O-GlcNAcylation of melanophilin enhances radiation resistance in glioblastoma via suppressing TRIM21 mediated ubiquitination
The molecular mechanism of glioblastoma (GBM) radiation resistance remains poorly understood. The aim of this study was to elucidate the potential role of Melanophilin (MLPH) O-GlcNAcylation and the specific mechanism through which it regulates GBM radiotherapy resistance. We found that MLPH was sig...
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| Veröffentlicht in: | Oncogene 2024-01, Vol.43 (1), p.61-75 |
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| creator | Xu, Lei Ye, Yangfan Tao, Zeqiang Wang, Tian Wei, Yutian Cai, Wanzhi Wan, Xin Zhao, Pengzhan Gu, Wei Gu, Bin Zhang, Liuchao Tian, Yufei Liu, Ning Tu, Yiming Ji, Jing |
| description | The molecular mechanism of glioblastoma (GBM) radiation resistance remains poorly understood. The aim of this study was to elucidate the potential role of Melanophilin (MLPH) O-GlcNAcylation and the specific mechanism through which it regulates GBM radiotherapy resistance. We found that MLPH was significantly upregulated in recurrent GBM tumor tissues after ionizing radiation (IR). MLPH induced radiotherapy resistance in GBM cells and xenotransplanted human tumors through regulating the NF-κB pathway. MLPH was O-GlcNAcylated at the conserved serine 510, and radiation-resistant GBM cells showed higher levels of O-GlcNAcylation of MLPH. O-GlcNAcylation of MLPH protected its protein stability and tripartite motif containing 21(TRIM21) was identified as an E3 ubiquitin ligase promoting MLPH degradation whose interaction with MLPH was affected by O-GlcNAcylation. Our data demonstrate that MLPH exerts regulatory functions in GBM radiation resistance by promoting the NF-κB signaling pathway and that O-GlcNAcylation of MLPH both stabilizes and protects it from TRIM21-mediated ubiquitination. These results identify a potential mechanism of GBM radiation resistance and suggest a potential therapeutic strategy for GBM treatment. |
| doi_str_mv | 10.1038/s41388-023-02881-6 |
| format | Article |
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The aim of this study was to elucidate the potential role of Melanophilin (MLPH) O-GlcNAcylation and the specific mechanism through which it regulates GBM radiotherapy resistance. We found that MLPH was significantly upregulated in recurrent GBM tumor tissues after ionizing radiation (IR). MLPH induced radiotherapy resistance in GBM cells and xenotransplanted human tumors through regulating the NF-κB pathway. MLPH was O-GlcNAcylated at the conserved serine 510, and radiation-resistant GBM cells showed higher levels of O-GlcNAcylation of MLPH. O-GlcNAcylation of MLPH protected its protein stability and tripartite motif containing 21(TRIM21) was identified as an E3 ubiquitin ligase promoting MLPH degradation whose interaction with MLPH was affected by O-GlcNAcylation. Our data demonstrate that MLPH exerts regulatory functions in GBM radiation resistance by promoting the NF-κB signaling pathway and that O-GlcNAcylation of MLPH both stabilizes and protects it from TRIM21-mediated ubiquitination. These results identify a potential mechanism of GBM radiation resistance and suggest a potential therapeutic strategy for GBM treatment.</description><identifier>ISSN: 0950-9232</identifier><identifier>ISSN: 1476-5594</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/s41388-023-02881-6</identifier><identifier>PMID: 37950039</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>101/58 ; 13/1 ; 13/2 ; 13/31 ; 13/51 ; 38/5 ; 42/109 ; 59/5 ; 631/337/1427/2122 ; 631/337/458/1524 ; 631/67/1922 ; 631/67/2327 ; 631/67/68 ; 64/114 ; 82/80 ; Apoptosis ; Brain cancer ; Cell Biology ; Cell Line, Tumor ; Glioblastoma ; Glioblastoma - genetics ; Glioblastoma - pathology ; Glioblastoma - radiotherapy ; Human Genetics ; Humans ; Internal Medicine ; Ionizing radiation ; Medicine ; Medicine & Public Health ; Molecular modelling ; Neoplasm Recurrence, Local ; NF-kappa B - genetics ; NF-κB protein ; O-GlcNAcylation ; Oncology ; Radiation therapy ; Signal transduction ; Ubiquitin-protein ligase ; Ubiquitination</subject><ispartof>Oncogene, 2024-01, Vol.43 (1), p.61-75</ispartof><rights>The Author(s), under exclusive licence to Springer Nature Limited 2023. corrected publication 2024. