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EZH2 suppression in glioblastoma shifts microglia toward M1 phenotype in tumor microenvironment
Glioblastoma multiforme (GBM) induces tumor immunosuppression through interacting with tumor-infiltrating microglia or macrophages (TAMs) with an unclear pathogenesis. Enhancer of zeste homolog 2 (EZH2) is abundant in GBM samples and cell lines and is involved in GBM proliferation, cell cycle, and i...
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Published in: | Journal of neuroinflammation 2017-11, Vol.14 (1), p.220-220, Article 220 |
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description | Glioblastoma multiforme (GBM) induces tumor immunosuppression through interacting with tumor-infiltrating microglia or macrophages (TAMs) with an unclear pathogenesis. Enhancer of zeste homolog 2 (EZH2) is abundant in GBM samples and cell lines and is involved in GBM proliferation, cell cycle, and invasion, whereas its association with innate immune response is not yet reported. Herein, the aim of this study was to investigate the role of EZH2 in GBM immune.
Co-culturing models of human/murine GBM cells with PBMC-derived macrophages/primary microglia were employed. EZH2 mRNAs and function were suppressed by siEZH2 and DZNep. Real-time PCR and flow cytometry were used to determine levels of microglia/macrophages markers. The fluorescence-labeled latex beads and flow cytometry were utilized to evaluate phagocytic abilities of microglia. CCK8 assay was performed to assess microglia proliferation.
EZH2 inhibition led to significant reduction of TGFβ1-3 and IL10 and elevation of IL1β and IL6 in human and murine GBM cells. More importantly, EZH2 suppression in GBM cells resulted in significant increase of M1 markers (TNFα and iNOS) and decrease of a pool of M2 markers in murine microglia. The proportion of CD206
cells was decreased in PBMC-derived macrophages as co-incubated with EZH2-inhibited GBM cells. Functional researches showed that phagocytic capacities of microglia were significantly ameliorated after EZH2 inhibition in co-culturing GBM cells and microglia proliferation was declined after addition of TGFβ2 antibodies to co-incubated GBM cells with EZH2 inhibition. Besides, we found that EZH2 suppression in GBM cells enhanced co-culturing microglia engulfment through activation of iNOS.
Our data demonstrates that EZH2 participates in GBM-induced immune deficient and EZH2 suppression in GBM can remodel microglia immune functions, which is beneficial for understanding GBM pathogenesis and suggests potential targets for therapeutic approaches. |
doi_str_mv | 10.1186/s12974-017-0993-4 |
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Co-culturing models of human/murine GBM cells with PBMC-derived macrophages/primary microglia were employed. EZH2 mRNAs and function were suppressed by siEZH2 and DZNep. Real-time PCR and flow cytometry were used to determine levels of microglia/macrophages markers. The fluorescence-labeled latex beads and flow cytometry were utilized to evaluate phagocytic abilities of microglia. CCK8 assay was performed to assess microglia proliferation.
EZH2 inhibition led to significant reduction of TGFβ1-3 and IL10 and elevation of IL1β and IL6 in human and murine GBM cells. More importantly, EZH2 suppression in GBM cells resulted in significant increase of M1 markers (TNFα and iNOS) and decrease of a pool of M2 markers in murine microglia. The proportion of CD206
cells was decreased in PBMC-derived macrophages as co-incubated with EZH2-inhibited GBM cells. Functional researches showed that phagocytic capacities of microglia were significantly ameliorated after EZH2 inhibition in co-culturing GBM cells and microglia proliferation was declined after addition of TGFβ2 antibodies to co-incubated GBM cells with EZH2 inhibition. Besides, we found that EZH2 suppression in GBM cells enhanced co-culturing microglia engulfment through activation of iNOS.
