ; Shoda, Katsutoshi ; Fujita, Yuji ; Ogino, Shinpei ; Takao, Koji ; Nanishi, Kenji ; Kosuga, Toshiyuki ; Komatsu, Shuhei ; Shiozaki, Atsushi ; Fujiwara, Hitoshi ; Okamoto, Kazuma ; Otsuji, Eigo</creator><creatorcontrib>Matsubara, Daiki ; Konishi, Hirotaka ; Arita, Tomohiro ; Shoda, Katsutoshi ; Fujita, Yuji ; Ogino, Shinpei ; Takao, Koji ; Nanishi, Kenji ; Kosuga, Toshiyuki ; Komatsu, Shuhei ; Shiozaki, Atsushi ; Fujiwara, Hitoshi ; Okamoto, Kazuma ; Otsuji, Eigo</creatorcontrib><description>Background
High-mobility group box-1 (HMGB1) is involved in a broad range of inflammatory responses and the progression of various types of malignancy. However, the roles of HMGB1 in the progression of esophageal squamous cell carcinoma (ESCC) are unclear. The aim of this study was to investigate the significance of intracellular and extracellular HMGB1 in ESCC.
Methods
HMGB1 levels were measured in the tissue and plasma of patients with ESCC, or in ESCC cell lines and their conditioned medium. The effects of downregulation of intracellular HMGB1 or upregulation of extracellular HMGB1 on proliferation, cell migration, and invasion were evaluated using proliferation, transwell, and wound healing assays.
Results
Downregulation of HMGB1 expression inhibited cell proliferation, migration, and invasion. On the other hand, upregulation of extracellular HMGB1 level by addition of recombinant HMGB1 promoted the migratory and invasive abilities of ESCC cells through increases of phosphorylation of the signal-regulated kinase 1/2 and NF-κBp65 proteins. These effects of extracellular HMGB1 were attenuated by treatment with recombinant soluble thrombomodulin, which adsorbs HMGB1. The expression of HMGB1 was significantly higher in tumor tissue (
p
= 0.008), and the concentration of HMGB1 in the plasma was significantly higher in patients with ESCC than in healthy volunteers (
p
= 0.04). Cancer-specific survival was worse in patients with high concentration of plasma HMGB1 (
p
= 0.01).
Conclusion
Increase of HMGB1 levels in tumor cells or plasma plays a crucial role in the malignant potential of ESCC. Intracellular and extracellular HMGB1 may be a therapeutic target in ESCC.</description><identifier>ISSN: 1068-9265</identifier><identifier>EISSN: 1534-4681</identifier><identifier>DOI: 10.1245/s10434-020-08363-3</identifier><identifier>PMID: 32221734</identifier><language>eng</language><publisher>Cham: Springer International Publishing</publisher><subject>Cell adhesion & migration ; Cell Line, Tumor ; Cell migration ; Cell Movement - physiology ; Cell proliferation ; Cell Proliferation - physiology ; Esophageal cancer ; Esophageal Neoplasms - genetics ; Esophageal Neoplasms - metabolism ; Esophageal Neoplasms - pathology ; Esophageal Squamous Cell Carcinoma - genetics ; Esophageal Squamous Cell Carcinoma - metabolism ; Esophageal Squamous Cell Carcinoma - pathology ; Esophagus ; HMGB1 protein ; HMGB1 Protein - genetics ; HMGB1 Protein - metabolism ; Humans ; Inflammation ; Intracellular ; Invasiveness ; Kinases ; Malignancy ; Medicine ; Medicine & Public Health ; Mobility ; Neoplasm Invasiveness ; Oncology ; Phosphorylation ; Plasma ; Squamous cell carcinoma ; Surgery ; Surgical Oncology ; Thrombomodulin ; Translational Research and Biomarkers ; Tumor cells ; Wound healing</subject><ispartof>Annals of surgical oncology, 2020-09, Vol.27 (9), p.3233-3244</ispartof><rights>Society of Surgical Oncology 2020</rights><rights>Society of Surgical Oncology 2020.