PTPRM methylation induced by FN1 promotes the development of glioblastoma by activating STAT3 signalling
The phosphorylation of signal transducer and activator of transcription protein 3 (STAT3) is up-regulated in glioblastoma (GBM) cells and is regulated by protein tyrosine phosphatase receptor type M (PTPRM). Fibronectin-1 (FN1) is also reported to be up-regulated in GBM. We explored the role of FN1-...
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| Veröffentlicht in: | Pharmaceutical biology 2021-01, Vol.59 (1), p.902-909 |
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| creator | Song, Jian Zhao, Di Sun, Guozhu Yang, Jiankai Lv, Zhongqiang Jiao, Baohua |
| description | The phosphorylation of signal transducer and activator of transcription protein 3 (STAT3) is up-regulated in glioblastoma (GBM) cells and is regulated by protein tyrosine phosphatase receptor type M (PTPRM). Fibronectin-1 (FN1) is also reported to be up-regulated in GBM.
We explored the role of FN1-induced PTPRM methylation in GBM.
The lentivirus particles of oe-PTPRM, sh-PTPRM, oe-FN1, sh-FN1, or their negative controls (NSCs) were transfected into GBM cells with or without stattic (0.5 μM, 24 h) or 5-aza (1 μM, 0, 2, 4 h) treatments. Methylation-specific PCR was performed to detect PTPRM methylation levels.
PTPRM was down-regulated (0.373 ± 0.124- and 0.455 ± 0.109-fold), FN1 and p-STAT3 were up-regulated (p |
| doi_str_mv | 10.1080/13880209.2021.1944220 |
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We explored the role of FN1-induced PTPRM methylation in GBM.
The lentivirus particles of oe-PTPRM, sh-PTPRM, oe-FN1, sh-FN1, or their negative controls (NSCs) were transfected into GBM cells with or without stattic (0.5 μM, 24 h) or 5-aza (1 μM, 0, 2, 4 h) treatments. Methylation-specific PCR was performed to detect PTPRM methylation levels.
PTPRM was down-regulated (0.373 ± 0.124- and 0.455 ± 0.109-fold), FN1 and p-STAT3 were up-regulated (p < 0.001) in A172 and U87 MG cells as compared to NSCs. Overexpressing PTPRM inhibited STAT3 phosphorylation. Interfering with PTPRM increased colony numbers in A172 and U-87 MG cells (2.253 ± 0.111- and 2.043 ± 0.19-fold), and stattic reduced them. Cell viability was reduced after treatment with 5-aza in A172 and U-87 MG cells (p < 0.05). P-STAT3 was down-regulated after 5-aza treatment. Overexpressing FN1 decreased PTPRM levels (p < 0.001), knockdown of FN1 decreased PTPRM methylation and inhibited STAT3 phosphorylation. Overexpressing FN1 increased cell viability (1.497 ± 0.114- and 1.460 ± 0.151-fold), and stattic or 5-aza reversed such effects (p < 0.05).
