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Eukaryotic initiation factor 4 A-3 promotes glioblastoma growth and invasion through the Notch1-dependent pathway

BACKGROUND: As an adult tumor with the most invasion and the highest mortality rate, the inherent heterogeneity of glioblastoma (GBM) is the main factor that causes treatment failure. Therefore, it is important to have a deeper understanding of the pathology of GBM. Some studies have shown that Euka...

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Autores principales: Wei, Lei, Pan, Mika, Jiang, Qiulan, Hu, Beiquan, Zhao, Jianyi, Zou, Chun, Chen, Liechun, Tang, Chunhai, Zou, Donghua
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10273507/
https://www.ncbi.nlm.nih.gov/pubmed/37322413
http://dx.doi.org/10.1186/s12885-023-10946-8
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author Wei, Lei
Pan, Mika
Jiang, Qiulan
Hu, Beiquan
Zhao, Jianyi
Zou, Chun
Chen, Liechun
Tang, Chunhai
Zou, Donghua
author_facet Wei, Lei
Pan, Mika
Jiang, Qiulan
Hu, Beiquan
Zhao, Jianyi
Zou, Chun
Chen, Liechun
Tang, Chunhai
Zou, Donghua
author_sort Wei, Lei
collection PubMed
description BACKGROUND: As an adult tumor with the most invasion and the highest mortality rate, the inherent heterogeneity of glioblastoma (GBM) is the main factor that causes treatment failure. Therefore, it is important to have a deeper understanding of the pathology of GBM. Some studies have shown that Eukaryotic Initiation Factor 4A-3 (EIF4A3) can promote the growth of many people’s tumors, and the role of specific molecules in GBM remains unclear. METHODS: The correlation between the expression of EIF4A3 gene and its prognosis was studied in 94 GBM patients using survival analysis. Further in vitro and in vivo experiments, the effect of EIF4A3 on GBM cells proliferation, migration, and the mechanism of EIF4A3 on GBM was explored. In addition, combined with bioinformatics analysis, we further confirmed that EIF4A3 contributes to the progress of GBM. RESULTS: The expression of EIF4A3 was upregulated in GBM tissues, and high expression of EIF4A3 is associated with poor prognosis in GBM. In vitro, knockdown of EIF4A3 significantly reduced the proliferation, migration, and invasion abilities of GBM cells, whereas overexpression of EIF4A3 led to the opposite effect. The analysis of differentially expressed genes related to EIF4A3 indicates that it is involved in many cancer-related pathways, such as Notch and JAK-STAT3 signal pathway. In Besides, we demonstrated the interaction between EIF4A3 and Notch1 by RNA immunoprecipitation. Finally, the biological function of EIF4A3-promoted GBM was confirmed in living organisms. CONCLUSION: The results of this study suggest that EIF4A3 may be a potential prognostic factor, and Notch1 participates in the proliferation and metastasis of GBM cells mediated by EIF4A3. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12885-023-10946-8.
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spelling pubmed-102735072023-06-17 Eukaryotic initiation factor 4 A-3 promotes glioblastoma growth and invasion through the Notch1-dependent pathway Wei, Lei Pan, Mika Jiang, Qiulan Hu, Beiquan Zhao, Jianyi Zou, Chun Chen, Liechun Tang, Chunhai Zou, Donghua BMC Cancer Research BACKGROUND: As an adult tumor with the most invasion and the highest mortality rate, the inherent heterogeneity of glioblastoma (GBM) is the main factor that causes treatment failure. Therefore, it is important to have a deeper understanding of the pathology of GBM. Some studies have shown that Eukaryotic Initiation Factor 4A-3 (EIF4A3) can promote the growth of many people’s tumors, and the role of specific molecules in GBM remains unclear. METHODS: The correlation between the expression of EIF4A3 gene and its prognosis was studied in 94 GBM patients using survival analysis. Further in vitro and in vivo experiments, the effect of EIF4A3 on GBM cells proliferation, migration, and the mechanism of EIF4A3 on GBM was explored. In addition, combined with bioinformatics analysis, we further confirmed that EIF4A3 contributes to the progress of GBM. RESULTS: The expression of EIF4A3 was upregulated in GBM tissues, and high expression of EIF4A3 is associated with poor prognosis in GBM. In vitro, knockdown of EIF4A3 significantly reduced the proliferation, migration, and invasion abilities of GBM cells, whereas overexpression of EIF4A3 led to the opposite effect. The analysis of differentially expressed genes related to EIF4A3 indicates that it is involved in many cancer-related pathways, such as Notch and JAK-STAT3 signal pathway. In Besides, we demonstrated the interaction between EIF4A3 and Notch1 by RNA immunoprecipitation. Finally, the biological function of EIF4A3-promoted GBM was confirmed in living organisms. CONCLUSION: The results of this study suggest that EIF4A3 may be a potential prognostic factor, and Notch1 participates in the proliferation and metastasis of GBM cells mediated by EIF4A3. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12885-023-10946-8. BioMed Central 2023-06-15 /pmc/articles/PMC10273507/ /pubmed/37322413 http://dx.doi.org/10.1186/s12885-023-10946-8 Text en © The Author(s) 2023 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
spellingShingle Research
Wei, Lei
Pan, Mika
Jiang, Qiulan
Hu, Beiquan
Zhao, Jianyi
Zou, Chun
Chen, Liechun
Tang, Chunhai
Zou, Donghua
Eukaryotic initiation factor 4 A-3 promotes glioblastoma growth and invasion through the Notch1-dependent pathway
title Eukaryotic initiation factor 4 A-3 promotes glioblastoma growth and invasion through the Notch1-dependent pathway
title_full Eukaryotic initiation factor 4 A-3 promotes glioblastoma growth and invasion through the Notch1-dependent pathway
title_fullStr Eukaryotic initiation factor 4 A-3 promotes glioblastoma growth and invasion through the Notch1-dependent pathway
title_full_unstemmed Eukaryotic initiation factor 4 A-3 promotes glioblastoma growth and invasion through the Notch1-dependent pathway
title_short Eukaryotic initiation factor 4 A-3 promotes glioblastoma growth and invasion through the Notch1-dependent pathway
title_sort eukaryotic initiation factor 4 a-3 promotes glioblastoma growth and invasion through the notch1-dependent pathway
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10273507/
https://www.ncbi.nlm.nih.gov/pubmed/37322413
http://dx.doi.org/10.1186/s12885-023-10946-8
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