Our data demonstrates that EZH2 participates in GBM-induced immune deficient and EZH2 suppression in GBM can remodel microglia immune functions, which is beneficial for understanding GBM pathogenesis and suggests potential targets for therapeutic approaches.</description><identifier>ISSN: 1742-2094</identifier><identifier>EISSN: 1742-2094</identifier><identifier>DOI: 10.1186/s12974-017-0993-4</identifier><identifier>PMID: 29132376</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Analysis ; Angiogenesis ; Animal models ; Apoptosis ; Brain cancer ; Cancer ; Cell cycle ; Cell growth ; Cell proliferation ; Cytokines ; Enhancer of zeste homolog 2 (EZH2) ; Flow cytometry ; Genetic aspects ; Genotype & phenotype ; Glioblastoma ; Glioblastomas ; Growth factors ; Immune response ; Immunosuppression ; Immunotherapy ; Innate immunity ; Interleukin 1 ; Interleukin 10 ; Interleukin 6 ; Latex beads ; Macrophages ; Medical prognosis ; Microglia ; Nitric oxide ; Nitric-oxide synthase ; Peripheral blood mononuclear cells ; Phagocytes ; Phenotypes ; Polarization ; Transforming growth factor-b1 ; Transforming growth factors ; Tumor necrosis factor-α ; Tumors</subject><ispartof>Journal of neuroinflammation, 2017-11, Vol.14 (1), p.220-220, Article 220</ispartof><rights>COPYRIGHT 2017 BioMed Central Ltd.</rights><rights>Copyright BioMed Central 2017</rights><rights>The Author(s). 2017</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c560t-54b5aac59408fbedc3b9740cb0db53c4f1c81ef65783bf3961196b274aa44d4e3</citedby><cites>FETCH-LOGICAL-c560t-54b5aac59408fbedc3b9740cb0db53c4f1c81ef65783bf3961196b274aa44d4e3</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/PMC5684749/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/1972444713?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,27924,27925,37012,37013,44590,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29132376$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yin, Yatao</creatorcontrib><creatorcontrib>Qiu, Shuwei</creatorcontrib><creatorcontrib>Li, Xiangpen</creatorcontrib><creatorcontrib>Huang, Bo</creatorcontrib><creatorcontrib>Xu, Yun</creatorcontrib><creatorcontrib>Peng, Ying</creatorcontrib><title>EZH2 suppression in glioblastoma shifts microglia toward M1 phenotype in tumor microenvironment</title><title>Journal of neuroinflammation</title><addtitle>J Neuroinflammation</addtitle><description>Glioblastoma multiforme (GBM) induces tumor immunosuppression through interacting with tumor-infiltrating microglia or macrophages (TAMs) with an unclear pathogenesis. Enhancer of zeste homolog 2 (EZH2) is abundant in GBM samples and cell lines and is involved in GBM proliferation, cell cycle, and invasion, whereas its association with innate immune response is not yet reported. Herein, the aim of this study was to investigate the role of EZH2 in GBM immune.
Co-culturing models of human/murine GBM cells with PBMC-derived macrophages/primary microglia were employed. EZH2 mRNAs and function were suppressed by siEZH2 and DZNep. Real-time PCR and flow cytometry were used to determine levels of microglia/macrophages markers. The fluorescence-labeled latex beads and flow cytometry were utilized to evaluate phagocytic abilities of microglia. CCK8 assay was performed to assess microglia proliferation.
EZH2 inhibition led to significant reduction of TGFβ1-3 and IL10 and elevation of IL1β and IL6 in human and murine GBM cells. More importantly, EZH2 suppression in GBM cells resulted in significant increase of M1 markers (TNFα and iNOS) and decrease of a pool of M2 markers in murine microglia. The proportion of CD206
cells was decreased in PBMC-derived macrophages as co-incubated with EZH2-inhibited GBM cells. Functional researches showed that phagocytic capacities of microglia were significantly ameliorated after EZH2 inhibition in co-culturing GBM cells and microglia proliferation was declined after addition of TGFβ2 antibodies to co-incubated GBM cells with EZH2 inhibition. Besides, we found that EZH2 suppression in GBM cells enhanced co-culturing microglia engulfment through activation of iNOS.
