ELAVL2 loss promotes aggressive mesenchymal transition in glioblastoma

Abstract Glioblastoma (GBM), the most lethal primary brain cancer, exhibits intratumoral heterogeneity and molecular plasticity, posing challenges for effective treatment. Despite this, the regulatory mechanisms underlying such plasticity, particularly mesenchymal (MES) transition, remain poorly und...
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Autor*in:	Yona Kim [verfasserIn] Ji Hyeon You [verfasserIn] Yeonjoo Ryu [verfasserIn] Gyuri Park [verfasserIn] Urim Lee [verfasserIn] Hyo Eun Moon [verfasserIn] Hye Ran Park [verfasserIn] Chang W. Song [verfasserIn] Ja-Lok Ku [verfasserIn] Sung-Hye Park [verfasserIn] Sun Ha Paek [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2024

Übergeordnetes Werk:	In: npj Precision Oncology - Nature Portfolio, 2017, 8(2024), 1, Seite 16
Übergeordnetes Werk:	volume:8 ; year:2024 ; number:1 ; pages:16

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1038/s41698-024-00566-1

Katalog-ID:	DOAJ097280135

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520			\|a Abstract Glioblastoma (GBM), the most lethal primary brain cancer, exhibits intratumoral heterogeneity and molecular plasticity, posing challenges for effective treatment. Despite this, the regulatory mechanisms underlying such plasticity, particularly mesenchymal (MES) transition, remain poorly understood. In this study, we elucidate the role of the RNA-binding protein ELAVL2 in regulating aggressive MES transformation in GBM. We found that ELAVL2 is most frequently deleted in GBM compared to other cancers and associated with distinct clinical and molecular features. Transcriptomic analysis revealed that ELAVL2-mediated alterations correspond to specific GBM subtype signatures. Notably, ELAVL2 expression negatively correlated with epithelial-to-mesenchymal transition (EMT)-related genes, and its loss promoted MES process and chemo-resistance in GBM cells, whereas ELAVL2 overexpression exerted the opposite effect. Further investigation via tissue microarray analysis demonstrated that high ELAVL2 protein expression confers a favorable survival outcome in GBM patients. Mechanistically, ELAVL2 was shown to directly bind to the transcripts of EMT-inhibitory molecules, SH3GL3 and DNM3, modulating their mRNA stability, potentially through an m6A-dependent mechanism. In summary, our findings identify ELAVL2 as a critical tumor suppressor and mRNA stabilizer that regulates MES transition in GBM, underscoring its role in transcriptomic plasticity and glioma progression.
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allfields	10.1038/s41698-024-00566-1 doi (DE-627)DOAJ097280135 (DE-599)DOAJ2a87bad4a8154cc9969bb2a939983550 DE-627 ger DE-627 rakwb eng RC254-282 Yona Kim verfasserin aut ELAVL2 loss promotes aggressive mesenchymal transition in glioblastoma 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Glioblastoma (GBM), the most lethal primary brain cancer, exhibits intratumoral heterogeneity and molecular plasticity, posing challenges for effective treatment. Despite this, the regulatory mechanisms underlying such plasticity, particularly mesenchymal (MES) transition, remain poorly understood. In this study, we elucidate the role of the RNA-binding protein ELAVL2 in regulating aggressive MES transformation in GBM. We found that ELAVL2 is most frequently deleted in GBM compared to other cancers and associated with distinct clinical and molecular features. Transcriptomic analysis revealed that ELAVL2-mediated alterations correspond to specific GBM subtype signatures. Notably, ELAVL2 expression negatively correlated with epithelial-to-mesenchymal transition (EMT)-related genes, and its loss promoted MES process and chemo-resistance in GBM cells, whereas ELAVL2 overexpression exerted the opposite effect. Further investigation via tissue microarray analysis demonstrated that high ELAVL2 protein expression confers a favorable survival outcome in GBM patients. Mechanistically, ELAVL2 was shown to directly bind to the transcripts of EMT-inhibitory molecules, SH3GL3 and DNM3, modulating their mRNA stability, potentially through an m6A-dependent mechanism. In summary, our findings identify ELAVL2 as a critical tumor suppressor and mRNA stabilizer that regulates MES transition in GBM, underscoring its role in transcriptomic plasticity and glioma progression. Neoplasms. Tumors. Oncology. Including cancer and carcinogens Ji Hyeon You verfasserin aut Yeonjoo Ryu verfasserin aut Gyuri Park verfasserin aut Urim Lee verfasserin aut Hyo Eun Moon verfasserin aut Hye Ran Park verfasserin aut Chang W. Song verfasserin aut Ja-Lok Ku verfasserin aut Sung-Hye Park verfasserin aut Sun Ha Paek verfasserin aut In npj Precision Oncology Nature Portfolio, 2017 8(2024), 1, Seite 16 (DE-627)884384454 (DE-600)2891458-2 2397768X nnns volume:8 year:2024 number:1 pages:16 https://doi.org/10.1038/s41698-024-00566-1 kostenfrei https://doaj.org/article/2a87bad4a8154cc9969bb2a939983550 kostenfrei https://doi.org/10.1038/s41698-024-00566-1 kostenfrei https://doaj.org/toc/2397-768X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2024 1 16
