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Suppression of long non-coding RNA PCAT19 inhibits glioma cell proliferation and invasion, and increases cell apoptosis through regulation of MELK targeted by miR-142-5p

Genes & Genomics 2020년 42권 11호 p.1299 ~ 1310
Xie Yu-Hua, Hu Jiao,
소속 상세정보
 ( Xie Yu-Hua ) - Chenzhou No. 1 People’s Hospital Department of Rehabilitation Medicine
 ( Hu Jiao ) - Chenzhou No. 1 People’s Hospital Emergency Department

Abstract


Background: Glioma has the chief type of primary brain tumors worldwide. The glioma may be controlled by regulators including some lncRNAs, miRNAs, and proteins.

Objective: Our study aims to discover the underlying mechanism for lncPCAT19/miR-142-5p/MELK axis in glioma progression.

Methods: The clinical samples were from patients with gliomas in our Hospital. Hematoxylin?eosin staining (H&E) was applied to determine the clinical pathological changes. Real time PCR was performed to measure the levels of lncPCAT19, miR-142-5p, MELK, and expression of other genes. Western blot was conducted to detect the protein level of MELK. RIP assay was performed to analyze the interaction between lncPCAT19 and miR-142-5p, and dual-luciferase reporter assay was used to determine the binding site between lncPCAT19 and miR-142-5p. CCK-8, colony formation assay, flow cytometry, and trans-well assay were carried out to confirm cell proliferation, colony formation, apoptosis, and invasion, respectively.

Results: LncPCAT19 was increased in cancer tissues. Then, lncPCAT19 could interact with and down-regulate miR-142-5p. Knockdown of lncPCAT19 distinctly inhibited tumor growth in vivo. Interfering lncPCAT19/overexpression of miR-142-5p decreased glioma cell proliferation, colony formation and invasion, and promoted cell apoptosis by down-regulating expression of Cyclin B1, CDK2, N-cadherin, Bcl-2, and by up-regulating expression of Bax and E-cadherin. Moreover, overexpression of lncPCAT19 overturned tumor-suppressing role of miR-142-5p in cells. Additionally, lncPCAT19 and miR-142-5p synergistically regulated expression of MELK. In conclusion, lncPCAT19 enhanced glioma development via increasing MELK by performing as a sponge of miR-142-5p.

Conclusions: LncPCAT19 promotes glioma progression by sponging miR-142-5p to upregulate MELK levels. Thus, lncPCAT19/miR-142-5p/MELK signaling would be a potential target for glioma treatment.

키워드

LncPCAT19; miR-142-5p; MELK; Xenografts; Glioma

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