4.6 Article

Circ_101064 regulates the proliferation, invasion and migration of glioma cells through miR-154-5p/PIWIL1 axis

Journal

Publisher

ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2019.12.096

Keywords

Circ_101064; miR-154-5p; PIWIL1; Glioma; Proliferation; Invasion; Migration

Funding

  1. National Natural Science Foundation of China [81801071]

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This study aimed to investigate the effects of Circ_101064 on glioma cell proliferation, invasion, migration and explore the underlying mechanisms. The expression levels of Circ_101064 in glioma/paracarcinoma tissues and glioma cells were analyzed using RT-qPCR. Moreover, U251 and U87 cells were transfected with si-Circ_101064 or miR-154-5p mimics. Cell proliferation rate was determined by CCK-8 assay; the invasion and migration activities were examined using Transwell assay; the expression levels of PIWIL1 were evaluated by RT-qPCR and western blotting. The expression level of Circ_101064 was significantly upregulated in glioma tissues compared with control, and was closely associated with tumor grading and diameter. Furthermore, increased Circ_101064 expression was detected in human glioma cell lines. In addition, knockdown of Circ_101064 remarkably suppressed cell proliferation, invasion and migration in glioma cells in vitro. Moreover, microRNA-154-5p (miR-154-5p) could be a target of Circ_101064. Additionally, PIWIL1 is a putative downstream molecule of miR-154-5p, and its expression was downregulated by knockdown of Circ_101064. The effects on cell growth and metastasis caused by si-Circ_101064 were notably enhanced by miR-154-5p mimics. However, the influences of miR-154-5p-suppressed proliferation, migration and invasion of glioma cells could be abolished by overexpressed PIWIL1. In summary, our findings provided novel insight into the regulatory functions of Circ_101064 during tumor development in glioma. More importantly, Circ_101064/miR-154-5p/PIWIL1 axis could be a promising therapeutic target for the treatment of this disease. (C) 2020 Elsevier Inc. All rights reserved.

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