spelling	10.1038/s41698-024-00566-1 doi (DE-627)DOAJ097280135 (DE-599)DOAJ2a87bad4a8154cc9969bb2a939983550 DE-627 ger DE-627 rakwb eng RC254-282 Yona Kim verfasserin aut ELAVL2 loss promotes aggressive mesenchymal transition in glioblastoma 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Glioblastoma (GBM), the most lethal primary brain cancer, exhibits intratumoral heterogeneity and molecular plasticity, posing challenges for effective treatment. Despite this, the regulatory mechanisms underlying such plasticity, particularly mesenchymal (MES) transition, remain poorly understood. In this study, we elucidate the role of the RNA-binding protein ELAVL2 in regulating aggressive MES transformation in GBM. We found that ELAVL2 is most frequently deleted in GBM compared to other cancers and associated with distinct clinical and molecular features. Transcriptomic analysis revealed that ELAVL2-mediated alterations correspond to specific GBM subtype signatures. Notably, ELAVL2 expression negatively correlated with epithelial-to-mesenchymal transition (EMT)-related genes, and its loss promoted MES process and chemo-resistance in GBM cells, whereas ELAVL2 overexpression exerted the opposite effect. Further investigation via tissue microarray analysis demonstrated that high ELAVL2 protein expression confers a favorable survival outcome in GBM patients. Mechanistically, ELAVL2 was shown to directly bind to the transcripts of EMT-inhibitory molecules, SH3GL3 and DNM3, modulating their mRNA stability, potentially through an m6A-dependent mechanism. In summary, our findings identify ELAVL2 as a critical tumor suppressor and mRNA stabilizer that regulates MES transition in GBM, underscoring its role in transcriptomic plasticity and glioma progression. Neoplasms. Tumors. Oncology. Including cancer and carcinogens Ji Hyeon You verfasserin aut Yeonjoo Ryu verfasserin aut Gyuri Park verfasserin aut Urim Lee verfasserin aut Hyo Eun Moon verfasserin aut Hye Ran Park verfasserin aut Chang W. Song verfasserin aut Ja-Lok Ku verfasserin aut Sung-Hye Park verfasserin aut Sun Ha Paek verfasserin aut In npj Precision Oncology Nature Portfolio, 2017 8(2024), 1, Seite 16 (DE-627)884384454 (DE-600)2891458-2 2397768X nnns volume:8 year:2024 number:1 pages:16 https://doi.org/10.1038/s41698-024-00566-1 kostenfrei https://doaj.org/article/2a87bad4a8154cc9969bb2a939983550 kostenfrei https://doi.org/10.1038/s41698-024-00566-1 kostenfrei https://doaj.org/toc/2397-768X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2024 1 16
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author	Yona Kim
spellingShingle	Yona Kim misc RC254-282 misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens ELAVL2 loss promotes aggressive mesenchymal transition in glioblastoma
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topic_title	RC254-282 ELAVL2 loss promotes aggressive mesenchymal transition in glioblastoma
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title	ELAVL2 loss promotes aggressive mesenchymal transition in glioblastoma
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title_full	ELAVL2 loss promotes aggressive mesenchymal transition in glioblastoma
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author_browse	Yona Kim Ji Hyeon You Yeonjoo Ryu Gyuri Park Urim Lee Hyo Eun Moon Hye Ran Park Chang W. Song Ja-Lok Ku Sung-Hye Park Sun Ha Paek
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title_sort	elavl2 loss promotes aggressive mesenchymal transition in glioblastoma
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title_auth	ELAVL2 loss promotes aggressive mesenchymal transition in glioblastoma
