Overexpression of lncRNA PTENP1 suppresses glioma cell proliferation and metastasis in vitro
Authors Hu S, Xu L, Li L, Luo D, Zhao H, Li D, Peng B
Received 3 August 2018
Accepted for publication 18 October 2018
Published 21 December 2018 Volume 2019:12 Pages 147—156
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Dr Andrew Yee
Peer reviewer comments 2
Editor who approved publication: Dr Leo Jen-Liang Su
Su Hu,1,* Li Xu,1,2,* Lihua Li,1 Dongdong Luo,1 Hailin Zhao,1 Dan Li,1 Biao Peng1
1Department of Neurosurgery, The Affiliated Cancer Hospital & Institute of Guangzhou Medical University, Guangzhou 510095, Guangdong, People’s Republic of China; 2Department of Neurosurgery, The Central People’s Hospital of Zhanjiang, Zhanjiang 524045, Guangdong, People’s Republic of China
*These authors contributed equally to this work
Background: Glioma is one of the most common malignancies of the central nervous system in adults. The lncRNA PTEN pseudogene-1 (PTENP1) has been reported to play an important role in the development and progression of various cancers. However, the molecular mechanism by which lncRNA PTENP1 affects the development and progression of gliomas remains unclear.
Materials and methods: The levels of PTENP1 expression in glioma tissues and normal brain tissues were detected by quantitative real-time PCR. Cell Counting Kit-8 and 5-ethynyl-2'-deoxyuridine staining assays were performed to detect cell proliferation. Flow cytometry was used to analyze cell cycle progression. Transwell assay and scratch test were used to detect cell migration and invasion, and Western blot studies were performed to detect protein expression.
Results: Our results showed that expression of lncRNA PTENP1 was decreased in glioma tissues when compared with normal brain tissues. Overexpression of PTENP1 suppressed SHG44 and U251 cell proliferation and significantly decreased the numbers of S-phase cells. Furthermore, the invasion and migration abilities of SHG44 and U251 cells were reduced after being transfected with a PTENP1 overexpression plasmid. Overexpression of PTENP1 induced the expression of p21 protein and suppressed the p38 signaling pathway.
Conclusion: Our study investigated the function of PTENP1 in glioma and provided new insights for treating that malignancy.
Keywords: lncRNA PTENP1, glioma, proliferation, invasion, migration
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