The up-regulation of FN1 reduced PTPRM by increasing its methylation, resulting in an increase of STAT3 phosphorylation and promoting GBM cell proliferation. Interfering with FN1 may be a potential therapeutic target for GBM.</description><identifier>ISSN: 1388-0209</identifier><identifier>EISSN: 1744-5116</identifier><identifier>DOI: 10.1080/13880209.2021.1944220</identifier><identifier>PMID: 34225581</identifier><language>eng</language><publisher>England: Taylor & Francis</publisher><subject>Brain cancer ; Brain Neoplasms - genetics ; Brain Neoplasms - pathology ; Cell Line, Tumor ; Cell proliferation ; Cell Proliferation - genetics ; Cell viability ; DNA Methylation ; Fibronectin ; Fibronectins - genetics ; GBM cells ; Glioblastoma ; Glioblastoma - genetics ; Glioblastoma - pathology ; Humans ; Kinases ; Methylation ; p-STAT3 ; Phosphorylation ; Phosphorylation - genetics ; proliferation ; Protein-tyrosine-phosphatase ; Receptor-Like Protein Tyrosine Phosphatases, Class 2 - genetics ; Signal Transduction - genetics ; Stat3 protein ; STAT3 Transcription Factor - genetics ; Therapeutic targets ; Up-Regulation</subject><ispartof>Pharmaceutical biology, 2021-01, Vol.59 (1), p.902-909</ispartof><rights>2021 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. 2021</rights><rights>2021 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. This work is licensed under the Creative Commons Attribution License http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2021 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. 2021 The Author(s)</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c562t-f27e1c510a78a16a6935f77155224af1a7c87cd62600524f32936376c9f876ea3</citedby><cites>FETCH-LOGICAL-c562t-f27e1c510a78a16a6935f77155224af1a7c87cd62600524f32936376c9f876ea3</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/PMC8259858/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8259858/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,724,777,781,861,882,2096,27483,27905,27906,53772,53774,59122,59123</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34225581$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Song, Jian</creatorcontrib><creatorcontrib>Zhao, Di</creatorcontrib><creatorcontrib>Sun, Guozhu</creatorcontrib><creatorcontrib>Yang, Jiankai</creatorcontrib><creatorcontrib>Lv, Zhongqiang</creatorcontrib><creatorcontrib>Jiao, Baohua</creatorcontrib><title>PTPRM methylation induced by FN1 promotes the development of glioblastoma by activating STAT3 signalling</title><title>Pharmaceutical biology</title><addtitle>Pharm Biol</addtitle><description>The phosphorylation of signal transducer and activator of transcription protein 3 (STAT3) is up-regulated in glioblastoma (GBM) cells and is regulated by protein tyrosine phosphatase receptor type M (PTPRM). Fibronectin-1 (FN1) is also reported to be up-regulated in GBM.
We explored the role of FN1-induced PTPRM methylation in GBM.
The lentivirus particles of oe-PTPRM, sh-PTPRM, oe-FN1, sh-FN1, or their negative controls (NSCs) were transfected into GBM cells with or without stattic (0.5 μM, 24 h) or 5-aza (1 μM, 0, 2, 4 h) treatments. Methylation-specific PCR was performed to detect PTPRM methylation levels.
PTPRM was down-regulated (0.373 ± 0.124- and 0.455 ± 0.109-fold), FN1 and p-STAT3 were up-regulated (p < 0.001) in A172 and U87 MG cells as compared to NSCs. Overexpressing PTPRM inhibited STAT3 phosphorylation. Interfering with PTPRM increased colony numbers in A172 and U-87 MG cells (2.253 ± 0.111- and 2.043 ± 0.19-fold), and stattic reduced them. Cell viability was reduced after treatment with 5-aza in A172 and U-87 MG cells (p < 0.05). P-STAT3 was down-regulated after 5-aza treatment. Overexpressing FN1 decreased PTPRM levels (p < 0.001), knockdown of FN1 decreased PTPRM methylation and inhibited STAT3 phosphorylation. Overexpressing FN1 increased cell viability (1.497 ± 0.114- and 1.460 ± 0.151-fold), and stattic or 5-aza reversed such effects (p < 0.05).