abstract	Abstract Glioblastoma (GBM), the most lethal primary brain cancer, exhibits intratumoral heterogeneity and molecular plasticity, posing challenges for effective treatment. Despite this, the regulatory mechanisms underlying such plasticity, particularly mesenchymal (MES) transition, remain poorly understood. In this study, we elucidate the role of the RNA-binding protein ELAVL2 in regulating aggressive MES transformation in GBM. We found that ELAVL2 is most frequently deleted in GBM compared to other cancers and associated with distinct clinical and molecular features. Transcriptomic analysis revealed that ELAVL2-mediated alterations correspond to specific GBM subtype signatures. Notably, ELAVL2 expression negatively correlated with epithelial-to-mesenchymal transition (EMT)-related genes, and its loss promoted MES process and chemo-resistance in GBM cells, whereas ELAVL2 overexpression exerted the opposite effect. Further investigation via tissue microarray analysis demonstrated that high ELAVL2 protein expression confers a favorable survival outcome in GBM patients. Mechanistically, ELAVL2 was shown to directly bind to the transcripts of EMT-inhibitory molecules, SH3GL3 and DNM3, modulating their mRNA stability, potentially through an m6A-dependent mechanism. In summary, our findings identify ELAVL2 as a critical tumor suppressor and mRNA stabilizer that regulates MES transition in GBM, underscoring its role in transcriptomic plasticity and glioma progression.
abstractGer	Abstract Glioblastoma (GBM), the most lethal primary brain cancer, exhibits intratumoral heterogeneity and molecular plasticity, posing challenges for effective treatment. Despite this, the regulatory mechanisms underlying such plasticity, particularly mesenchymal (MES) transition, remain poorly understood. In this study, we elucidate the role of the RNA-binding protein ELAVL2 in regulating aggressive MES transformation in GBM. We found that ELAVL2 is most frequently deleted in GBM compared to other cancers and associated with distinct clinical and molecular features. Transcriptomic analysis revealed that ELAVL2-mediated alterations correspond to specific GBM subtype signatures. Notably, ELAVL2 expression negatively correlated with epithelial-to-mesenchymal transition (EMT)-related genes, and its loss promoted MES process and chemo-resistance in GBM cells, whereas ELAVL2 overexpression exerted the opposite effect. Further investigation via tissue microarray analysis demonstrated that high ELAVL2 protein expression confers a favorable survival outcome in GBM patients. Mechanistically, ELAVL2 was shown to directly bind to the transcripts of EMT-inhibitory molecules, SH3GL3 and DNM3, modulating their mRNA stability, potentially through an m6A-dependent mechanism. In summary, our findings identify ELAVL2 as a critical tumor suppressor and mRNA stabilizer that regulates MES transition in GBM, underscoring its role in transcriptomic plasticity and glioma progression.
abstract_unstemmed	Abstract Glioblastoma (GBM), the most lethal primary brain cancer, exhibits intratumoral heterogeneity and molecular plasticity, posing challenges for effective treatment. Despite this, the regulatory mechanisms underlying such plasticity, particularly mesenchymal (MES) transition, remain poorly understood. In this study, we elucidate the role of the RNA-binding protein ELAVL2 in regulating aggressive MES transformation in GBM. We found that ELAVL2 is most frequently deleted in GBM compared to other cancers and associated with distinct clinical and molecular features. Transcriptomic analysis revealed that ELAVL2-mediated alterations correspond to specific GBM subtype signatures. Notably, ELAVL2 expression negatively correlated with epithelial-to-mesenchymal transition (EMT)-related genes, and its loss promoted MES process and chemo-resistance in GBM cells, whereas ELAVL2 overexpression exerted the opposite effect. Further investigation via tissue microarray analysis demonstrated that high ELAVL2 protein expression confers a favorable survival outcome in GBM patients. Mechanistically, ELAVL2 was shown to directly bind to the transcripts of EMT-inhibitory molecules, SH3GL3 and DNM3, modulating their mRNA stability, potentially through an m6A-dependent mechanism. In summary, our findings identify ELAVL2 as a critical tumor suppressor and mRNA stabilizer that regulates MES transition in GBM, underscoring its role in transcriptomic plasticity and glioma progression.
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title_short	ELAVL2 loss promotes aggressive mesenchymal transition in glioblastoma
url	https://doi.org/10.1038/s41698-024-00566-1 https://doaj.org/article/2a87bad4a8154cc9969bb2a939983550 https://doaj.org/toc/2397-768X
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