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c441t-5b4539db05aef7dae70b1ddd9e2156baef9a7d2a8721926bb891ed6fc9382cde3</citedby><cites>FETCH-LOGICAL-c441t-5b4539db05aef7dae70b1ddd9e2156baef9a7d2a8721926bb891ed6fc9382cde3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1245/s10434-020-08363-3$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1245/s10434-020-08363-3$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32221734$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Matsubara, Daiki</creatorcontrib><creatorcontrib>Konishi, Hirotaka</creatorcontrib><creatorcontrib>Arita, Tomohiro</creatorcontrib><creatorcontrib>Shoda, Katsutoshi</creatorcontrib><creatorcontrib>Fujita, Yuji</creatorcontrib><creatorcontrib>Ogino, Shinpei</creatorcontrib><creatorcontrib>Takao, Koji</creatorcontrib><creatorcontrib>Nanishi, Kenji</creatorcontrib><creatorcontrib>Kosuga, Toshiyuki</creatorcontrib><creatorcontrib>Komatsu, Shuhei</creatorcontrib><creatorcontrib>Shiozaki, Atsushi</creatorcontrib><creatorcontrib>Fujiwara, Hitoshi</creatorcontrib><creatorcontrib>Okamoto, Kazuma</creatorcontrib><creatorcontrib>Otsuji, Eigo</creatorcontrib><title>Involvement of Intracellular and Extracellular High-Mobility Group Box-1 in the Progression of Esophageal Squamous Cell Carcinoma</title><title>Annals of surgical oncology</title><addtitle>Ann Surg Oncol</addtitle><addtitle>Ann Surg Oncol</addtitle><description>Background
High-mobility group box-1 (HMGB1) is involved in a broad range of inflammatory responses and the progression of various types of malignancy. However, the roles of HMGB1 in the progression of esophageal squamous cell carcinoma (ESCC) are unclear. The aim of this study was to investigate the significance of intracellular and extracellular HMGB1 in ESCC.
Methods
HMGB1 levels were measured in the tissue and plasma of patients with ESCC, or in ESCC cell lines and their conditioned medium. The effects of downregulation of intracellular HMGB1 or upregulation of extracellular HMGB1 on proliferation, cell migration, and invasion were evaluated using proliferation, transwell, and wound healing assays.
Results
Downregulation of HMGB1 expression inhibited cell proliferation, migration, and invasion. On the other hand, upregulation of extracellular HMGB1 level by addition of recombinant HMGB1 promoted the migratory and invasive abilities of ESCC cells through increases of phosphorylation of the signal-regulated kinase 1/2 and NF-κBp65 proteins. These effects of extracellular HMGB1 were attenuated by treatment with recombinant soluble thrombomodulin, which adsorbs HMGB1. The expression of HMGB1 was significantly higher in tumor tissue (
p
= 0.008), and the concentration of HMGB1 in the plasma was significantly higher in patients with ESCC than in healthy volunteers (
p
= 0.04). Cancer-specific survival was worse in patients with high concentration of plasma HMGB1 (
p
= 0.01).
Conclusion
Increase of HMGB1 levels in tumor cells or plasma plays a crucial role in the malignant potential of ESCC. Intracellular and extracellular HMGB1 may be a therapeutic target in ESCC.</description><subject>Cell adhesion & migration</subject><subject>Cell Line, Tumor</subject><subject>Cell migration</subject><subject>Cell Movement - physiology</subject><subject>Cell proliferation</subject><subject>Cell Proliferation - physiology</subject><subject>Esophageal cancer</subject><subject>Esophageal Neoplasms - genetics</subject><subject>Esophageal Neoplasms - metabolism</subject><subject>Esophageal Neoplasms - pathology</subject><subject>Esophageal Squamous Cell Carcinoma - genetics</subject><subject>Esophageal Squamous Cell Carcinoma - metabolism</subject><subject>Esophageal Squamous Cell Carcinoma - pathology</subject><subject>Esophagus</subject><subject>HMGB1 protein</subject><subject>HMGB1 Protein - genetics</subject><subject>HMGB1 Protein - metabolism</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Intracellular</subject><subject>Invasiveness</subject><subject>Kinases</subject><subject>Malignancy</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Mobility</subject><subject>Neoplasm Invasiveness</subject><subject>Oncology</subject><subject>Phosphorylation</subject><subject>Plasma</subject><subject>Squamous cell carcinoma</subject><subject>Surgery</subject><subject>Surgical Oncology</subject><subject>Thrombomodulin</subject><subject>Translational Research and Biomarkers</subject><subject>Tumor cells</subject><subject>Wound