Overexpression of PPM1B inhibited chemoresistance to temozolomide and proliferation in glioma cells
Protein phosphatase magnesium‐dependent 1B (PPM1B) functions as IKKβ phosphatases to terminate nuclear factor kappa B (NF‐κB) signaling. NF‐κB signaling was constitutively activated in glioma cells. At present, little is known about the role of PPM1B in glioma. In the current study, we found that th...
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| Veröffentlicht in: | Cell biology international 2024-02, Vol.48 (2), p.143-153 |
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| creator | Yu, Yunhu Liu, Qian Ran, Qishan Cao, Fang |
| description | Protein phosphatase magnesium‐dependent 1B (PPM1B) functions as IKKβ phosphatases to terminate nuclear factor kappa B (NF‐κB) signaling. NF‐κB signaling was constitutively activated in glioma cells. At present, little is known about the role of PPM1B in glioma. In the current study, we found that the expression of PPM1B was reduced in glioma tissues and cells, and decreased expression of PPM1B was related to poor overall survival of patients. Overexpression of PPM1B inhibited the proliferation and promoted apoptosis of glioma cells. Moreover, PPM1B overexpression reduced the phosphorylation of IKKβ and inhibited the nuclear localization of NF‐κBp65. PDTC, an inhibitor of NF‐κB signaling, reversed PPM1B‐knockdown‐induced cell proliferation. Furthermore, overexpression of PPM1B enhanced the sensitivity of glioma cells to temozolomide. In vivo experiments showed that overexpression of PPM1B could inhibit tumor growth, improve the survival rate of nude mice, and enhance the sensitivity to temozolomide. In conclusion, PPM1B suppressed glioma cell proliferation and the IKKβ‐NF‐κB signaling pathway, and enhanced temozolomide sensitivity of glioma cells. |
| doi_str_mv | 10.1002/cbin.12092 |
| format | Article |
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NF‐κB signaling was constitutively activated in glioma cells. At present, little is known about the role of PPM1B in glioma. In the current study, we found that the expression of PPM1B was reduced in glioma tissues and cells, and decreased expression of PPM1B was related to poor overall survival of patients. Overexpression of PPM1B inhibited the proliferation and promoted apoptosis of glioma cells. Moreover, PPM1B overexpression reduced the phosphorylation of IKKβ and inhibited the nuclear localization of NF‐κBp65. PDTC, an inhibitor of NF‐κB signaling, reversed PPM1B‐knockdown‐induced cell proliferation. Furthermore, overexpression of PPM1B enhanced the sensitivity of glioma cells to temozolomide. In vivo experiments showed that overexpression of PPM1B could inhibit tumor growth, improve the survival rate of nude mice, and enhance the sensitivity to temozolomide. In conclusion, PPM1B suppressed glioma cell proliferation and the IKKβ‐NF‐κB signaling pathway, and enhanced temozolomide sensitivity of glioma cells.</description><identifier>ISSN: 1065-6995</identifier><identifier>EISSN: 1095-8355</identifier><identifier>DOI: 10.1002/cbin.12092</identifier><identifier>PMID: 37798941</identifier><language>eng</language><publisher>England: Wiley Subscription Services, Inc</publisher><subject>Animals ; Apoptosis ; Cell growth ; Cell Line, Tumor ; Cell Proliferation ; Chemoresistance ; Drug Resistance, Neoplasm ; Glioma ; Glioma - metabolism ; Glioma cells ; Humans ; I-kappa B Kinase - metabolism ; IKKβ‐NF‐κB ; Localization ; Magnesium ; Mice ; Mice, Nude ; NF-kappa B - metabolism ; Phosphoprotein Phosphatases ; Phosphorylation ; PPM1B ; proliferation ; Protein phosphatase ; Protein Phosphatase 2C ; Signal transduction ; Temozolomide ; Temozolomide - pharmacology ; temozolomide resistance</subject><ispartof>Cell biology international, 2024-02, Vol.48 (2), p.143-153</ispartof><rights>2023 International Federation of Cell Biology.</rights><rights>2024 International Federation for Cell Biology.