lncRNA KTN1‑AS1 promotes glioma cell proliferation and invasion by negatively regulating miR‑505‑3p
- Yulong Mu
- Qiang Tang
- Haiyan Feng
- Luwen Zhu
- Yan Wang
Affiliations: Department of Surgery, Hanan Branch of The Second Affiliated Hospital of Heilongjiang University of Chinese Medicine, Harbin, Heilongjiang 150001, P.R. China, Rehabilitation Medicine Center of the Second Affiliated Hospital of Heilongjiang University of Chinese Medicine, Harbin, Heilongjiang 150001, P.R. China, Shanghai Public Health Clinical Center, Jinshan, Shanghai 200001, P.R. China
- Published online on: October 22, 2020 https://doi.org/10.3892/or.2020.7821
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Glioblastoma (GBM) is one of the most prevalent and aggressive central nervous tumors with high mobility and mortality. The prognosis of patients with GBM is poor. It is therefore essential to explore the therapeutic strategies for the treatment of GBM. Previous studies have demonstrated that the long non‑coding RNA (lncRNA) Kinectin 1‑Antisense RNA 1 (KTN1‑AS1) can participate in the development of several types of cancer. However, the underlying mechanism of KTN1‑AS1 in GBM remains unknown. The present study aimed to determine the potential role of KTN1‑AS1 in GBM. In this study, reverse transcription quantitative PCR analysis was conducted and the results demonstrated that KTN1‑AS1 was upregulated in GBM tissues and cell lines compared with normal tissues and astrocytes (NHA). Furthermore, KTN1‑AS1 knockdown decreased the viability and invasive ability of glioma cells in vitro and in vivo. In addition, high level of KTN1‑AS1 was correlated with poor prognosis in TCGA GBM database. Furthermore, microRNA‑505‑3p (miR‑505‑3p) was a promising target of KTN1‑AS1, and the suppressing effects of miR‑505‑3p on cell proliferation and invasive ability was reversed by downregulating KTN1‑AS1. Taken together, the results from the present provided novel insights into the roles of KTN1‑AS1 in GBM, and suggested that the KTN1‑AS1/miR‑505‑3p axis may be considered as a novel therapeutic target for the treatment of patients with GBM.