healing</subject><issn>1068-9265</issn><issn>1534-4681</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp9kctO5DAQRS3EaHjM_AALZIkNG4OfeSyh1UBLoEFiZm05caU7KLEbO2nBkj_HTTOAWLBy6frUrSpdhA4YPWFcqtPIqBSSUE4JLUQmiNhCu0wlSWYF2041zQpS8kztoL0Y7ylluaDqJ9oRnPNUy130PHMr362gBzdg3-CZG4KpoevGzgRsnMXTx8_KVTtfkBtftV07POHL4MclPvePhOHW4WEB-Db4eYAYW-_WftPolwszB9Phu4fR9H6MeJLM8MSEunW-N7_Qj8Z0EX6_vfvo38X07-SKXP-5nE3OrkktJRuIqqQSpa2oMtDk1kBOK2atLYEzlVVJLE1uuSlyztLJVVWUDGzW1KUoeG1B7KPjje8y-IcR4qD7Nq7vMg7SVpqLQnIqsyxP6NEX9N6PwaXtNJeCFixXiieKb6g6-BgDNHoZ2t6EJ82oXgekNwHpFJB-DUiL1HT4Zj1WPdj3lv-JJEBsgJi-3BzCx-xvbF8A5LidBA</recordid><startdate>20200901</startdate><enddate>20200901</enddate><creator>Matsubara, Daiki</creator><creator>Konishi, Hirotaka</creator><creator>Arita, Tomohiro</creator><creator>Shoda, Katsutoshi</creator><creator>Fujita, Yuji</creator><creator>Ogino, Shinpei</creator><creator>Takao, Koji</creator><creator>Nanishi, Kenji</creator><creator>Kosuga, Toshiyuki</creator><creator>Komatsu, Shuhei</creator><creator>Shiozaki, Atsushi</creator><creator>Fujiwara, Hitoshi</creator><creator>Okamoto, Kazuma</creator><creator>Otsuji, Eigo</creator><general>Springer International Publishing</general><general>Springer Nature B.V</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>3V.</scope><scope>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20200901</creationdate><title>Involvement of Intracellular and Extracellular High-Mobility Group Box-1 in the Progression of Esophageal Squamous Cell Carcinoma</title><author>Matsubara, Daiki ; Konishi, Hirotaka ; Arita, Tomohiro ; Shoda, Katsutoshi ; Fujita, Yuji ; Ogino, Shinpei ; Takao, Koji ; Nanishi, Kenji ; Kosuga, Toshiyuki ; Komatsu, Shuhei ; Shiozaki, Atsushi ; Fujiwara, Hitoshi ; Okamoto, Kazuma ; Otsuji, Eigo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c441t-5b4539db05aef7dae70b1ddd9e2156baef9a7d2a8721926bb891ed6fc9382cde3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Cell adhesion & migration</topic><topic>Cell Line, Tumor</topic><topic>Cell migration</topic><topic>Cell Movement - physiology</topic><topic>Cell proliferation</topic><topic>Cell Proliferation - physiology</topic><topic>Esophageal cancer</topic><topic>Esophageal Neoplasms - genetics</topic><topic>Esophageal Neoplasms - metabolism</topic><topic>Esophageal Neoplasms - pathology</topic><topic>Esophageal Squamous Cell Carcinoma - genetics</topic><topic>Esophageal Squamous Cell Carcinoma - metabolism</topic><topic>Esophageal Squamous Cell Carcinoma - pathology</topic><topic>Esophagus</topic><topic>HMGB1 protein</topic><topic>HMGB1 Protein - genetics</topic><topic>HMGB1 Protein - metabolism</topic><topic>Humans</topic><topic>Inflammation</topic><topic>Intracellular</topic><topic>Invasiveness</topic><topic>Kinases</topic><topic>Malignancy</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Mobility</topic><topic>Neoplasm Invasiveness</topic><topic>Oncology</topic><topic>Phosphorylation</topic><topic>Plasma</topic><topic>Squamous cell carcinoma</topic><topic>Surgery</topic><topic>Surgical Oncology</topic><topic>Thrombomodulin</topic><topic>Translational Research and Biomarkers</topic><topic>Tumor cells</topic><topic>Wound healing</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Matsubara, Daiki</creatorcontrib><creatorcontrib>Konishi, Hirotaka</creatorcontrib><creatorcontrib>Arita, Tomohiro</creatorcontrib><creatorcontrib>Shoda, Katsutoshi</creatorcontrib><creatorcontrib>Fujita, Yuji</creatorcontrib><creatorcontrib>Ogino, Shinpei</creatorcontrib><creatorcontrib>Takao, Koji</creatorcontrib><creatorcontrib>Nanishi, Kenji</creatorcontrib><creatorcontrib>Kosuga, Toshiyuki</creatorcontrib><creatorcontrib>Komatsu, Shuhei</creatorcontrib><creatorcontrib>Shiozaki, Atsushi</creatorcontrib><creatorcontrib>Fujiwara, Hitoshi</creatorcontrib><creatorcontrib>Okamoto, Kazuma</creatorcontrib><creatorcontrib>Otsuji, Eigo</creatorcontrib><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>Oncogenes and Growth Factors Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma 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</collection><collection>ProQuest One Community College</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>Medical 