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3572-32d6abb388cc890bbbfc60b82f7a761a97305a0f360fc7daf435a34f05e3d3dc3</citedby><cites>FETCH-LOGICAL-c3572-32d6abb388cc890bbbfc60b82f7a761a97305a0f360fc7daf435a34f05e3d3dc3</cites><orcidid>0000-0002-4900-8957</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fcbin.12092$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fcbin.12092$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37798941$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yu, Yunhu</creatorcontrib><creatorcontrib>Liu, Qian</creatorcontrib><creatorcontrib>Ran, Qishan</creatorcontrib><creatorcontrib>Cao, Fang</creatorcontrib><title>Overexpression of PPM1B inhibited chemoresistance to temozolomide and proliferation in glioma cells</title><title>Cell biology international</title><addtitle>Cell Biol Int</addtitle><description>Protein phosphatase magnesium‐dependent 1B (PPM1B) functions as IKKβ phosphatases to terminate nuclear factor kappa B (NF‐κB) signaling. NF‐κB signaling was constitutively activated in glioma cells. At present, little is known about the role of PPM1B in glioma. In the current study, we found that the expression of PPM1B was reduced in glioma tissues and cells, and decreased expression of PPM1B was related to poor overall survival of patients. Overexpression of PPM1B inhibited the proliferation and promoted apoptosis of glioma cells. Moreover, PPM1B overexpression reduced the phosphorylation of IKKβ and inhibited the nuclear localization of NF‐κBp65. PDTC, an inhibitor of NF‐κB signaling, reversed PPM1B‐knockdown‐induced cell proliferation. Furthermore, overexpression of PPM1B enhanced the sensitivity of glioma cells to temozolomide. In vivo experiments showed that overexpression of PPM1B could inhibit tumor growth, improve the survival rate of nude mice, and enhance the sensitivity to temozolomide. In conclusion, PPM1B suppressed glioma cell proliferation and the IKKβ‐NF‐κB signaling pathway, and enhanced temozolomide sensitivity of glioma cells.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation</subject><subject>Chemoresistance</subject><subject>Drug Resistance, Neoplasm</subject><subject>Glioma</subject><subject>Glioma - metabolism</subject><subject>Glioma cells</subject><subject>Humans</subject><subject>I-kappa B Kinase - metabolism</subject><subject>IKKβ‐NF‐κB</subject><subject>Localization</subject><subject>Magnesium</subject><subject>Mice</subject><subject>Mice, Nude</subject><subject>NF-kappa B - metabolism</subject><subject>Phosphoprotein Phosphatases</subject><subject>Phosphorylation</subject><subject>PPM1B</subject><subject>proliferation</subject><subject>Protein phosphatase</subject><subject>Protein Phosphatase 2C</subject><subject>Signal transduction</subject><subject>Temozolomide</subject><subject>Temozolomide - pharmacology</subject><subject>temozolomide resistance</subject><issn>1065-6995</issn><issn>1095-8355</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kMlKxTAUhoMozhsfQAJuRKhmaJpk6b04gdNC1yFJE420zTXpdXp6W6-6cOHqHM75-Pj5AdjB6BAjRI6sCd0hJkiSJbCOkWSFoIwtj3vFikpKtgY2cn5CCONSVKtgjXIuhSzxOrA3Ly65t1lyOYfYwejh7e0VnsDQPQYTeldD--jaOPxD7nVnHewj7IfLR2xiG2oHdVfDWYpN8C7pfpSEDj40IbYaWtc0eQuseN1kt_09N8H96cnd9Ly4vDm7mB5fFpYyTgpK6kobQ4WwVkhkjPG2QkYQzzWvsJacIqaRpxXyltfal5RpWnrEHK1pbekm2F94hzTPc5d71YY8JtCdi_OsiOAlqZAo5YDu_UGf4jx1QzpFJGZUcIlG6mBB2RRzTs6rWQqtTu8KIzVWr8bq1Vf1A7z7rZyb1tW_6E_XA4AXwGto3Ps_KjWdXFwvpJ9-n49U</recordid><startdate>202402</startdate><enddate>202402</enddate><creator>Yu, Yunhu</creator><creator>Liu, Qian</creator><creator>Ran, Qishan</creator><creator>Cao, Fang</creator><general>Wiley Subscription Services, Inc</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>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>8FD</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-4900-8957</orcidid></search><sort><creationdate>202402</creationdate><title>Overexpression