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长链非编码 RNA KTN1-AS1 通过负调控 miR-505-3p 促进神经胶质瘤细胞的增殖和侵袭。

lncRNA KTN1‑AS1 promotes glioma cell proliferation and invasion by negatively regulating miR‑505‑3p.

机构信息

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.

出版信息

Oncol Rep. 2020 Dec;44(6):2645-2655. doi: 10.3892/or.2020.7821. Epub 2020 Oct 22.

DOI:10.3892/or.2020.7821
PMID:33125151
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7640367/
Abstract

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.

摘要

胶质母细胞瘤(GBM)是最常见和侵袭性最强的中枢神经系统肿瘤之一,具有高迁移性和高死亡率。GBM 患者的预后较差,因此探索治疗 GBM 的治疗策略至关重要。先前的研究表明,长链非编码 RNA(lncRNA)Kinectin 1-反义 RNA 1(KTN1-AS1)可以参与多种类型癌症的发展。然而,KTN1-AS1 在 GBM 中的潜在机制尚不清楚。本研究旨在确定 KTN1-AS1 在 GBM 中的潜在作用。在这项研究中,进行了逆转录定量 PCR 分析,结果表明,与正常组织和星形胶质细胞(NHA)相比,GBM 组织和细胞系中 KTN1-AS1 上调。此外,KTN1-AS1 敲低降低了体外和体内神经胶质瘤细胞的活力和侵袭能力。此外,TCGA GBM 数据库中高水平的 KTN1-AS1 与预后不良相关。此外,miR-505-3p(miR-505-3p)是 KTN1-AS1 的一个有前途的靶点,下调 KTN1-AS1 逆转了 miR-505-3p 对细胞增殖和侵袭能力的抑制作用。综上所述,本研究为 KTN1-AS1 在 GBM 中的作用提供了新的见解,并表明 KTN1-AS1/miR-505-3p 轴可能被认为是治疗 GBM 患者的新治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0832/7640367/8b52d64d51e7/OR-44-06-2645-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0832/7640367/8851aee73f5d/OR-44-06-2645-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0832/7640367/c480ebf5df13/OR-44-06-2645-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0832/7640367/19bbd033cfeb/OR-44-06-2645-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0832/7640367/07723749019f/OR-44-06-2645-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0832/7640367/c23d652d005a/OR-44-06-2645-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0832/7640367/8b52d64d51e7/OR-44-06-2645-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0832/7640367/8851aee73f5d/OR-44-06-2645-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0832/7640367/c480ebf5df13/OR-44-06-2645-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0832/7640367/19bbd033cfeb/OR-44-06-2645-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0832/7640367/07723749019f/OR-44-06-2645-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0832/7640367/c23d652d005a/OR-44-06-2645-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0832/7640367/8b52d64d51e7/OR-44-06-2645-g05.jpg

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