Interferon-γ inducible protein 30 promotes the epithelial-mesenchymal transition-like phenotype and chemoresistance by activating EGFR/AKT/GSK3β/β-catenin pathway in glioma
Previous studies have indicated that IFI30 plays a protective role in human cancers. However, its potential roles in regulating glioma development are not fully understood. Public datasets, immunohistochemistry, and western blotting (WB) were used to evaluate the expression of IFI30 in glioma. The p...
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| Veröffentlicht in: | CNS neuroscience & therapeutics 2023-12, Vol.29 (12), p.4124-4138 |
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| creator | Chen, Ying Xu, Hui Yu, Pei Wang, Qing Li, Shenggang Ji, Fufu Wu, Chunwang Lan, Qing |
| description | Previous studies have indicated that IFI30 plays a protective role in human cancers. However, its potential roles in regulating glioma development are not fully understood.
Public datasets, immunohistochemistry, and western blotting (WB) were used to evaluate the expression of IFI30 in glioma. The potential functions and mechanisms of IFI30 were examined by public dataset analysis; quantitative real-time PCR; WB; limiting dilution analysis; xenograft tumor assays; CCK-8, colony formation, wound healing, and transwell assays; and immunofluorescence microscopy and flow cytometry.
IFI30 was significantly upregulated in glioma tissues and cell lines compared with corresponding controls, and the expression level of IFI30 was positively associated with tumor grade. Functionally, both in vivo and in vitro evidence showed that IFI30 regulated the migration and invasion of glioma cells. Mechanistically, we found that IFI30 dramatically promoted the epithelial-mesenchymal transition (EMT)-like process by activating the EGFR/AKT/GSK3β/β-catenin pathway. In addition, IFI30 regulated the chemoresistance of glioma cells to temozolomide directly via the expression of the transcription factor Slug, a key regulator of the EMT-like process.
The present study suggests that IFI30 is a regulator of the EMT-like phenotype and acts not only as a prognostic marker but also as a potential therapeutic target for temozolomide-resistant glioma. |
| doi_str_mv | 10.1111/cns.14334 |
| format | Article |
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Public datasets, immunohistochemistry, and western blotting (WB) were used to evaluate the expression of IFI30 in glioma. The potential functions and mechanisms of IFI30 were examined by public dataset analysis; quantitative real-time PCR; WB; limiting dilution analysis; xenograft tumor assays; CCK-8, colony formation, wound healing, and transwell assays; and immunofluorescence microscopy and flow cytometry.
IFI30 was significantly upregulated in glioma tissues and cell lines compared with corresponding controls, and the expression level of IFI30 was positively associated with tumor grade. Functionally, both in vivo and in vitro evidence showed that IFI30 regulated the migration and invasion of glioma cells. Mechanistically, we found that IFI30 dramatically promoted the epithelial-mesenchymal transition (EMT)-like process by activating the EGFR/AKT/GSK3β/β-catenin pathway. In addition, IFI30 regulated the chemoresistance of glioma cells to temozolomide directly via the expression of the transcription factor Slug, a key regulator of the EMT-like process.