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</rights><rights>2023. 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The aim of this study was to elucidate the potential role of Melanophilin (MLPH) O-GlcNAcylation and the specific mechanism through which it regulates GBM radiotherapy resistance. We found that MLPH was significantly upregulated in recurrent GBM tumor tissues after ionizing radiation (IR). MLPH induced radiotherapy resistance in GBM cells and xenotransplanted human tumors through regulating the NF-κB pathway. MLPH was O-GlcNAcylated at the conserved serine 510, and radiation-resistant GBM cells showed higher levels of O-GlcNAcylation of MLPH. O-GlcNAcylation of MLPH protected its protein stability and tripartite motif containing 21(TRIM21) was identified as an E3 ubiquitin ligase promoting MLPH degradation whose interaction with MLPH was affected by O-GlcNAcylation. Our data demonstrate that MLPH exerts regulatory functions in GBM radiation resistance by promoting the NF-κB signaling pathway and that O-GlcNAcylation of MLPH both stabilizes and protects it from TRIM21-mediated ubiquitination. 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The aim of this study was to elucidate the potential role of Melanophilin (MLPH) O-GlcNAcylation and the specific mechanism through which it regulates GBM radiotherapy resistance. We found that MLPH was significantly upregulated in recurrent GBM tumor tissues after ionizing radiation (IR). MLPH induced radiotherapy resistance in GBM cells and xenotransplanted human tumors through regulating the NF-κB pathway. MLPH was O-GlcNAcylated at the conserved serine 510, and radiation-resistant GBM cells showed higher levels of O-GlcNAcylation of MLPH. O-GlcNAcylation of MLPH protected its protein stability and tripartite motif containing 21(TRIM21) was identified as an E3 ubiquitin ligase promoting MLPH degradation whose interaction with MLPH was affected by O-GlcNAcylation. Our data demonstrate that MLPH exerts regulatory functions in GBM radiation resistance by promoting the NF-κB signaling pathway and that O-GlcNAcylation of MLPH both stabilizes and protects it from TRIM21-mediated ubiquitination. These results identify a potential mechanism of GBM radiation resistance and suggest a potential therapeutic strategy for GBM treatment.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>37950039</pmid><doi>10.1038/s41388-023-02881-6</doi><tpages>15</tpages><orcidid>https://orcid.org/0000-0002-7372-024X</orcidid></addata></record> |
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| subjects | 101/58 13/1 13/2 13/31 13/51 38/5 42/109 59/5 631/337/1427/2122 631/337/458/1524 631/67/1922 631/67/2327 631/67/68 64/114 82/80 Apoptosis Brain cancer Cell Biology Cell Line, Tumor Glioblastoma Glioblastoma - genetics Glioblastoma - pathology Glioblastoma - radiotherapy Human Genetics Humans Internal Medicine Ionizing radiation Medicine Medicine & Public Health Molecular modelling Neoplasm Recurrence, Local NF-kappa B - genetics NF-κB protein O-GlcNAcylation Oncology Radiation therapy Signal transduction Ubiquitin-protein ligase Ubiquitination |
| title | O-GlcNAcylation of melanophilin enhances radiation resistance in glioblastoma via suppressing TRIM21 mediated ubiquitination |
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