Upregulation of Nogo‐B by hypoxia inducible factor‐1 and activator protein‐1 in hepatocellular carcinoma
Nogo‐B is an important regulator of tumor angiogenesis. Expression of Nogo‐B is remarkably upregulated in multiple tumor types, especially hepatocellular carcinoma (HCC). Here, we show the transcriptional regulation mechanisms of Nogo‐B in liver cancer. In response to hypoxia, expression of Nogo‐B s...
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| Veröffentlicht in: | Cancer science 2021-07, Vol.112 (7), p.2728-2738 |
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| creator | Han, Dingding Yang, Penggao Qin, Bo Ji, Guoqing Wu, Yanhua Yu, Long Zhang, Hong |
| description | Nogo‐B is an important regulator of tumor angiogenesis. Expression of Nogo‐B is remarkably upregulated in multiple tumor types, especially hepatocellular carcinoma (HCC). Here, we show the transcriptional regulation mechanisms of Nogo‐B in liver cancer. In response to hypoxia, expression of Nogo‐B significantly increased in HCC tissues and cells. The distal hypoxia‐responsive element in the promoter was essential for transcriptional activation of Nogo‐B under hypoxic conditions, which is the specific site for hypoxia inducible factor‐1α (HIF‐1α) binding. In addition, Nogo‐B expression was associated with c‐Fos expression in HCC tissues. Nogo‐B expression was induced by c‐Fos, yet inhibited by a dominant negative mutant A‐Fos. Deletion and mutation analysis of the predicted activator protein‐1 binding sites revealed that functional element mediated the induction of Nogo‐B promoter activity, which was confirmed by ChIP. These results indicate that HIF‐1α and c‐Fos induce the expression of Nogo‐B depending on tumor microenvironments, such as hypoxia and low levels of nutrients, and play a role in upregulation of Nogo‐B in tumor angiogenesis.
Our results indicated that, although Nogo‐B played a complementary and parallel role in tumor angiogenesis to that of vascular endothelial growth factor, they shared a common induction mechanism of hypoxia inducible factor‐1 and activator protein‐1 activation, which might provide novel treatment options in hepatocellular carcinoma. |
| doi_str_mv | 10.1111/cas.14941 |
| format | Article |
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Our results indicated that, although Nogo‐B played a complementary and parallel role in tumor angiogenesis to that of vascular endothelial growth factor, they shared a common induction mechanism of hypoxia inducible factor‐1 and activator protein‐1 activation, which might provide novel treatment options in hepatocellular carcinoma.</description><identifier>ISSN: 1347-9032</identifier><identifier>EISSN: 1349-7006</identifier><identifier>DOI: 10.1111/cas.14941</identifier><identifier>PMID: 33963651</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>Analysis ; Angiogenesis ; Animals ; Binding sites ; Binding Sites - genetics ; Biotechnology ; Carcinoma, Hepatocellular - blood supply ; Carcinoma, Hepatocellular - metabolism ; c‐Fos ; Gene Deletion ; Gene regulation ; Hepatic Artery ; Hepatocellular carcinoma ; Hepatoma ; HIF‐1α ; Humans ; Hypoxia ; Hypoxia-Inducible Factor 1 - metabolism ; Laboratory animals ; Ligation ; Liver cancer ; Liver Neoplasms - blood supply ; Liver Neoplasms - metabolism ; Male ; Microenvironments ; Mutagenesis ; Mutation ; Neoplasm Proteins - genetics ; Neoplasm Proteins - metabolism ; Neovascularization, Pathologic ; Nogo protein ; Nogo Proteins - genetics ; Nogo Proteins - metabolism ; Nogo‐B ; Original ; Plasmids ; Promoter Regions, Genetic ; Protein binding ; Proteins ; Proto-Oncogene Proteins c-fyn - metabolism ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Regulatory sequences ; Transcription activation ; Transcription Factor AP-1 - genetics ; Transcription Factor AP-1 - metabolism ; Transcriptional Activation ; Tumor Hypoxia - physiology ; Tumor Microenvironment ; Tumors ; Up-Regulation ; Vascular endothelial growth factor</subject><ispartof>Cancer science, 2021-07, Vol.112 (7), p.2728-2738</ispartof><rights>2021 The Authors. published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association.