Αρχειοθήκη ιστολογίου

Τρίτη 3 Απριλίου 2018

CPEB4 regulates glioblastoma cell proliferation and predicts poor outcome of patients

Publication date: Available online 3 April 2018
Source:Clinical Neurology and Neurosurgery
Author(s): Hong-xiang Wang, Rong Qin, Jian Mao, Qi-lin Huang, Fan Hong, Feng Li, Zhen-yu Gong, Tao Xu, Yong Yan, Shao-hui Chao, Shi-kun Zhang, Ju-xiang Chen
ObjectiveCytoplasmic polyadenylation element binding protein 4 (CPEB4) is a regulator of gene expression at transcriptional level and has been reported to be associated with biological malignancy in cancers. However, little was known about the correlation between CPEB4 and glioblastoma cell proliferation and the prognostic significance in patients. Our aim was to investigate the functional role and prognostic value of CPEB4 in glioblastoma.Patients and methodsWe determined the expression of CPEB4 protein using immunohistochemistry in tissue microarrays containing 278 glioma patients (including 98 primary glioblastomas) and evaluated its association with pathological grades and clinical outcome by univariate and multivariate analyses. And then, lentiviral-mediated RNAi targeting CPEB4 was utilized to study the role of CPEB4 in glioblastoma cell proliferation.ResultsIn our cohort, CPEB4 expression was positively related to glioma pathological grade (p < 0.01) and elevated in glioblastoma (p < 0.01). High expression of CPEB4 was associated with significantly poor prognosis, and could be identified as an independent risk factor for overall survival (OS) and progression-free survival (PFS) of glioblastoma patients (hazard ratio (HR) = 1.730, p = 0.014 and HR = 1.877, p = 0.004, respectively). In vitro studies further showed that downregulation of CPEB4 significantly reduced the growth rate of T98G and U251 cells comparing with the controls.ConclusionOur study indicated that increased expression of CPEB4 in primary glioblastoma is a novel biomarker for predicting poor outcome of patients and suppression of CPEB4 inhibit tumor cell proliferation, suggesting a potential therapeutic target for glioblastoma.



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