Our data demonstrates that EZH2 participates in GBM-induced immune deficient and EZH2 suppression in GBM can remodel microglia immune functions, which is beneficial for understanding GBM pathogenesis and suggests potential targets for therapeutic approaches.</description><subject>Analysis</subject><subject>Angiogenesis</subject><subject>Animal models</subject><subject>Apoptosis</subject><subject>Brain cancer</subject><subject>Cancer</subject><subject>Cell cycle</subject><subject>Cell growth</subject><subject>Cell proliferation</subject><subject>Cytokines</subject><subject>Enhancer of zeste homolog 2 (EZH2)</subject><subject>Flow cytometry</subject><subject>Genetic aspects</subject><subject>Genotype & phenotype</subject><subject>Glioblastoma</subject><subject>Glioblastomas</subject><subject>Growth factors</subject><subject>Immune response</subject><subject>Immunosuppression</subject><subject>Immunotherapy</subject><subject>Innate immunity</subject><subject>Interleukin 1</subject><subject>Interleukin 10</subject><subject>Interleukin 6</subject><subject>Latex beads</subject><subject>Macrophages</subject><subject>Medical prognosis</subject><subject>Microglia</subject><subject>Nitric oxide</subject><subject>Nitric-oxide synthase</subject><subject>Peripheral blood mononuclear cells</subject><subject>Phagocytes</subject><subject>Phenotypes</subject><subject>Polarization</subject><subject>Transforming growth factor-b1</subject><subject>Transforming growth factors</subject><subject>Tumor necrosis factor-α</subject><subject>Tumors</subject><issn>1742-2094</issn><issn>1742-2094</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNptUk1v1DAUjBCIlsIP4IIiceGS4o9ne3NBqqrSViriAhculu3Yu14ldrCTov57nKaULkI-2PKbmed5nqp6i9Epxhv-MWPSCmgQFg1qW9rAs-oYCyANQS08f3I-ql7lvEeIEsbJy-qItJgSKvhxJS9-XJE6z-OYbM4-htqHetv7qHuVpzioOu-8m3I9eJNiKah6ir9U6uovuB53NsTpbrQLaZqHmFaYDbc-xTDYML2uXjjVZ_vmYT-pvn---HZ-1dx8vbw-P7tpDONoahhoppRhLaCN07YzVBdnyGjUaUYNOGw22DrOxIZqR1uOccs1EaAUQAeWnlTXq24X1V6OyQ8q3cmovLy_iGkrVZq86a1kFAmjGHDQCCjlresUIKQoA2ysQUXr06o1znoobyk2kuoPRA8rwe_kNt5KxjcgoC0CHx4EUvw52zzJwWdj-14FG-csy9uBCAxUFOj7f6D7OKdQRlVQggCAwPQvaquKAR9cLH3NIirPihEkEGZL29P_oMrqbPmWGKzz5f6AgFdC-bOck3WPHjGSS8LkmjBZEiaXhEkonHdPh_PI-BMp-hs9-Mt3</recordid><startdate>20171113</startdate><enddate>20171113</enddate><creator>Yin, Yatao</creator><creator>Qiu, Shuwei</creator><creator>Li, Xiangpen</creator><creator>Huang, Bo</creator><creator>Xu, Yun</creator><creator>Peng, Ying</creator><general>BioMed Central Ltd</general><general>BioMed Central</general><general>BMC</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7T5</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20171113</creationdate><title>EZH2 suppression in glioblastoma shifts microglia toward M1 phenotype in tumor microenvironment</title><author>Yin, Yatao ; Qiu, Shuwei ; Li, Xiangpen ; Huang, Bo ; Xu, Yun ; Peng, Ying</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c560t-54b5aac59408fbedc3b9740cb0db53c4f1c81ef65783bf3961196b274aa44d4e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Analysis</topic><topic>Angiogenesis</topic><topic>Animal models</topic><topic>Apoptosis</topic><topic>Brain cancer</topic><topic>Cancer</topic><topic>Cell cycle</topic><topic>Cell growth</topic><topic>Cell proliferation</topic><topic>Cytokines</topic><topic>Enhancer of zeste homolog 2 (EZH2)</topic><topic>Flow cytometry</topic><topic>Genetic aspects</topic><topic>Genotype & phenotype</topic><topic>Glioblastoma</topic><topic>Glioblastomas</topic><topic>Growth factors</topic><topic>Immune response</topic><topic>Immunosuppression</topic><topic>Immunotherapy</topic><topic>Innate immunity</topic><topic>Interleukin 1</topic><topic>Interleukin 10</topic><topic>Interleukin 6</topic><topic>Latex beads</topic><topic>Macrophages</topic><topic>Medical prognosis</topic><topic>Microglia</topic><topic>Nitric oxide</topic><topic>Nitric-oxide synthase</topic><topic>Peripheral blood mononuclear cells</topic><topic>Phagocytes</topic><topic>Phenotypes</topic><topic>Polarization</topic><topic>Transforming growth factor-b1</topic><topic>Transforming growth factors</topic><topic>Tumor necrosis