The present study suggests that IFI30 is a regulator of the EMT-like phenotype and acts not only as a prognostic marker but also as a potential therapeutic target for temozolomide-resistant glioma.</description><identifier>ISSN: 1755-5930</identifier><identifier>EISSN: 1755-5949</identifier><identifier>DOI: 10.1111/cns.14334</identifier><identifier>PMID: 37408388</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>AKT protein ; beta Catenin - genetics ; beta Catenin - metabolism ; Brain cancer ; Cancer therapies ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Chemoresistance ; Cholecystokinin ; Datasets ; Drug Resistance, Neoplasm ; Epidermal growth factor receptors ; Epithelial-Mesenchymal Transition ; ErbB Receptors - metabolism ; Flow cytometry ; Gene Expression Regulation, Neoplastic ; Genomes ; Glioma ; Glioma - genetics ; Glioma cells ; Glycogen Synthase Kinase 3 beta ; Humans ; Immunofluorescence ; Immunohistochemistry ; Interferon ; Interferon-gamma - metabolism ; Medical prognosis ; Phenotype ; Phenotypes ; Protein expression ; Proteins ; Proto-Oncogene Proteins c-akt - metabolism ; Stem cells ; Temozolomide ; Temozolomide - pharmacology ; Temozolomide - therapeutic use ; Therapeutic targets ; Tumors ; Western blotting ; Wound healing ; β-Catenin ; γ-Interferon</subject><ispartof>CNS neuroscience & therapeutics, 2023-12, Vol.29 (12), p.4124-4138</ispartof><rights>2023 The Authors. CNS Neuroscience & Therapeutics Published by John Wiley & Sons Ltd.</rights><rights>2023. This work is published under 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><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c348t-ac6cac972744123f6ef82a0eea38f0ba7858d07ee97acccf54d615a76be497a3</citedby><cites>FETCH-LOGICAL-c348t-ac6cac972744123f6ef82a0eea38f0ba7858d07ee97acccf54d615a76be497a3</cites><orcidid>0000-0002-0709-3874 ; 0000-0002-8468-4942</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,860,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37408388$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chen, Ying</creatorcontrib><creatorcontrib>Xu, Hui</creatorcontrib><creatorcontrib>Yu, Pei</creatorcontrib><creatorcontrib>Wang, Qing</creatorcontrib><creatorcontrib>Li, Shenggang</creatorcontrib><creatorcontrib>Ji, Fufu</creatorcontrib><creatorcontrib>Wu, Chunwang</creatorcontrib><creatorcontrib>Lan, Qing</creatorcontrib><title>Interferon-γ inducible protein 30 promotes the epithelial-mesenchymal transition-like phenotype and chemoresistance by activating EGFR/AKT/GSK3β/β-catenin pathway in glioma</title><title>CNS neuroscience & therapeutics</title><addtitle>CNS Neurosci Ther</addtitle><description>Previous studies have indicated that IFI30 plays a protective role in human cancers. However, its potential roles in regulating glioma development are not fully understood.
Public datasets, immunohistochemistry, and western blotting (WB) were used to evaluate the expression of IFI30 in glioma. The potential functions and mechanisms of IFI30 were examined by public dataset analysis; quantitative real-time PCR; WB; limiting dilution analysis; xenograft tumor assays; CCK-8, colony formation, wound healing, and transwell assays; and immunofluorescence microscopy and flow cytometry.
IFI30 was significantly upregulated in glioma tissues and cell lines compared with corresponding controls, and the expression level of IFI30 was positively associated with tumor grade. Functionally, both in vivo and in vitro evidence showed that IFI30 regulated the migration and invasion of glioma cells. Mechanistically, we found that IFI30 dramatically promoted the epithelial-mesenchymal transition (EMT)-like process by activating the EGFR/AKT/GSK3β/β-catenin pathway. In addition, IFI30 regulated the chemoresistance of glioma cells to temozolomide directly via the expression of the transcription factor Slug, a key regulator of the EMT-like process.
The present study suggests that IFI30 is a regulator of the EMT-like phenotype and acts not only as a prognostic marker but also as a potential therapeutic target for temozolomide-resistant glioma.</description><subject>AKT protein</subject><subject>beta Catenin - genetics</subject><subject>beta Catenin - metabolism</subject><subject>Brain cancer</subject><subject>Cancer therapies</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement</subject><subject>Cell Proliferation</subject><subject>Chemoresistance</subject><subject>Cholecystokinin</subject><subject>Datasets</subject><subject>Drug Resistance, Neoplasm</subject><subject>Epidermal growth factor receptors</subject><subject>Epithelial-Mesenchymal Transition</subject><subject>ErbB Receptors - metabolism</subject><subject>Flow cytometry</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genomes</subject><subject>Glioma</subject><subject>Glioma - genetics</subject><subject>Glioma