of PPM1B inhibited chemoresistance to temozolomide and proliferation in glioma cells</title><author>Yu, Yunhu ; Liu, Qian ; Ran, Qishan ; Cao, Fang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3572-32d6abb388cc890bbbfc60b82f7a761a97305a0f360fc7daf435a34f05e3d3dc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation</topic><topic>Chemoresistance</topic><topic>Drug Resistance, Neoplasm</topic><topic>Glioma</topic><topic>Glioma - metabolism</topic><topic>Glioma cells</topic><topic>Humans</topic><topic>I-kappa B Kinase - metabolism</topic><topic>IKKβ‐NF‐κB</topic><topic>Localization</topic><topic>Magnesium</topic><topic>Mice</topic><topic>Mice, Nude</topic><topic>NF-kappa B - metabolism</topic><topic>Phosphoprotein Phosphatases</topic><topic>Phosphorylation</topic><topic>PPM1B</topic><topic>proliferation</topic><topic>Protein phosphatase</topic><topic>Protein Phosphatase 2C</topic><topic>Signal transduction</topic><topic>Temozolomide</topic><topic>Temozolomide - pharmacology</topic><topic>temozolomide resistance</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yu, Yunhu</creatorcontrib><creatorcontrib>Liu, Qian</creatorcontrib><creatorcontrib>Ran, Qishan</creatorcontrib><creatorcontrib>Cao, Fang</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Cell biology international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yu, Yunhu</au><au>Liu, Qian</au><au>Ran, Qishan</au><au>Cao, Fang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Overexpression of PPM1B inhibited chemoresistance to temozolomide and proliferation in glioma cells</atitle><jtitle>Cell biology international</jtitle><addtitle>Cell Biol Int</addtitle><date>2024-02</date><risdate>2024</risdate><volume>48</volume><issue>2</issue><spage>143</spage><epage>153</epage><pages>143-153</pages><issn>1065-6995</issn><eissn>1095-8355</eissn><abstract>Protein phosphatase magnesium‐dependent 1B (PPM1B) functions as IKKβ phosphatases to terminate nuclear factor kappa B (NF‐κB) signaling. NF‐κB signaling was constitutively activated in glioma cells. At present, little is known about the role of PPM1B in glioma. In the current study, we found that the expression of PPM1B was reduced in glioma tissues and cells, and decreased expression of PPM1B was related to poor overall survival of patients. Overexpression of PPM1B inhibited the proliferation and promoted apoptosis of glioma cells. Moreover, PPM1B overexpression reduced the phosphorylation of IKKβ and inhibited the nuclear localization of NF‐κBp65. PDTC, an inhibitor of NF‐κB signaling, reversed PPM1B‐knockdown‐induced cell proliferation. Furthermore, overexpression of PPM1B enhanced the sensitivity of glioma cells to temozolomide. In vivo experiments showed that overexpression of PPM1B could inhibit tumor growth, improve the survival rate of nude mice, and enhance the sensitivity to temozolomide. In conclusion, PPM1B suppressed glioma cell proliferation and the IKKβ‐NF‐κB signaling pathway, and enhanced temozolomide sensitivity of glioma cells.</abstract><cop>England</cop><pub>Wiley Subscription Services, Inc</pub><pmid>37798941</pmid><doi>10.1002/cbin.12092</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0002-4900-8957</orcidid></addata></record> |
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| subjects | Animals Apoptosis Cell growth Cell Line, Tumor Cell Proliferation Chemoresistance Drug Resistance, Neoplasm Glioma Glioma - metabolism Glioma cells Humans I-kappa B Kinase - metabolism IKKβ‐NF‐κB Localization Magnesium Mice Mice, Nude NF-kappa B - metabolism Phosphoprotein Phosphatases Phosphorylation PPM1B proliferation Protein phosphatase Protein Phosphatase 2C Signal transduction Temozolomide Temozolomide - pharmacology temozolomide resistance |
| title | Overexpression of PPM1B inhibited chemoresistance to temozolomide and proliferation in glioma cells |
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