The up-regulation of FN1 reduced PTPRM by increasing its methylation, resulting in an increase of STAT3 phosphorylation and promoting GBM cell proliferation. Interfering with FN1 may be a potential therapeutic target for GBM.</description><subject>Brain cancer</subject><subject>Brain Neoplasms - genetics</subject><subject>Brain Neoplasms - pathology</subject><subject>Cell Line, Tumor</subject><subject>Cell proliferation</subject><subject>Cell Proliferation - genetics</subject><subject>Cell viability</subject><subject>DNA Methylation</subject><subject>Fibronectin</subject><subject>Fibronectins - genetics</subject><subject>GBM cells</subject><subject>Glioblastoma</subject><subject>Glioblastoma - genetics</subject><subject>Glioblastoma - pathology</subject><subject>Humans</subject><subject>Kinases</subject><subject>Methylation</subject><subject>p-STAT3</subject><subject>Phosphorylation</subject><subject>Phosphorylation - genetics</subject><subject>proliferation</subject><subject>Protein-tyrosine-phosphatase</subject><subject>Receptor-Like Protein Tyrosine Phosphatases, Class 2 - genetics</subject><subject>Signal Transduction - genetics</subject><subject>Stat3 protein</subject><subject>STAT3 Transcription Factor - genetics</subject><subject>Therapeutic targets</subject><subject>Up-Regulation</subject><issn>1388-0209</issn><issn>1744-5116</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>0YH</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>DOA</sourceid><recordid>eNp9kktvEzEURkcIRB_wE0AjsWGT4Pdjg6gqCpUKVBDW1o3HkzjyjIPtBOXf1yFpRVmwsmWfe-xrf03zCqMpRgq9w1QpRJCeEkTwFGvGCEFPmlMsGZtwjMXTOq_MZA-dNGc5rxBCnFL-vDmhFeZc4dNmeTu7_f6lHVxZ7gIUH8fWj93Guq6d79qrr7hdpzjE4nJblq7t3NaFuB7cWNrYt4vg4zxALnGAPQ-2-G21jIv2x-xiRtvsFyOEUBdeNM96CNm9PI7nzc-rj7PLz5Obb5-uLy9uJpYLUiY9kQ5bjhFIBViA0JT3UmLOCWHQY5BWSdsJImozhPWUaCqoFFb3SgoH9Ly5Pni7CCuzTn6AtDMRvPmzENPCQCreBmc4YGBEk7kEx3RH1JxK7SQCzBkBiavr_cG13swH19nadYLwSPp4Z_RLs4hbowjXiqsqeHsUpPhr43Ixg8_WhQCji5tsCGdKI6YFqeibf9BV3KT6eJUSGtevxIpXih8om2LOyfUPl8HI7HNh7nNh9rkwx1zUutd_d_JQdR-ECnw4AH7sYxrgd0yhMwV2IaY-wWh9NvT_Z9wBfvLFyA</recordid><startdate>20210101</startdate><enddate>20210101</enddate><creator>Song, Jian</creator><creator>Zhao, Di</creator><creator>Sun, Guozhu</creator><creator>Yang, Jiankai</creator><creator>Lv, Zhongqiang</creator><creator>Jiao, Baohua</creator><general>Taylor & Francis</general><general>Taylor & Francis Ltd</general><general>Taylor & Francis Group</general><scope>0YH</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>8FD</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>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20210101</creationdate><title>PTPRM methylation induced by FN1 promotes the development of glioblastoma by activating STAT3 signalling</title><author>Song, Jian ; Zhao, Di ; Sun, Guozhu ; Yang, Jiankai ; Lv, Zhongqiang ; Jiao, Baohua</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c562t-f27e1c510a78a16a6935f77155224af1a7c87cd62600524f32936376c9f876ea3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Brain cancer</topic><topic>Brain Neoplasms - genetics</topic><topic>Brain Neoplasms - pathology</topic><topic>Cell Line, Tumor</topic><topic>Cell proliferation</topic><topic>Cell Proliferation - genetics</topic><topic>Cell viability</topic><topic>DNA Methylation</topic><topic>Fibronectin</topic><topic>Fibronectins - genetics</topic><topic>GBM cells</topic><topic>Glioblastoma</topic><topic>Glioblastoma - genetics</topic><topic>Glioblastoma - pathology</topic><topic>Humans</topic><topic>Kinases</topic><topic>Methylation</topic><topic>p-STAT3</topic><topic>Phosphorylation</topic><topic>Phosphorylation - genetics</topic><topic>proliferation</topic><topic>Protein-tyrosine-phosphatase</topic><topic>Receptor-Like Protein Tyrosine Phosphatases, Class 2 - genetics</topic><topic>Signal Transduction - genetics</topic><topic>Stat3 protein</topic><topic>STAT3 Transcription Factor - genetics</topic><topic>Therapeutic