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EphB3 receptor suppressor invasion, migration and proliferation in glioma by inhibiting EGFR-PI3K/AKT signaling pathway.
Xiao, Zumu; Huang, Shengxuan; Qiu, Wenjin; Pang, Mengru; Zeng, Xi; Xu, Xu; Yang, Yushi; Yang, Binglin; Chu, Liangzhao.
Afiliación
  • Xiao Z; Department of Neurosurgery, Sanming First Hospital Affiliated to Fujian Medical University, Sanming, Fujian, China; Department of Neurosurgery, the Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou, China.
  • Huang S; Department of Neurosurgery, Sanming First Hospital Affiliated to Fujian Medical University, Sanming, Fujian, China.
  • Qiu W; Department of Neurosurgery, the Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou, China.
  • Pang M; Department of Burn and Plastic Surgery, the Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou, China.
  • Zeng X; Department of Neurosurgery, the Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou, China.
  • Xu X; Department of Neurosurgery, the Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou, China.
  • Yang Y; Department of Neurosurgery, the Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou, China. Electronic address: 903026198@qq.com.
  • Yang B; Department of Breast, Sanming First Hospital Affiliated to Fujian Medical University, Sanming, Fujian, China. Electronic address: yangbinglin2005@126.com.
  • Chu L; Department of Neurosurgery, the Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou, China. Electronic address: 365446506@qq.com.
Brain Res ; 1830: 148796, 2024 May 01.
Article en En | MEDLINE | ID: mdl-38341169
ABSTRACT
Eph receptors are the largest subfamily of receptor tyrosine kinases, and they have been shown to play a crucial role in glioma. The EphB3 receptor is a member of this family, and its effect on the invasion, migration and proliferation of glioma cells was examined in this study. It was found that the expression of EphB3 was decreased in glioma specimens with increasing tumor grade. Additionally, the U87MG and U251 cell lines showed low levels of EphB3 expression. This finding was consistent with the negative correlation between EphB3 expression in glioma tissues and tumor grade. Depletion of EphB3 gene in U87MG and U251 cell lines resulted in a substantial enhancement of their invasion, migration, and proliferation capacities in vitro. Furthermore, the knockdown of EphB3 led to an upregulation of EGFR, p-PI3K, and p-AKT protein levels. On the other hand, EphB3 overexpression reduced the invasiveness, proliferative capacity and migration rate of U87MG and U251 cells, and downregulated EGFR, p-PI3K and p-AKT. These findings indicate that EphB3 functions as a tumor suppressor in glioma, and its downregulation enhances the malignant potential of glioma cells by activating the EGFR-PI3K/AKT pathway. Thus, EphB3 is a promising diagnostic marker for glioma, and the EphB3-EGFR-PI3K / AKT axis deserves further investigation as a potential therapeutic target.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Proteínas Proto-Oncogénicas c-akt / Glioma Límite: Humans Idioma: En Revista: Brain Res Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación: Países Bajos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Proteínas Proto-Oncogénicas c-akt / Glioma Límite: Humans Idioma: En Revista: Brain Res Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación: Países Bajos