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The tumorigenic effect of the high expression of ABRACL in glioma and its potential as a therapeutic target.
Zhao, Chenhui; Wu, Zeyu; Yao, Zhipeng; Zhang, Fan; Zhao, Rui; Cao, Xiaoxiang; Ling, Shizhang; Jiang, Xiaochun.
Afiliación
  • Zhao C; Department of Neurosurgery, Shandong Provincial Third Hospital, Shandong University, Jinan, China.
  • Wu Z; Translational Research Institute for Neurological Disorders, The First Affiliated Hospital of Wannan Medical College (Yijishan Hospital of Wannan Medical College), Wannan Medical College, Wuhu, China.
  • Yao Z; School of Chemistry and Chemical Engineering, Southeast University, Nanjing, China.
  • Zhang F; School of Chemistry and Chemical Engineering, Southeast University, Nanjing, China.
  • Zhao R; Translational Research Institute for Neurological Disorders, The First Affiliated Hospital of Wannan Medical College (Yijishan Hospital of Wannan Medical College), Wannan Medical College, Wuhu, China.
  • Cao X; Translational Research Institute for Neurological Disorders, The First Affiliated Hospital of Wannan Medical College (Yijishan Hospital of Wannan Medical College), Wannan Medical College, Wuhu, China.
  • Ling S; Translational Research Institute for Neurological Disorders, The First Affiliated Hospital of Wannan Medical College (Yijishan Hospital of Wannan Medical College), Wannan Medical College, Wuhu, China.
  • Jiang X; Department of Neurosurgery, Shandong Provincial Third Hospital, Shandong University, Jinan, China.
Heliyon ; 10(17): e36597, 2024 Sep 15.
Article en En | MEDLINE | ID: mdl-39286126
ABSTRACT
Gliomas are the most common malignant intracranial tumors, with no effective treatments. Better understanding and identification of novel targets are urgently warranted. Actin-binding Rho activating C-terminal like (ABRACL) has been reported as an oncogene in several cancer types. However, the potential roles of ABRACL in the tumorigenesis of malignant glioma remain unknown. We discovered that ABRACL is highly expressed in different sub-types of gliomas in both CGGA and TCGA databases, which was further validated in glioblastoma cell lines and normal human astrocyte lines. RT-qPCR, Western blotting and immunohistochemistry demonstrated that ABRACL expression in glioma tissues was upregulated along with the increasing WHO grades. Further survival analysis of glioma patients also revealed that the overall survival of patients in the ABRACL high expression level group were significantly shorter than those in the low expression level group. Knockdown of ABRACL inhibited the proliferation, cell migration, invasion and cytodynamics behaviors in glioma cell lines via activating STAT3 signaling, which also induced apoptosis and cell cycle arrest. Conversely, overexpressing ABRACL promoted cell renewing and migration, enabled more flexible cell deformation, supporting ABRACL being a bona fide oncogene. Intracranial orthotopic xenograft experiment further confirmed that ABRACL downregulation significantly suppressed glioma growth. These results have demonstrated that the tumorigenic effect of ABRACL is partly mediated by STAT3, whose expression also correlates with clinical prognosis. ABRACL facilitates glioma malignancy phenotype through regulating the cytoskeleton by activating STAT3 pathway, suggesting that it may represent a potential therapeutic target for glioblastoma.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Heliyon Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación: Reino Unido
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Heliyon Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación: Reino Unido