</rights><rights>2021 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association.</rights><rights>COPYRIGHT 2021 John Wiley & Sons, Inc.</rights><rights>2021. This work is published under http://creativecommons.org/licenses/by-nc-nd/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-c5621-c096f1c397deb1ad2c147f046aa00fad64140ed10444ca7e4e47f6495e31e5bc3</citedby><cites>FETCH-LOGICAL-c5621-c096f1c397deb1ad2c147f046aa00fad64140ed10444ca7e4e47f6495e31e5bc3</cites><orcidid>0000-0003-0963-6286</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/PMC8253276/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8253276/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,1411,11541,27901,27902,45550,45551,46027,46451,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33963651$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Han, Dingding</creatorcontrib><creatorcontrib>Yang, Penggao</creatorcontrib><creatorcontrib>Qin, Bo</creatorcontrib><creatorcontrib>Ji, Guoqing</creatorcontrib><creatorcontrib>Wu, Yanhua</creatorcontrib><creatorcontrib>Yu, Long</creatorcontrib><creatorcontrib>Zhang, Hong</creatorcontrib><title>Upregulation of Nogo‐B by hypoxia inducible factor‐1 and activator protein‐1 in hepatocellular carcinoma</title><title>Cancer science</title><addtitle>Cancer Sci</addtitle><description>Nogo‐B is an important regulator of tumor angiogenesis. Expression of Nogo‐B is remarkably upregulated in multiple tumor types, especially hepatocellular carcinoma (HCC). Here, we show the transcriptional regulation mechanisms of Nogo‐B in liver cancer. In response to hypoxia, expression of Nogo‐B significantly increased in HCC tissues and cells. The distal hypoxia‐responsive element in the promoter was essential for transcriptional activation of Nogo‐B under hypoxic conditions, which is the specific site for hypoxia inducible factor‐1α (HIF‐1α) binding. In addition, Nogo‐B expression was associated with c‐Fos expression in HCC tissues. Nogo‐B expression was induced by c‐Fos, yet inhibited by a dominant negative mutant A‐Fos. Deletion and mutation analysis of the predicted activator protein‐1 binding sites revealed that functional element mediated the induction of Nogo‐B promoter activity, which was confirmed by ChIP. These results indicate that HIF‐1α and c‐Fos induce the expression of Nogo‐B depending on tumor microenvironments, such as hypoxia and low levels of nutrients, and play a role in upregulation of Nogo‐B in tumor angiogenesis.
Our results indicated that, although Nogo‐B played a complementary and parallel role in tumor angiogenesis to that of vascular endothelial growth factor, they shared a common induction mechanism of hypoxia inducible factor‐1 and activator protein‐1 activation, which might provide novel treatment options in hepatocellular carcinoma.</description><subject>Analysis</subject><subject>Angiogenesis</subject><subject>Animals</subject><subject>Binding sites</subject><subject>Binding Sites - genetics</subject><subject>Biotechnology</subject><subject>Carcinoma, Hepatocellular - blood supply</subject><subject>Carcinoma, Hepatocellular - metabolism</subject><subject>c‐Fos</subject><subject>Gene Deletion</subject><subject>Gene regulation</subject><subject>Hepatic Artery</subject><subject>Hepatocellular carcinoma</subject><subject>Hepatoma</subject><subject>HIF‐1α</subject><subject>Humans</subject><subject>Hypoxia</subject><subject>Hypoxia-Inducible Factor 1 - metabolism</subject><subject>Laboratory animals</subject><subject>Ligation</subject><subject>Liver cancer</subject><subject>Liver Neoplasms - blood supply</subject><subject>Liver Neoplasms - metabolism</subject><subject>Male</subject><subject>Microenvironments</subject><subject>Mutagenesis</subject><subject>Mutation</subject><subject>Neoplasm Proteins - genetics</subject><subject>Neoplasm Proteins - metabolism</subject><subject>Neovascularization, Pathologic</subject><subject>Nogo protein</subject><subject>Nogo Proteins - genetics</subject><subject>Nogo Proteins - metabolism</subject><subject>Nogo‐B</subject><subject>Original</subject><subject>Plasmids</subject><subject>Promoter