Academic Journal

BEX1 and BEX4 Induce GBM Progression through Regulation of Actin Polymerization and Activation of YAP/TAZ Signaling

التفاصيل البيبلوغرافية
العنوان: BEX1 and BEX4 Induce GBM Progression through Regulation of Actin Polymerization and Activation of YAP/TAZ Signaling
المؤلفون: Sungmin Lee, Hyunkoo Kang, Eunguk Shin, Jaewan Jeon, HyeSook Youn, BuHyun Youn
المصدر: International Journal of Molecular Sciences; Volume 22; Issue 18; Pages: 9845
بيانات النشر: Multidisciplinary Digital Publishing Institute
سنة النشر: 2021
المجموعة: MDPI Open Access Publishing
مصطلحات موضوعية: glioblastoma, actin polymerization, BEX1, BEX4, latrunculin B
جغرافية الموضوع: agris
الوصف: GBM is a high-grade cancer that originates from glial cells and has a poor prognosis. Although a combination of surgery, radiotherapy, and chemotherapy is prescribed to patients, GBM is highly resistant to therapies, and surviving cells show increased aggressiveness. In this study, we investigated the molecular mechanism underlying GBM progression after radiotherapy by establishing a GBM orthotopic xenograft mouse model. Based on transcriptomic analysis, we found that the expression of BEX1 and BEX4 was upregulated in GBM cells surviving radiotherapy. We also found that upregulated expression of BEX1 and BEX4 was involved in the formation of the filamentous cytoskeleton and altered mechanotransduction, which resulted in the activation of the YAP/TAZ signaling pathway. BEX1- and BEX4-mediated YAP/TAZ activation enhanced the tumor formation, growth, and radioresistance of GBM cells. Additionally, latrunculin B inhibited GBM progression after radiotherapy by suppressing actin polymerization in an orthotopic xenograft mouse model. Taken together, we suggest the involvement of cytoskeleton formation in radiation-induced GBM progression and latrunculin B as a GBM radiosensitizer.
نوع الوثيقة: text
وصف الملف: application/pdf
اللغة: English
Relation: Biochemistry; https://dx.doi.org/10.3390/ijms22189845
DOI: 10.3390/ijms22189845
الاتاحة: https://doi.org/10.3390/ijms22189845
Rights: https://creativecommons.org/licenses/by/4.0/
رقم الانضمام: edsbas.580D774D
قاعدة البيانات: BASE
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