Open Access

ARTICLE

Knockdown of lncRNA PVT1 Inhibits Glioma Progression by Regulating miR-424 Expression

Yanjie Han^*1, Xinxin Li^*1, Fei He^†1, Jiliang Yan^*, Chunyan Ma^*, Xiaoli Zheng^‡, Jinli Zhang^*, Donghui Zhang^*, Cuiping Meng^*, Zhen Zhang^*, Xinying Ji^§

* Clinical Laboratory and Functional Laboratory, Kaifeng Central Hospital, Kaifeng, Henan, P.R. China
† Department of Cardiothoracic Surgery, Huai-He Hospital, College of Medicine, Henan University, Kaifeng, Henan, P.R. China
‡ Hospital Infection Control Office, First Affiliated Hospital of Henan University, Kaifeng, Henan, P.R. China
§ Henan International Joint Laboratory of Nuclear Protein Regulation, Henan University College of Medicine, Kaifeng, Henan, P.R. China

Oncology Research 2019, 27(6), 681-690. https://doi.org/10.3727/096504018X15424939990246

Abstract

Plasmacytoma variability translocation 1 (PVT1), an oncogene, has been reported to be highly expressed in many tumors, including human glioma, gastric cancer, and non-small cell lung cancer. Functionally, it could also regulate the development of tumor cells. However, its specific roles and pathogenesis in human gliomas are still not clear. This study investigated the function and mechanism of PVT1 knockdown in the proliferation and malignant transformation of human gliomas. We first examined the expression levels of PVT1 and miR- 424 in human glioma tissues and cell lines. We also used gene manipulation techniques to explore the effects of PVT1 knockdown on cell viability, migration, invasion, and miR-424. We found that PVT1 knockdown effectively inhibited cell viability, migration, and invasion of human glioma cells and increased miR-424 expression. Based on the negative correlation between PVT1 and miR-424, we then confirmed the direct interaction between PVT1 and miR-424 using RNA immunoprecipitation (RIP) and luciferase reporter assays. Further, we established a xenograft nude mouse model to determine the role and mechanism of PVT1 on tumor growth in vivo. In addition, PVT1 knockdown was shown to promote miR-424 in vivo. In summary, the present study demonstrated that PVT1 knockdown could negatively regulate miR-424 to inhibit human glioma cell activity, migration, and invasiveness. PVT1 knockdown could negatively regulate miR-424 to inhibit cellular activity, migration, and invasiveness in human gliomas, which explained the oncogenic mechanism of PVT1 in human gliomas. It also suggested that PVT1 might be a novel therapeutic target for human gliomas.

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