cells</subject><subject>Glycogen Synthase Kinase 3 beta</subject><subject>Humans</subject><subject>Immunofluorescence</subject><subject>Immunohistochemistry</subject><subject>Interferon</subject><subject>Interferon-gamma - 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genetics</topic><topic>beta Catenin - metabolism</topic><topic>Brain cancer</topic><topic>Cancer therapies</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement</topic><topic>Cell Proliferation</topic><topic>Chemoresistance</topic><topic>Cholecystokinin</topic><topic>Datasets</topic><topic>Drug Resistance, Neoplasm</topic><topic>Epidermal growth factor receptors</topic><topic>Epithelial-Mesenchymal Transition</topic><topic>ErbB Receptors - metabolism</topic><topic>Flow cytometry</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Genomes</topic><topic>Glioma</topic><topic>Glioma - genetics</topic><topic>Glioma cells</topic><topic>Glycogen Synthase Kinase 3 beta</topic><topic>Humans</topic><topic>Immunofluorescence</topic><topic>Immunohistochemistry</topic><topic>Interferon</topic><topic>Interferon-gamma - metabolism</topic><topic>Medical prognosis</topic><topic>Phenotype</topic><topic>Phenotypes</topic><topic>Protein expression</topic><topic>Proteins</topic><topic>Proto-Oncogene Proteins c-akt - 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Academic</collection><jtitle>CNS neuroscience & therapeutics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chen, Ying</au><au>Xu, Hui</au><au>Yu, Pei</au><au>Wang, Qing</au><au>Li, Shenggang</au><au>Ji, Fufu</au><au>Wu, Chunwang</au><au>Lan, Qing</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Interferon-γ inducible protein 30 promotes the epithelial-mesenchymal transition-like phenotype and chemoresistance by activating EGFR/AKT/GSK3β/β-catenin pathway in glioma</atitle><jtitle>CNS neuroscience & therapeutics</jtitle><addtitle>CNS Neurosci Ther</addtitle><date>2023-12</date><risdate>2023</risdate><volume>29</volume><issue>12</issue><spage>4124</spage><epage>4138</epage><pages>4124-4138</pages><issn>1755-5930</issn><eissn>1755-5949</eissn><abstract>Previous studies have indicated that IFI30 plays a protective role in human cancers. However, its potential roles in regulating glioma development are not fully understood.
Public datasets, immunohistochemistry, and western blotting (WB) were used to evaluate the expression of IFI30 in glioma. The potential functions and mechanisms of IFI30 were examined by public dataset analysis; quantitative real-time PCR; WB; limiting dilution analysis; xenograft tumor assays; CCK-8, colony formation, wound healing, and transwell assays; and immunofluorescence microscopy and flow cytometry.
IFI30 was significantly upregulated in glioma tissues and cell lines compared with corresponding controls, and the expression level of IFI30 was positively associated with tumor grade. Functionally, both in vivo and in vitro evidence showed that IFI30 regulated the migration and invasion of glioma cells. Mechanistically, we found that IFI30 dramatically promoted the epithelial-mesenchymal transition (EMT)-like process by activating the EGFR/AKT/GSK3β/β-catenin pathway. In addition, IFI30 regulated the chemoresistance of glioma cells to temozolomide directly via the expression of the transcription factor Slug, a key regulator of the EMT-like process.
The present study suggests that IFI30 is a regulator of the EMT-like phenotype and acts not only as a prognostic marker but also as a potential therapeutic target for temozolomide-resistant glioma.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>37408388</pmid><doi>10.1111/cns.14334</doi><tpages>15</tpages><orcidid>https://orcid.org/0000-0002-0709-3874</orcidid><orcidid>https://orcid.org/0000-0002-8468-4942</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | AKT protein beta Catenin - genetics beta Catenin - metabolism Brain cancer Cancer therapies Cell Line, Tumor Cell Movement Cell Proliferation Chemoresistance Cholecystokinin Datasets Drug Resistance, Neoplasm Epidermal growth factor receptors Epithelial-Mesenchymal Transition ErbB Receptors - metabolism Flow cytometry Gene Expression Regulation, Neoplastic Genomes Glioma Glioma - genetics Glioma cells Glycogen Synthase Kinase 3 beta Humans Immunofluorescence Immunohistochemistry Interferon Interferon-gamma - metabolism Medical prognosis Phenotype Phenotypes Protein expression Proteins Proto-Oncogene Proteins c-akt - metabolism Stem cells Temozolomide Temozolomide - pharmacology Temozolomide - therapeutic use Therapeutic targets Tumors Western blotting Wound healing β-Catenin γ-Interferon |
| title | Interferon-γ inducible protein 30 promotes the epithelial-mesenchymal transition-like phenotype and chemoresistance by activating EGFR/AKT/GSK3β/β-catenin pathway in glioma |
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