Regions, Genetic</subject><subject>Protein binding</subject><subject>Proteins</subject><subject>Proto-Oncogene Proteins c-fyn - metabolism</subject><subject>Random Allocation</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Regulatory sequences</subject><subject>Transcription activation</subject><subject>Transcription Factor AP-1 - genetics</subject><subject>Transcription Factor AP-1 - metabolism</subject><subject>Transcriptional Activation</subject><subject>Tumor Hypoxia - physiology</subject><subject>Tumor Microenvironment</subject><subject>Tumors</subject><subject>Up-Regulation</subject><subject>Vascular endothelial growth factor</subject><issn>1347-9032</issn><issn>1349-7006</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp9ks9u1DAQxi0EoqVw4AWQJU4csvXEjr25IG1X_JMqOEDPluOMd10ldnCSwt54BJ6RJ8HdLYVKgH2wPd9vvrGtIeQpsAXkcWrNuABRC7hHjoGLulCMyfv7vSpqxssj8mgcLxnjMlMPyRHnteSygmMSLoaEm7kzk4-BRkffx0388e37GW12dLsb4ldvqA_tbH3TIXXGTjFlHagJLc0nf2VyhA4pTujDXvGBbnHIYYtdl60TtSZZH2JvHpMHznQjPrlZT8jF61ef1m-L8w9v3q1X54WtZAmFZbV0YHmtWmzAtKUFoRwT0hjGnGmlAMGwBSaEsEahwCznt1XIAavG8hPy8uA7zE2PrcUwJdPpIfnepJ2Oxuu7SvBbvYlXellWvFQyGzy_MUjx84zjpC_jnEK-sy6resnZEkr-f0qoStYMxG9qYzrUPriYS9rej1avFDAlONTXXou_UHm22HsbAzqf43cSXhwSbIrjmNDdPg-Yvu4LnftC7_sis8_-_I9b8lcjZOD0AHzJVXb_dtLr1ceD5U8WOcQf</recordid><startdate>202107</startdate><enddate>202107</enddate><creator>Han, Dingding</creator><creator>Yang, Penggao</creator><creator>Qin, Bo</creator><creator>Ji, Guoqing</creator><creator>Wu, Yanhua</creator><creator>Yu, Long</creator><creator>Zhang, Hong</creator><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</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>8FE</scope><scope>8FH</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>GNUQQ</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0003-0963-6286</orcidid></search><sort><creationdate>202107</creationdate><title>Upregulation of Nogo‐B by hypoxia inducible factor‐1 and activator protein‐1 in hepatocellular carcinoma</title><author>Han, Dingding ; Yang, Penggao ; Qin, Bo ; Ji, Guoqing ; Wu, Yanhua ; Yu, Long ; Zhang, Hong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5621-c096f1c397deb1ad2c147f046aa00fad64140ed10444ca7e4e47f6495e31e5bc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Analysis</topic><topic>Angiogenesis</topic><topic>Animals</topic><topic>Binding sites</topic><topic>Binding Sites - genetics</topic><topic>Biotechnology</topic><topic>Carcinoma, Hepatocellular - blood supply</topic><topic>Carcinoma, Hepatocellular - metabolism</topic><topic>c‐Fos</topic><topic>Gene Deletion</topic><topic>Gene regulation</topic><topic>Hepatic Artery</topic><topic>Hepatocellular carcinoma</topic><topic>Hepatoma</topic><topic>HIF‐1α</topic><topic>Humans</topic><topic>Hypoxia</topic><topic>Hypoxia-Inducible Factor 1 - metabolism</topic><topic>Laboratory animals</topic><topic>Ligation</topic><topic>Liver cancer</topic><topic>Liver Neoplasms - blood supply</topic><topic>Liver Neoplasms - metabolism</topic><topic>Male</topic><topic>Microenvironments</topic><topic>Mutagenesis</topic><topic>Mutation</topic><topic>Neoplasm Proteins - genetics</topic><topic>Neoplasm Proteins - metabolism</topic><topic>Neovascularization, Pathologic</topic><topic>Nogo protein</topic><topic>Nogo Proteins - genetics</topic><topic>Nogo Proteins - metabolism</topic><topic>Nogo‐B</topic><topic>Original</topic><topic>Plasmids</topic><topic>Promoter Regions, Genetic</topic><topic>Protein binding</topic><topic>Proteins</topic><topic>Proto-Oncogene Proteins c-fyn - metabolism</topic><topic>Random Allocation</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Regulatory sequences</topic><topic>Transcription activation</topic><topic>Transcription Factor AP-1 - genetics</topic><topic>Transcription Factor AP-1 - metabolism</topic><topic>Transcriptional Activation</topic><topic>Tumor Hypoxia - physiology</topic><topic>Tumor Microenvironment</topic><topic>Tumors</topic><topic>Up-Regulation</topic><topic>Vascular endothelial growth