Wang Shuwei, Guo Xinru, Lv Wenying, Li Yanteng, Zhang Leiming, Dong Chao, Zhang Jianning, Cheng Gang
Department of Neurosurgery, Sixth Medical Center, Chinese PLA General Hospital, Beijing 100048, People's Republic of China.
Cancer Manag Res. 2020 Apr 15;12:2541-2547. doi: 10.2147/CMAR.S227496. eCollection 2020.
Ribosomal protein SA pseudogene 52 (RPSAP52) has been characterized as an oncogenic lncRNA in pituitary tumors. Analysis of TCGA dataset revealed the upregulation of RPSAP52 in glioblastoma (GBM). We, therefore, investigated the roles of RPSAP52 in GBM.
A total of 50 GBM patients (33 males and 20 females; 54-75 years; mean age: 61.8±5.8 years) were selected from the 89 cases of GBM patients. Under the guidance of MRI, brain biopsy was performed to collect GBM tissues from each patient for the diagnosis of GBM. U-373 MG cells were employed and had transient transfections. qRNA, Western blot, and a series of experiments were performed to characterize their associations.
The results showed that RPSAP52 was upregulated in GBM patients, and its high expression levels predicted poor survival. In GBM tissues, expression levels of RPSAP52 were significantly and positively correlated with that of TGF-β1. In GBM tissues, RPSAP52 positively regulated the expression of TGF-β1. Cell stemness assay showed that, compared to C and NC groups, overexpression of RPSAP52 and TGF-β1 led to increased, while silencing of RPSAP52 led to decreased CD133+ cells. Overexpression of TGF-β1 attenuated the effects of RPSAP52 siRNA silencing.
Therefore, RPSAP52 upregulates TGF-β1 to increase cancer cell stemness and predict postoperative survival in GBM.
核糖体蛋白SA假基因52（RPSAP52）已被鉴定为垂体肿瘤中的一种致癌长链非编码RNA。对TCGA数据集的分析显示，胶质母细胞瘤（GBM）中RPSAP52表达上调。因此，我们研究了RPSAP52在GBM中的作用。
从89例GBM患者中选取50例（男33例，女20例；年龄54 - 75岁；平均年龄：61.8±5.8岁）。在MRI引导下进行脑活检，从每位患者收集GBM组织用于GBM诊断。采用U - 373 MG细胞并进行瞬时转染。进行qRNA、蛋白质印迹及一系列实验以表征它们之间的关联。
结果显示，GBM患者中RPSAP52上调，其高表达水平预示着较差的生存率。在GBM组织中，RPSAP52的表达水平与TGF-β1的表达水平显著正相关。在GBM组织中，RPSAP52正向调节TGF-β1的表达。细胞干性分析表明，与C组和NC组相比，RPSAP52和TGF-β1过表达导致CD133 +细胞增加，而RPSAP52沉默则导致CD133 +细胞减少。TGF-β1过表达减弱了RPSAP52 siRNA沉默的作用。
因此，RPSAP52上调TGF-β1以增加GBM中的癌细胞干性并预测术后生存率。