targets</topic><topic>Up-Regulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Song, Jian</creatorcontrib><creatorcontrib>Zhao, Di</creatorcontrib><creatorcontrib>Sun, Guozhu</creatorcontrib><creatorcontrib>Yang, Jiankai</creatorcontrib><creatorcontrib>Lv, Zhongqiang</creatorcontrib><creatorcontrib>Jiao, Baohua</creatorcontrib><collection>Taylor & Francis 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 Central (Corporate)</collection><collection>ProQuest Health and Medical</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Technology Research Database</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</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Biotechnology and BioEngineering Abstracts</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>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>Directory of Open Access Journals</collection><jtitle>Pharmaceutical biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Song, Jian</au><au>Zhao, Di</au><au>Sun, Guozhu</au><au>Yang, Jiankai</au><au>Lv, Zhongqiang</au><au>Jiao, Baohua</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>PTPRM methylation induced by FN1 promotes the development of glioblastoma by activating STAT3 signalling</atitle><jtitle>Pharmaceutical biology</jtitle><addtitle>Pharm Biol</addtitle><date>2021-01-01</date><risdate>2021</risdate><volume>59</volume><issue>1</issue><spage>902</spage><epage>909</epage><pages>902-909</pages><issn>1388-0209</issn><eissn>1744-5116</eissn><abstract>The phosphorylation of signal transducer and activator of transcription protein 3 (STAT3) is up-regulated in glioblastoma (GBM) cells and is regulated by protein tyrosine phosphatase receptor type M (PTPRM). Fibronectin-1 (FN1) is also reported to be up-regulated in GBM.
We explored the role of FN1-induced PTPRM methylation in GBM.
The lentivirus particles of oe-PTPRM, sh-PTPRM, oe-FN1, sh-FN1, or their negative controls (NSCs) were transfected into GBM cells with or without stattic (0.5 μM, 24 h) or 5-aza (1 μM, 0, 2, 4 h) treatments. Methylation-specific PCR was performed to detect PTPRM methylation levels.
PTPRM was down-regulated (0.373 ± 0.124- and 0.455 ± 0.109-fold), FN1 and p-STAT3 were up-regulated (p < 0.001) in A172 and U87 MG cells as compared to NSCs. Overexpressing PTPRM inhibited STAT3 phosphorylation. Interfering with PTPRM increased colony numbers in A172 and U-87 MG cells (2.253 ± 0.111- and 2.043 ± 0.19-fold), and stattic reduced them. Cell viability was reduced after treatment with 5-aza in A172 and U-87 MG cells (p < 0.05). P-STAT3 was down-regulated after 5-aza treatment. Overexpressing FN1 decreased PTPRM levels (p < 0.001), knockdown of FN1 decreased PTPRM methylation and inhibited STAT3 phosphorylation. Overexpressing FN1 increased cell viability (1.497 ± 0.114- and 1.460 ± 0.151-fold), and stattic or 5-aza reversed such effects (p < 0.05).
The up-regulation of FN1 reduced PTPRM by increasing its methylation, resulting in an increase of STAT3 phosphorylation and promoting GBM cell proliferation. Interfering with FN1 may be a potential therapeutic target for GBM.</abstract><cop>England</cop><pub>Taylor & Francis</pub><pmid>34225581</pmid><doi>10.1080/13880209.2021.1944220</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Brain cancer Brain Neoplasms - genetics Brain Neoplasms - pathology Cell Line, Tumor Cell proliferation Cell Proliferation - genetics Cell viability DNA Methylation Fibronectin Fibronectins - genetics GBM cells Glioblastoma Glioblastoma - genetics Glioblastoma - pathology Humans Kinases Methylation p-STAT3 Phosphorylation Phosphorylation - genetics proliferation Protein-tyrosine-phosphatase Receptor-Like Protein Tyrosine Phosphatases, Class 2 - genetics Signal Transduction - genetics Stat3 protein STAT3 Transcription Factor - genetics Therapeutic targets Up-Regulation |
| title | PTPRM methylation induced by FN1 promotes the development of glioblastoma by activating STAT3 signalling |
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