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자료유형
학술저널
저자정보
Yu‑hua Xie (Chenzhou No. 1 People’s Hospital) Jiao Hu (Chenzhou No. 1 People’s Hospital)
저널정보
한국유전학회 Genes & Genomics Genes & Genomics Vol.42 No.11
발행연도
2020.1
수록면
1,299 - 1,310 (12page)

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Background Glioma has the chief type of primary brain tumors worldwide. The glioma may be controlled by regulatorsincluding some lncRNAs, miRNAs, and proteins. Objective Our study aims to discover the underlying mechanism for lncPCAT19/miR-142-5p/MELK axis in gliomaprogression. Methods The clinical samples were from patients with gliomas in our Hospital. Hematoxylin–eosin staining (H&E) wasapplied 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. RIPassay was performed to analyze the interaction between lncPCAT19 and miR-142-5p, and dual-luciferase reporter assay wasused 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-142-5pdecreased glioma cell proliferation, colony formation and invasion, and promoted cell apoptosis by down-regulating expressionof Cyclin B1, CDK2, N-cadherin, Bcl-2, and by up-regulating expression of Bax and E-cadherin. Moreover, overexpressionof lncPCAT19 overturned tumor-suppressing role of miR-142-5p in cells. Additionally, lncPCAT19 and miR-142-5psynergistically regulated expression of MELK. In conclusion, lncPCAT19 enhanced glioma development via increasingMELK 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.

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