factor-α</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yin, Yatao</creatorcontrib><creatorcontrib>Qiu, Shuwei</creatorcontrib><creatorcontrib>Li, Xiangpen</creatorcontrib><creatorcontrib>Huang, Bo</creatorcontrib><creatorcontrib>Xu, Yun</creatorcontrib><creatorcontrib>Peng, Ying</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</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)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>AUTh Library subscriptions: ProQuest Central</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>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>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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>Directory of Open Access Journals</collection><jtitle>Journal of neuroinflammation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yin, Yatao</au><au>Qiu, Shuwei</au><au>Li, Xiangpen</au><au>Huang, Bo</au><au>Xu, Yun</au><au>Peng, Ying</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>EZH2 suppression in glioblastoma shifts microglia toward M1 phenotype in tumor microenvironment</atitle><jtitle>Journal of neuroinflammation</jtitle><addtitle>J Neuroinflammation</addtitle><date>2017-11-13</date><risdate>2017</risdate><volume>14</volume><issue>1</issue><spage>220</spage><epage>220</epage><pages>220-220</pages><artnum>220</artnum><issn>1742-2094</issn><eissn>1742-2094</eissn><abstract>Glioblastoma multiforme (GBM) induces tumor immunosuppression through interacting with tumor-infiltrating microglia or macrophages (TAMs) with an unclear pathogenesis. Enhancer of zeste homolog 2 (EZH2) is abundant in GBM samples and cell lines and is involved in GBM proliferation, cell cycle, and invasion, whereas its association with innate immune response is not yet reported. Herein, the aim of this study was to investigate the role of EZH2 in GBM immune.
Co-culturing models of human/murine GBM cells with PBMC-derived macrophages/primary microglia were employed. EZH2 mRNAs and function were suppressed by siEZH2 and DZNep. Real-time PCR and flow cytometry were used to determine levels of microglia/macrophages markers. The fluorescence-labeled latex beads and flow cytometry were utilized to evaluate phagocytic abilities of microglia. CCK8 assay was performed to assess microglia proliferation.
EZH2 inhibition led to significant reduction of TGFβ1-3 and IL10 and elevation of IL1β and IL6 in human and murine GBM cells. More importantly, EZH2 suppression in GBM cells resulted in significant increase of M1 markers (TNFα and iNOS) and decrease of a pool of M2 markers in murine microglia. The proportion of CD206
cells was decreased in PBMC-derived macrophages as co-incubated with EZH2-inhibited GBM cells. Functional researches showed that phagocytic capacities of microglia were significantly ameliorated after EZH2 inhibition in co-culturing GBM cells and microglia proliferation was declined after addition of TGFβ2 antibodies to co-incubated GBM cells with EZH2 inhibition. Besides, we found that EZH2 suppression in GBM cells enhanced co-culturing microglia engulfment through activation of iNOS.
Our data demonstrates that EZH2 participates in GBM-induced immune deficient and EZH2 suppression in GBM can remodel microglia immune functions, which is beneficial for understanding GBM pathogenesis and suggests potential targets for therapeutic approaches.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>29132376</pmid><doi>10.1186/s12974-017-0993-4</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Analysis Angiogenesis Animal models Apoptosis Brain cancer Cancer Cell cycle Cell growth Cell proliferation Cytokines Enhancer of zeste homolog 2 (EZH2) Flow cytometry Genetic aspects Genotype & phenotype Glioblastoma Glioblastomas Growth factors Immune response Immunosuppression Immunotherapy Innate immunity Interleukin 1 Interleukin 10 Interleukin 6 Latex beads Macrophages Medical prognosis Microglia Nitric oxide Nitric-oxide synthase Peripheral blood mononuclear cells Phagocytes Phenotypes Polarization Transforming growth factor-b1 Transforming growth factors Tumor necrosis factor-α Tumors |
title | EZH2 suppression in glioblastoma shifts microglia toward M1 phenotype in tumor microenvironment |
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