TUBA1C expression promotes proliferation by regulating the cell cycle and indicates poor prognosis in glioma

被引:25
作者
Gui, Shikai [1 ,3 ]
Chen, Peng [1 ]
Liu, Yu [1 ]
Chen, Qiaorong [1 ]
Cheng, Tianxiang [1 ]
Lv, Shulong [1 ]
Zhou, Tong [1 ]
Song, Zhen [1 ]
Xiao, Juexian [1 ]
He, Wei [1 ]
Yuan, Shengtao [2 ]
Cheng, Zujue [1 ,3 ]
机构
[1] Nanchang Univ, Affiliated Hosp 2, Dept Neurosurg, Nanchang 330000, Jiangxi, Peoples R China
[2] China Pharmaceut Univ, Jiangsu Ctr Pharmacodynam Res & Evaluat, Nanjing 210000, Jiangsu, Peoples R China
[3] Nanchang Univ, Nanchang 330000, Jiangxi, Peoples R China
关键词
Glioma; TUBA1C; Prognosis; Proliferation; Cell cycle; CLASSIFICATION;
D O I
10.1016/j.bbrc.2021.08.079
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Gliomas are the major type of primary brain tumors. Accumulating research has demonstrated that tubulin is connected with the development and malignant progression of tumors. TUBA1C is a subtype of a-tubulin and is linked to prognosis in multiple cancers. In this study, the prognosis-related gene TUBA1C in glioma was identified and analyzed by bioinformatic approaches such as Kaplan-Meier (KM) survival time analysis, univariate and multivariate Cox analysis, receiver operating characteristic (ROC) analysis and functional enrichment analysis. Based on the above analyses, we found that glioma tissues had significantly higher expression of TUBA1C than normal brain tissues, and high expression of TUBA1C has worse prognosis in glioma. Gene set enrichment analysis (GSEA) revealed the signaling pathways related to the cell cycle. Furthermore, knockdown of TUBA1C also inhibited proliferation and migration and caused apoptosis and G2/M phase arrest in glioma cells. This study demonstrated that high TUBA1C expression correlated with poor outcomes in glioma patients and that knocking down TUBA1C suppressed glioma cell proliferation via cell cycle arrest. In addition, TUBA1C might be a therapeutic biomarker for gliomas. (C) 2021 Elsevier Inc. All rights reserved.
引用
收藏
页码:130 / 138
页数:9
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