HMGB1/RAGE axis mediates the apoptosis, invasion, autophagy, and angiogenesis of the renal cell carcinoma
High mobility group box 1 protein (HMGB1) is a sort of non-histone protein in chromatin, which plays an important role in tumor proliferation, invasion, and immune escape. HMGB1-RAGE (receptor for advanced glycation end products) interactions have been reported to be important in a number of cancers...
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| Veröffentlicht in: | OncoTargets and therapy 2018, Vol.11, p.4501-4510 |
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| creator | Wu, Cun-Zao Zheng, Jian-Jian Bai, Yong-Heng Xia, Peng Zhang, Hai-Cong Guo, Yong |
| description | High mobility group box 1 protein (HMGB1) is a sort of non-histone protein in chromatin, which plays an important role in tumor proliferation, invasion, and immune escape. HMGB1-RAGE (receptor for advanced glycation end products) interactions have been reported to be important in a number of cancers.
CCK8, flow cytometry and qRT-PCR were used to detected cell viability, apoptosis and gene expression, respectively.
In the present study, we demonstrated that HMGB1/RAGE axis regulated the cell proliferation, apoptosis, and invasion of the renal cell carcinoma (RCC). Further, we discovered that HMGB1/RAGE axis increased the expression of autophagic proteins LC3 and Beclin-1 in RCC. Finally, we used a coculture model of human umbilical vein endothelial cells with RCC cell lines to find out that HMGB1 also increased the expression of VEGF and VEGFR2 in human umbilical vein endothelial cells. An in vivo study further confirmed that HMGB1 knockdown inhibited RCC tumor growth.
Our results illustrated that HMGB1/RAGE axis mediated RCC cell viability, apoptosis, invasion, autophagy, and angiogenesis, which provides a novel theoretical basis for using HMGB1 as the target in RCC. |
| doi_str_mv | 10.2147/OTT.S167197 |
| format | Article |
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CCK8, flow cytometry and qRT-PCR were used to detected cell viability, apoptosis and gene expression, respectively.
In the present study, we demonstrated that HMGB1/RAGE axis regulated the cell proliferation, apoptosis, and invasion of the renal cell carcinoma (RCC). Further, we discovered that HMGB1/RAGE axis increased the expression of autophagic proteins LC3 and Beclin-1 in RCC. Finally, we used a coculture model of human umbilical vein endothelial cells with RCC cell lines to find out that HMGB1 also increased the expression of VEGF and VEGFR2 in human umbilical vein endothelial cells. An in vivo study further confirmed that HMGB1 knockdown inhibited RCC tumor growth.
Our results illustrated that HMGB1/RAGE axis mediated RCC cell viability, apoptosis, invasion, autophagy, and angiogenesis, which provides a novel theoretical basis for using HMGB1 as the target in RCC.</description><identifier>ISSN: 1178-6930</identifier><identifier>EISSN: 1178-6930</identifier><identifier>DOI: 10.2147/OTT.S167197</identifier><identifier>PMID: 30122942</identifier><language>eng</language><publisher>New Zealand: Taylor & Francis Ltd</publisher><subject>Alzheimer's disease ; Angiogenesis ; Apoptosis ; Autophagy ; Bladder cancer ; Bone cancer ; Cell adhesion & migration ; Cell viability ; Chemotherapy ; Flow cytometry ; Hospitals ; Inflammation ; Kidney cancer ; Laboratories ; Ligands ; Medical prognosis ; Metastasis ; Original Research ; Proteins ; Radiation therapy ; Renal cell carcinoma ; Tumors</subject><ispartof>OncoTargets and therapy, 2018, Vol.11, p.4501-4510</ispartof><rights>2018. This work is licensed under https://creativecommons.org/licenses/by-nc/3.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2018 Wu et al. This work is published and licensed by Dove Medical Press Limited 2018</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3907-608c2394f0c410257df32a422db3d2bea61471975a4e1e311fe102ff071c9ce83</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6078191/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6078191/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,3849,4010,27902,27903,27904,53769,53771</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30122942$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wu, Cun-Zao</creatorcontrib><creatorcontrib>Zheng, Jian-Jian</creatorcontrib><creatorcontrib>Bai, Yong-Heng</creatorcontrib><creatorcontrib>Xia, Peng</creatorcontrib><creatorcontrib>Zhang, Hai-Cong</creatorcontrib><creatorcontrib>Guo, Yong</creatorcontrib><title>HMGB1/RAGE axis mediates the apoptosis, invasion, autophagy, and angiogenesis of the renal cell carcinoma</title><title>OncoTargets and therapy</title><addtitle>Onco Targets Ther</addtitle><description>High mobility group box 1 protein (HMGB1) is a sort of non-histone protein in chromatin, which plays an important role in tumor proliferation, invasion, and immune escape. HMGB1-RAGE (receptor for advanced glycation end products) interactions have been reported to be important in a number of cancers.
