KIF4A promotes epithelial–mesenchymal transition by activating the TGF-β/SMAD signaling pathway in glioma cells
Gliomas are the most prevalent type of primary brain tumor, with poor prognosis reported in patients with high-grade glioma. Kinesin family member 4 A (KIF4A) stimulates the proliferation, migration, and invasion of tumor cells. However, its function in gliomas has not been clearly established. Ther...
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| Veröffentlicht in: | Molecular and cellular biochemistry 2025-01, Vol.480 (1), p.217-230 |
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| creator | Xu, Yao Xue, Guangren Zhou, Lei Wu, Gaotian Hu, Lingji Ma, Shuchen Zhang, Jian Li, Xiangdong |
| description | Gliomas are the most prevalent type of primary brain tumor, with poor prognosis reported in patients with high-grade glioma. Kinesin family member 4 A (KIF4A) stimulates the proliferation, migration, and invasion of tumor cells. However, its function in gliomas has not been clearly established. Therefore, this study aimed to investigate the effects of KIF4A on the epithelial–mesenchymal transition and invasion of glioma cells. We searched The Cancer Genome Atlas and Chinese Glioma Genome Atlas databases to identify KIF4A-related signaling pathways and downstream genes. We further validated them using western blotting, transwell migration and invasion, wound-healing scratch, and dual-luciferase reporter assays in U251 and U87 human glioblastoma cells. Our analysis of the Cancer Genome Atlas and Chinese Glioma Genome Atlas data showed elevated KIF4A expression in patients with gliomas and was associated with clinical grade. Here, KIF4A overexpression promoted the migration, invasion, and proliferation of glioma cells, whereas KIF4A knockdown showed contrasting results. Gene Ontology (GO) and Gene Set Enrichment Analysis (GSEA) analyses demonstrated that KIF4A positively controls TGF-β/SMAD signaling in glioma cells. Additionally, genetic correlation analysis revealed that KIF4A transcriptionally controls benzimidazoles-1 expression in glioma cells. KIF4A promotes the epithelial–mesenchymal transition by regulating the TGF-β/SMAD signaling pathway via benzimidazoles-1 in glioma cells. |
| doi_str_mv | 10.1007/s11010-024-04943-z |
| format | Article |
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Kinesin family member 4 A (KIF4A) stimulates the proliferation, migration, and invasion of tumor cells. However, its function in gliomas has not been clearly established. Therefore, this study aimed to investigate the effects of KIF4A on the epithelial–mesenchymal transition and invasion of glioma cells. We searched The Cancer Genome Atlas and Chinese Glioma Genome Atlas databases to identify KIF4A-related signaling pathways and downstream genes. We further validated them using western blotting, transwell migration and invasion, wound-healing scratch, and dual-luciferase reporter assays in U251 and U87 human glioblastoma cells. Our analysis of the Cancer Genome Atlas and Chinese Glioma Genome Atlas data showed elevated KIF4A expression in patients with gliomas and was associated with clinical grade. Here, KIF4A overexpression promoted the migration, invasion, and proliferation of glioma cells, whereas KIF4A knockdown showed contrasting results. Gene Ontology (GO) and Gene Set Enrichment Analysis (GSEA) analyses demonstrated that KIF4A positively controls TGF-β/SMAD signaling in glioma cells. Additionally, genetic correlation analysis revealed that KIF4A transcriptionally controls benzimidazoles-1 expression in glioma cells. KIF4A promotes the epithelial–mesenchymal transition by regulating the TGF-β/SMAD signaling pathway via benzimidazoles-1 in glioma cells.