factor</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Han, Dingding</creatorcontrib><creatorcontrib>Yang, Penggao</creatorcontrib><creatorcontrib>Qin, Bo</creatorcontrib><creatorcontrib>Ji, Guoqing</creatorcontrib><creatorcontrib>Wu, Yanhua</creatorcontrib><creatorcontrib>Yu, Long</creatorcontrib><creatorcontrib>Zhang, Hong</creatorcontrib><collection>Wiley Online Library Open Access</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 SciTech Collection</collection><collection>ProQuest Natural Science Collection</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>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Biological Science Collection</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 China</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cancer science</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Han, Dingding</au><au>Yang, Penggao</au><au>Qin, Bo</au><au>Ji, Guoqing</au><au>Wu, Yanhua</au><au>Yu, Long</au><au>Zhang, Hong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Upregulation of Nogo‐B by hypoxia inducible factor‐1 and activator protein‐1 in hepatocellular carcinoma</atitle><jtitle>Cancer science</jtitle><addtitle>Cancer Sci</addtitle><date>2021-07</date><risdate>2021</risdate><volume>112</volume><issue>7</issue><spage>2728</spage><epage>2738</epage><pages>2728-2738</pages><issn>1347-9032</issn><eissn>1349-7006</eissn><abstract>Nogo‐B is an important regulator of tumor angiogenesis. Expression of Nogo‐B is remarkably upregulated in multiple tumor types, especially hepatocellular carcinoma (HCC). Here, we show the transcriptional regulation mechanisms of Nogo‐B in liver cancer. In response to hypoxia, expression of Nogo‐B significantly increased in HCC tissues and cells. The distal hypoxia‐responsive element in the promoter was essential for transcriptional activation of Nogo‐B under hypoxic conditions, which is the specific site for hypoxia inducible factor‐1α (HIF‐1α) binding. In addition, Nogo‐B expression was associated with c‐Fos expression in HCC tissues. Nogo‐B expression was induced by c‐Fos, yet inhibited by a dominant negative mutant A‐Fos. Deletion and mutation analysis of the predicted activator protein‐1 binding sites revealed that functional element mediated the induction of Nogo‐B promoter activity, which was confirmed by ChIP. These results indicate that HIF‐1α and c‐Fos induce the expression of Nogo‐B depending on tumor microenvironments, such as hypoxia and low levels of nutrients, and play a role in upregulation of Nogo‐B in tumor angiogenesis.
Our results indicated that, although Nogo‐B played a complementary and parallel role in tumor angiogenesis to that of vascular endothelial growth factor, they shared a common induction mechanism of hypoxia inducible factor‐1 and activator protein‐1 activation, which might provide novel treatment options in hepatocellular carcinoma.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>33963651</pmid><doi>10.1111/cas.14941</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0003-0963-6286</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Analysis Angiogenesis Animals Binding sites Binding Sites - genetics Biotechnology Carcinoma, Hepatocellular - blood supply Carcinoma, Hepatocellular - metabolism c‐Fos Gene Deletion Gene regulation Hepatic Artery Hepatocellular carcinoma Hepatoma HIF‐1α Humans Hypoxia Hypoxia-Inducible Factor 1 - metabolism Laboratory animals Ligation Liver cancer Liver Neoplasms - blood supply Liver Neoplasms - metabolism Male Microenvironments Mutagenesis Mutation Neoplasm Proteins - genetics Neoplasm Proteins - metabolism Neovascularization, Pathologic Nogo protein Nogo Proteins - genetics Nogo Proteins - metabolism Nogo‐B Original Plasmids Promoter Regions, Genetic Protein binding Proteins Proto-Oncogene Proteins c-fyn - metabolism Random Allocation Rats Rats, Sprague-Dawley Regulatory sequences Transcription activation Transcription Factor AP-1 - genetics Transcription Factor AP-1 - metabolism Transcriptional Activation Tumor Hypoxia - physiology Tumor Microenvironment Tumors Up-Regulation Vascular endothelial growth factor |
| title | Upregulation of Nogo‐B by hypoxia inducible factor‐1 and activator protein‐1 in hepatocellular carcinoma |
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