CCK8, flow cytometry and qRT-PCR were used to detected cell viability, apoptosis and gene expression, respectively.
In the present study, we demonstrated that HMGB1/RAGE axis regulated the cell proliferation, apoptosis, and invasion of the renal cell carcinoma (RCC). Further, we discovered that HMGB1/RAGE axis increased the expression of autophagic proteins LC3 and Beclin-1 in RCC. Finally, we used a coculture model of human umbilical vein endothelial cells with RCC cell lines to find out that HMGB1 also increased the expression of VEGF and VEGFR2 in human umbilical vein endothelial cells. An in vivo study further confirmed that HMGB1 knockdown inhibited RCC tumor growth.
Our results illustrated that HMGB1/RAGE axis mediated RCC cell viability, apoptosis, invasion, autophagy, and angiogenesis, which provides a novel theoretical basis for using HMGB1 as the target in RCC.</description><subject>Alzheimer's disease</subject><subject>Angiogenesis</subject><subject>Apoptosis</subject><subject>Autophagy</subject><subject>Bladder cancer</subject><subject>Bone cancer</subject><subject>Cell adhesion & migration</subject><subject>Cell viability</subject><subject>Chemotherapy</subject><subject>Flow cytometry</subject><subject>Hospitals</subject><subject>Inflammation</subject><subject>Kidney cancer</subject><subject>Laboratories</subject><subject>Ligands</subject><subject>Medical prognosis</subject><subject>Metastasis</subject><subject>Original Research</subject><subject>Proteins</subject><subject>Radiation therapy</subject><subject>Renal cell carcinoma</subject><subject>Tumors</subject><issn>1178-6930</issn><issn>1178-6930</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpdkUtLLDEQhYMovlfuLw1uBB3Ny05nI6joKCiCjutQk66eicwkbdIt-u-NOorXRSoF9dWhDoeQHUYPOZPq6G40OnxgpWJaLZF1xlQ1KLWgy7_6NbKR0hOlZVlxuUrWBGWca8nXibu6HZ6xo_vT4UUBry4Vc6wddJiKbooFtKHtQnLpoHD-BZIL_qCAvgvtFCZvufV1fhMXJugxY0VoPvciepgVFme5QLTOhzlskZUGZgm3F_8meby8GJ1fDW7uhtfnpzcDKzRVg5JWlgstG2olo_xY1Y3gIDmvx6LmY4Qye85Wj0EiQ8FYgxlrGqqY1RYrsUlOvnTbfpzNWPRdhJlpo5tDfDMBnPl_4t3UTMKLKamqmGZZYG8hEMNzj6kzc5c-vIDH0CfDqaZCSK50Rnf_oE-hj9l7prjkUkhNaab2vygbQ0oRm59jGDUfEZocoVlEmOl_v-__Yb8zE-9WyZYi</recordid><startdate>2018</startdate><enddate>2018</enddate><creator>Wu, Cun-Zao</creator><creator>Zheng, Jian-Jian</creator><creator>Bai, Yong-Heng</creator><creator>Xia, Peng</creator><creator>Zhang, Hai-Cong</creator><creator>Guo, Yong</creator><general>Taylor & Francis Ltd</general><general>Dove Medical Press</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</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>GUQSH</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>2018</creationdate><title>HMGB1/RAGE axis mediates the apoptosis, invasion, autophagy, and angiogenesis of the renal cell carcinoma</title><author>Wu, Cun-Zao ; Zheng, Jian-Jian ; Bai, Yong-Heng ; Xia, Peng ; Zhang, Hai-Cong ; Guo, Yong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3907-608c2394f0c410257df32a422db3d2bea61471975a4e1e311fe102ff071c9ce83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Alzheimer's disease</topic><topic>Angiogenesis</topic><topic>Apoptosis</topic><topic>Autophagy</topic><topic>Bladder cancer</topic><topic>Bone cancer</topic><topic>Cell adhesion & migration</topic><topic>Cell viability</topic><topic>Chemotherapy</topic><topic>Flow cytometry</topic><topic>Hospitals</topic><topic>Inflammation</topic><topic>Kidney cancer</topic><topic>Laboratories</topic><topic>Ligands</topic><topic>Medical prognosis</topic><topic>Metastasis</topic><topic>Original