</description><identifier>ISSN: 0300-8177</identifier><identifier>ISSN: 1573-4919</identifier><identifier>EISSN: 1573-4919</identifier><identifier>DOI: 10.1007/s11010-024-04943-z</identifier><identifier>PMID: 38411896</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Benzimidazoles ; Biochemistry ; Biomedical and Life Sciences ; Brain cancer ; Brain Neoplasms - genetics ; Brain Neoplasms - metabolism ; Brain Neoplasms - pathology ; Brain tumors ; Cancer ; Cancer Research ; Cardiology ; Cell Line, Tumor ; Cell migration ; Cell Movement ; Cell Proliferation ; Correlation analysis ; Epithelial-Mesenchymal Transition ; Gene Expression Regulation, Neoplastic ; Gene set enrichment analysis ; Genetic analysis ; Genomes ; Genomic analysis ; Glioblastoma ; Glioblastoma cells ; Glioma ; Glioma - genetics ; Glioma - metabolism ; Glioma - pathology ; Glioma cells ; Humans ; Kinesin ; Kinesins - genetics ; Kinesins - metabolism ; Life Sciences ; Medical Biochemistry ; Neoplasm Proteins - genetics ; Neoplasm Proteins - metabolism ; Signal Transduction ; Smad protein ; Smad Proteins - metabolism ; Transforming Growth Factor beta - metabolism ; Transforming growth factor-b ; Tumor cells ; Tumors ; Western blotting ; Wound healing</subject><ispartof>Molecular and cellular biochemistry, 2025-01, Vol.480 (1), p.217-230</ispartof><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 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>2024. 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Kinesin family member 4 A (KIF4A) stimulates the proliferation, migration, and invasion of tumor cells. However, its function in gliomas has not been clearly established. Therefore, this study aimed to investigate the effects of KIF4A on the epithelial–mesenchymal transition and invasion of glioma cells. We searched The Cancer Genome Atlas and Chinese Glioma Genome Atlas databases to identify KIF4A-related signaling pathways and downstream genes. We further validated them using western blotting, transwell migration and invasion, wound-healing scratch, and dual-luciferase reporter assays in U251 and U87 human glioblastoma cells. Our analysis of the Cancer Genome Atlas and Chinese Glioma Genome Atlas data showed elevated KIF4A expression in patients with gliomas and was associated with clinical grade. Here, KIF4A overexpression promoted the migration, invasion, and proliferation of glioma cells, whereas KIF4A knockdown showed contrasting results. Gene Ontology (GO) and Gene Set Enrichment Analysis (GSEA) analyses demonstrated that KIF4A positively controls TGF-β/SMAD signaling in glioma cells. Additionally, genetic correlation analysis revealed that KIF4A transcriptionally controls benzimidazoles-1 expression in glioma cells. KIF4A promotes the epithelial–mesenchymal transition by regulating the TGF-β/SMAD signaling pathway via benzimidazoles-1 in glioma cells.</description><subject>Benzimidazoles</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Brain cancer</subject><subject>Brain Neoplasms - genetics</subject><subject>Brain Neoplasms - metabolism</subject><subject>Brain Neoplasms - pathology</subject><subject>Brain tumors</subject><subject>Cancer</subject><subject>Cancer Research</subject><subject>Cardiology</subject><subject>Cell Line, Tumor</subject><subject>Cell migration</subject><subject>Cell Movement</subject><subject>Cell Proliferation</subject><subject>Correlation analysis</subject><subject>Epithelial-Mesenchymal Transition</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Gene set enrichment analysis</subject><subject>Genetic analysis</subject><subject>Genomes</subject><subject>Genomic analysis</subject><subject>Glioblastoma</subject><subject>Glioblastoma cells</subject><subject>Glioma</subject><subject>Glioma - genetics</subject><subject>Glioma - metabolism</subject><subject>Glioma - pathology</subject><subject>Glioma cells</subject><subject>Humans</subject><subject>Kinesin</subject><subject>Kinesins - genetics</subject><subject>Kinesins - metabolism</subject><subject>Life Sciences</subject><subject>Medical Biochemistry</subject><subject>Neoplasm Proteins - genetics</subject><subject>Neoplasm Proteins - metabolism</subject><subject>Signal Transduction</subject><subject>Smad protein</subject><subject>Smad Proteins - metabolism</subject><subject>Transforming Growth Factor beta - metabolism</subject><subject>Transforming growth factor-b</subject><subject>Tumor cells</subject><subject>Tumors</subject><subject>Western