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LncRNA RPSAP52 Upregulates TGF-β1 to Increase Cancer Cell Stemness and Predict Postoperative Survival in Glioblastoma

Authors Wang S, Guo X, Lv W, Li Y, Zhang L, Dong C, Zhang J, Cheng G

Received 16 August 2019

Accepted for publication 11 February 2020

Published 15 April 2020 Volume 2020:12 Pages 2541—2547

DOI https://doi.org/10.2147/CMAR.S227496

Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 2

Editor who approved publication: Dr Seema Singh


Shuwei Wang, Xinru Guo, Wenying Lv, Yanteng Li, Leiming Zhang, Chao Dong, Jianning Zhang, Gang Cheng

Department of Neurosurgery, Sixth Medical Center, Chinese PLA General Hospital, Beijing 100048, People’s Republic of China

Correspondence: Jianning Zhang; Gang Cheng
Department of Neurosurgery, Sixth Medical Center, Chinese PLA General Hospital, No. 6 Pucheng Road, Beijing 100048, People’s Republic of China
Tel +86 10-66951351
Email jianningz36@aliyun.com; bgsvsaswgxo6@163.com

Introduction: 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.
Methods: 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.
Results: 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-β 1. In GBM tissues, RPSAP52 positively regulated the expression of TGF-β 1. Cell stemness assay showed that, compared to C and NC groups, overexpression of RPSAP52 and TGF-β 1 led to increased, while silencing of RPSAP52 led to decreased CD133+ cells. Overexpression of TGF-β 1 attenuated the effects of RPSAP52 siRNA silencing.
Conclusion: Therefore, RPSAP52 upregulates TGF-β 1 to increase cancer cell stemness and predict postoperative survival in GBM.

Keywords: glioblastoma, RPSAP52, TGF-β 1, survival, stemness


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