Research</topic><topic>Proteins</topic><topic>Radiation therapy</topic><topic>Renal cell carcinoma</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wu, Cun-Zao</creatorcontrib><creatorcontrib>Zheng, Jian-Jian</creatorcontrib><creatorcontrib>Bai, Yong-Heng</creatorcontrib><creatorcontrib>Xia, Peng</creatorcontrib><creatorcontrib>Zhang, Hai-Cong</creatorcontrib><creatorcontrib>Guo, Yong</creatorcontrib><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>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>Research Library (Alumni Edition)</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>Research Library Prep</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>Research Library</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</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>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>OncoTargets and therapy</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wu, Cun-Zao</au><au>Zheng, Jian-Jian</au><au>Bai, Yong-Heng</au><au>Xia, Peng</au><au>Zhang, Hai-Cong</au><au>Guo, Yong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>HMGB1/RAGE axis mediates the apoptosis, invasion, autophagy, and angiogenesis of the renal cell carcinoma</atitle><jtitle>OncoTargets and therapy</jtitle><addtitle>Onco Targets Ther</addtitle><date>2018</date><risdate>2018</risdate><volume>11</volume><spage>4501</spage><epage>4510</epage><pages>4501-4510</pages><issn>1178-6930</issn><eissn>1178-6930</eissn><abstract>High mobility group box 1 protein (HMGB1) is a sort of non-histone protein in chromatin, which plays an important role in tumor proliferation, invasion, and immune escape. HMGB1-RAGE (receptor for advanced glycation end products) interactions have been reported to be important in a number of cancers.
CCK8, flow cytometry and qRT-PCR were used to detected cell viability, apoptosis and gene expression, respectively.
In the present study, we demonstrated that HMGB1/RAGE axis regulated the cell proliferation, apoptosis, and invasion of the renal cell carcinoma (RCC). Further, we discovered that HMGB1/RAGE axis increased the expression of autophagic proteins LC3 and Beclin-1 in RCC. Finally, we used a coculture model of human umbilical vein endothelial cells with RCC cell lines to find out that HMGB1 also increased the expression of VEGF and VEGFR2 in human umbilical vein endothelial cells. An in vivo study further confirmed that HMGB1 knockdown inhibited RCC tumor growth.
Our results illustrated that HMGB1/RAGE axis mediated RCC cell viability, apoptosis, invasion, autophagy, and angiogenesis, which provides a novel theoretical basis for using HMGB1 as the target in RCC.</abstract><cop>New Zealand</cop><pub>Taylor & Francis Ltd</pub><pmid>30122942</pmid><doi>10.2147/OTT.S167197</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| source | Taylor & Francis Open Access; DOVE Medical Press Journals; EZB-FREE-00999 freely available EZB journals; PubMed Central; PubMed Central Open Access |
| subjects | Alzheimer's disease Angiogenesis Apoptosis Autophagy Bladder cancer Bone cancer Cell adhesion & migration Cell viability Chemotherapy Flow cytometry Hospitals Inflammation Kidney cancer Laboratories Ligands Medical prognosis Metastasis Original Research Proteins Radiation therapy Renal cell carcinoma Tumors |
| title | HMGB1/RAGE axis mediates the apoptosis, invasion, autophagy, and angiogenesis of the renal cell carcinoma |
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