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><jtitle>Annals of surgical oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Matsubara, Daiki</au><au>Konishi, Hirotaka</au><au>Arita, Tomohiro</au><au>Shoda, Katsutoshi</au><au>Fujita, Yuji</au><au>Ogino, Shinpei</au><au>Takao, Koji</au><au>Nanishi, Kenji</au><au>Kosuga, Toshiyuki</au><au>Komatsu, Shuhei</au><au>Shiozaki, Atsushi</au><au>Fujiwara, Hitoshi</au><au>Okamoto, Kazuma</au><au>Otsuji, Eigo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Involvement of Intracellular and Extracellular High-Mobility Group Box-1 in the Progression of Esophageal Squamous Cell Carcinoma</atitle><jtitle>Annals of surgical oncology</jtitle><stitle>Ann Surg Oncol</stitle><addtitle>Ann Surg Oncol</addtitle><date>2020-09-01</date><risdate>2020</risdate><volume>27</volume><issue>9</issue><spage>3233</spage><epage>3244</epage><pages>3233-3244</pages><issn>1068-9265</issn><eissn>1534-4681</eissn><abstract>Background
High-mobility group box-1 (HMGB1) is involved in a broad range of inflammatory responses and the progression of various types of malignancy. However, the roles of HMGB1 in the progression of esophageal squamous cell carcinoma (ESCC) are unclear. The aim of this study was to investigate the significance of intracellular and extracellular HMGB1 in ESCC.
Methods
HMGB1 levels were measured in the tissue and plasma of patients with ESCC, or in ESCC cell lines and their conditioned medium. The effects of downregulation of intracellular HMGB1 or upregulation of extracellular HMGB1 on proliferation, cell migration, and invasion were evaluated using proliferation, transwell, and wound healing assays.
Results
Downregulation of HMGB1 expression inhibited cell proliferation, migration, and invasion. On the other hand, upregulation of extracellular HMGB1 level by addition of recombinant HMGB1 promoted the migratory and invasive abilities of ESCC cells through increases of phosphorylation of the signal-regulated kinase 1/2 and NF-κBp65 proteins. These effects of extracellular HMGB1 were attenuated by treatment with recombinant soluble thrombomodulin, which adsorbs HMGB1. The expression of HMGB1 was significantly higher in tumor tissue (
p
= 0.008), and the concentration of HMGB1 in the plasma was significantly higher in patients with ESCC than in healthy volunteers (
p
= 0.04). Cancer-specific survival was worse in patients with high concentration of plasma HMGB1 (
p
= 0.01).
Conclusion
Increase of HMGB1 levels in tumor cells or plasma plays a crucial role in the malignant potential of ESCC. Intracellular and extracellular HMGB1 may be a therapeutic target in ESCC.</abstract><cop>Cham</cop><pub>Springer International Publishing</pub><pmid>32221734</pmid><doi>10.1245/s10434-020-08363-3</doi><tpages>12</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1068-9265 |
| ispartof | Annals of surgical oncology, 2020-09, Vol.27 (9), p.3233-3244 |
| issn | 1068-9265 1534-4681 |
| language | eng |
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| source | MEDLINE; SpringerLink Journals - AutoHoldings |
| subjects | Cell adhesion & migration Cell Line, Tumor Cell migration Cell Movement - physiology Cell proliferation Cell Proliferation - physiology Esophageal cancer Esophageal Neoplasms - genetics Esophageal Neoplasms - metabolism Esophageal Neoplasms - pathology Esophageal Squamous Cell Carcinoma - genetics Esophageal Squamous Cell Carcinoma - metabolism Esophageal Squamous Cell Carcinoma - pathology Esophagus HMGB1 protein HMGB1 Protein - genetics HMGB1 Protein - metabolism Humans Inflammation Intracellular Invasiveness Kinases Malignancy Medicine Medicine & Public Health Mobility Neoplasm Invasiveness Oncology Phosphorylation Plasma Squamous cell carcinoma Surgery Surgical Oncology Thrombomodulin Translational Research and Biomarkers Tumor cells Wound healing |
| title | Involvement of Intracellular and Extracellular High-Mobility Group Box-1 in the Progression of Esophageal Squamous Cell Carcinoma |
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