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 |