[HTML][HTML] High expression of Bruton's tyrosine kinase (BTK) is required for EGFR-induced NF-κB activation and predicts poor prognosis in human glioma
C Yue, M Niu, QQ Shan, T Zhou, Y Tu, P Xie… - Journal of Experimental …, 2017 - Springer
C Yue, M Niu, QQ Shan, T Zhou, Y Tu, P Xie, L Hua, R Yu, X Liu
Journal of Experimental & Clinical Cancer Research, 2017•SpringerBackground Malignant glioma is the most common primary brain tumor in adults and has a
poor prognosis. However, there are no effective targeted therapies for glioma patients. Thus,
the development of novel targeted therapeutics for glioma is urgently needed. Methods In
this study, we examined the prognostic significance BTK expression in patients with glioma.
Furthermore, we investigated the mechanism and therapeutic potential of ibrutinib in the
treatment of human glioma in vitro and in vivo. Results Our data demonstrate that high …
poor prognosis. However, there are no effective targeted therapies for glioma patients. Thus,
the development of novel targeted therapeutics for glioma is urgently needed. Methods In
this study, we examined the prognostic significance BTK expression in patients with glioma.
Furthermore, we investigated the mechanism and therapeutic potential of ibrutinib in the
treatment of human glioma in vitro and in vivo. Results Our data demonstrate that high …
Background
Malignant glioma is the most common primary brain tumor in adults and has a poor prognosis. However, there are no effective targeted therapies for glioma patients. Thus, the development of novel targeted therapeutics for glioma is urgently needed.
Methods
In this study, we examined the prognostic significance BTK expression in patients with glioma. Furthermore, we investigated the mechanism and therapeutic potential of ibrutinib in the treatment of human glioma in vitro and in vivo.
Results
Our data demonstrate that high expression of BTK is a novel prognostic marker for poor survival in patients with glioma. BTK-specific inhibitor ibrutinib effectively inhibits the proliferation, migration and invasion ability of glioma cells. Furthermore, ibrutinib can induce G1 cell-cycle arrest by regulating multiple cell cycle-associated proteins. More importantly, we found that BTK inhibition significantly blocks the degradation of IκBα and prevents the nuclear accumulation of NF-κB p65 subunit induced by EGF in glioma cells.
Conclusions
Taken together, our study suggests that BTK is a novel prognostic marker and molecular therapeutic target for glioma. BTK is required for EGFR-induced NF-κB activation in glioma cells. These findings provide the basis for future clinical studies of ibrutinib for the treatment of glioma.
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