blotting</subject><subject>Wound healing</subject><issn>0300-8177</issn><issn>1573-4919</issn><issn>1573-4919</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2025</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kUtOWzEUhq2qCAJ0Ax1UljrpxHDO9ePeO4ygoQhQB9Cx5Vw7idF9pLbTKozYAzthIV1EV1KHQJE66MiD853_-NdHyHuEIwQojyMiIDAoBANRC87u3pARypIzUWP9loyAA7AKy3KP7Md4C5kGxF2yxyuBWNVqRMLF-USM6TIM3ZBcpG7p08K13rS_7x86F13fLNadaWkKpo8--aGn0zU1TfI_TPL9nGac3pxN2K_H4-ur8SmNft6bdjNZmrT4adbU93Te-qEztHFtGw_Jzsy00b17fg_It8nnm5Mv7PLr2fnJ-JI1vFCJVU6q3K-YgZVWlCqXVdZJ66CRteEIjVKGV8agFRzsVKpyWs2stVgCL6ziB-TTNjeX-75yMenOx80PTO-GVdRFzQvBMywz-vEf9HZYhVwjao4S6lqWRZWpYks1YYgxuJleBt-ZsNYIemNEb43obEQ_GdF3eenDc_Rq2jn7d-VFQQb4Foh51M9deL39n9g_hNaYNw</recordid><startdate>20250101</startdate><enddate>20250101</enddate><creator>Xu, Yao</creator><creator>Xue, Guangren</creator><creator>Zhou, Lei</creator><creator>Wu, Gaotian</creator><creator>Hu, Lingji</creator><creator>Ma, Shuchen</creator><creator>Zhang, Jian</creator><creator>Li, Xiangdong</creator><general>Springer US</general><general>Springer Nature B.V</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>7QL</scope><scope>7QP</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20250101</creationdate><title>KIF4A promotes epithelial–mesenchymal transition by activating the TGF-β/SMAD signaling pathway in glioma cells</title><author>Xu, Yao ; 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Kinesin family member 4 A (KIF4A) stimulates the proliferation, migration, and invasion of tumor cells. However, its function in gliomas has not been clearly established. Therefore, this study aimed to investigate the effects of KIF4A on the epithelial–mesenchymal transition and invasion of glioma cells. We searched The Cancer Genome Atlas and Chinese Glioma Genome Atlas databases to identify KIF4A-related signaling pathways and downstream genes. We further validated them using western blotting, transwell migration and invasion, wound-healing scratch, and dual-luciferase reporter assays in U251 and U87 human glioblastoma cells. Our analysis of the Cancer Genome Atlas and Chinese Glioma Genome Atlas data showed elevated KIF4A expression in patients with gliomas and was associated with clinical grade. Here, KIF4A overexpression promoted the migration, invasion, and proliferation of glioma cells, whereas KIF4A knockdown showed contrasting results. Gene Ontology (GO) and Gene Set Enrichment Analysis (GSEA) analyses demonstrated that KIF4A positively controls TGF-β/SMAD signaling in glioma cells. Additionally, genetic correlation analysis revealed that KIF4A transcriptionally controls benzimidazoles-1 expression in glioma cells. KIF4A promotes the epithelial–mesenchymal transition by regulating the TGF-β/SMAD signaling pathway via benzimidazoles-1 in glioma cells.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>38411896</pmid><doi>10.1007/s11010-024-04943-z</doi><tpages>14</tpages></addata></record> |
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| subjects | Benzimidazoles Biochemistry Biomedical and Life Sciences Brain cancer Brain Neoplasms - genetics Brain Neoplasms - metabolism Brain Neoplasms - pathology Brain tumors Cancer Cancer Research Cardiology Cell Line, Tumor Cell migration Cell Movement Cell Proliferation Correlation analysis Epithelial-Mesenchymal Transition Gene Expression Regulation, Neoplastic Gene set enrichment analysis Genetic analysis Genomes Genomic analysis Glioblastoma Glioblastoma cells Glioma Glioma - genetics Glioma - metabolism Glioma - pathology Glioma cells Humans Kinesin Kinesins - genetics Kinesins - metabolism Life Sciences Medical Biochemistry Neoplasm Proteins - genetics Neoplasm Proteins - metabolism Signal Transduction Smad protein Smad Proteins - metabolism Transforming Growth Factor beta - metabolism Transforming growth factor-b Tumor cells Tumors Western blotting Wound healing |
| title | KIF4A promotes epithelial–mesenchymal transition by activating the TGF-β/SMAD signaling pathway in glioma cells |
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