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Open Access MicroRNA-598 Inhibits Cell Proliferation and Invasion of Glioblastoma by Directly Targeting Metastasis Associated in Colon Cancer-1 (MACC1)

The dysregulation of microRNA (miRNA) expression is closely related with tumorigenesis and tumor development in glioblastoma (GBM). In this study, we found that miRNA-598 (miR-598) expression was significantly downregulated in GBM tissues and cell lines. Restoring miR-598 expression inhibited cell proliferation and invasion in GBM. Moreover, we validated that metastasis associated in colon cancer-1 (MACC1) is a novel target of miR-598 in GBM. Restoring MACC1 expression reversed the inhibitory effects of miR-598 overexpression on GBM cells. In addition, miR-598 overexpression suppressed Met/AKT pathway activation in GBM. Our results provided compelling evidence that miR-598 serves tumor-suppressive roles in GBM and that its antioncogenic effects are mediated chiefly through the direct suppression of MACC1 expression and regulation of the Met/AKT signaling pathway. Therefore, miR-598 is a potential target in the treatment of GBM.

Keywords: Glioblastoma; Invasion; Metastasis associated in colon cancer-1 (MACC1); MicroRNA-598; Proliferation

Document Type: Research Article

Affiliations: 1: Department of Neurosurgery, Xiangyang No. 1 People’s Hospital, Hubei University of Medicine, Hubei, P.R. China 2: Department of Anesthesiology, Xiangyang No. 1 People’s Hospital, Hubei University of Medicine, Hubei, P.R. China 3: Department of Neurosurgery, China-Japan Union Hospital, Jilin University, Jilin, P.R. China

Publication date: 14 September 2018

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  • Formerly: Oncology Research Incorporating Anti-Cancer Drug Design
    Oncology Research Featuring Preclinical and Clincal Cancer Therapeutics publishes research of the highest quality that contributes to an understanding of cancer in areas of molecular biology, cell biology, biochemistry, biophysics, genetics, biology, endocrinology, and immunology, as well as studies on the mechanism of action of carcinogens and therapeutic agents, reports dealing with cancer prevention and epidemiology, and clinical trials delineating effective new therapeutic regimens.

    From Volume 23, Oncology Research Featuring Preclinical and Clinical Cancer Therapeutics is Open Access under the terms of the Creative Commons CC BY-NC-ND license.

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