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长链非编码 RNA MYCNOS 通过调控 miR-216b/FOXM1 轴促进胶质母细胞瘤细胞增殖。

LncRNA MYCNOS promotes glioblastoma cell proliferation by regulating miR-216b/FOXM1 axis.

机构信息

Department of Pediatric Surgery, Gansu Provincial Maternity and Child-Care Hospital, No.143 Qilihe North Street, Lanzhou City, Gansu Province, 730050, People's Republic of China.

出版信息

Metab Brain Dis. 2021 Aug;36(6):1185-1189. doi: 10.1007/s11011-021-00729-0. Epub 2021 Apr 19.

Abstract

MYCNOS is an oncogenic lncRNA in liver cancer, but its role in glioblastoma (GBM) is unknown. We predicted that MYCNOS might interact with miR-216b, which targets FOXM1 to perform tumor suppressive roles. This study was performed to analyze the role of MYCNOS in GBM and explore its potential interactions with miR-216b and FOXM1. MYCNOS expression in paired GBM and non-tumor tissues from 62 GBM patients was analyzed by RT-qPCR. The interaction between MYCNOS and miR-216b was predicted by IntaRNA 2.0 and confirmed by dual luciferase activity assay. Overexpression of MYCNOS, miR-216b, and FOXM1 was achieved in GBM cells, followed by performing RT-qPCR and Western blot to explore the relationship among them. CCK-8 assay was performed to explore the role of MYCNOS, miR-216b, and FOXM1 in regulating GBM cell proliferation. MYCNOS was upregulated in GBM tissues compared to the paired non-tumor tissues. MYCNOS is predicted to interact with miR-216b, but overexpression of MYCNOS and miR-216b failed to affect each other's expression significantly. Dual luciferase activity assay showed that MYCNOS and miR-216b could directly interact with each other. MYCNOS overexpression increased the expression of FOXM1, which is a direct target of miR-216b. Cell proliferation assay showed that MYCNOS and FOXM1 overexpression resulted in an increased proliferation rate of GBM cells, while miR-216b overexpression suppressed cell proliferation. Moreover, MYCNOS overexpression suppressed the role of miR-216b. MYCNOS may regulate FOXM1 expression of by serving as an endogenous sponge of miR-216b axis to promote the proliferation of GBM cells.

摘要

MYCNOS 是肝癌中的致癌 lncRNA,但它在胶质母细胞瘤(GBM)中的作用尚不清楚。我们预测 MYCNOS 可能与 miR-216b 相互作用,miR-216b 靶向 FOXM1 发挥肿瘤抑制作用。本研究旨在分析 MYCNOS 在 GBM 中的作用,并探讨其与 miR-216b 和 FOXM1 之间的潜在相互作用。通过 RT-qPCR 分析了 62 例 GBM 患者配对的 GBM 组织和非肿瘤组织中的 MYCNOS 表达。通过 IntaRNA 2.0 预测 MYCNOS 和 miR-216b 之间的相互作用,并通过双荧光素酶活性测定进行验证。在 GBM 细胞中过表达 MYCNOS、miR-216b 和 FOXM1,然后进行 RT-qPCR 和 Western blot 以探索它们之间的关系。CCK-8 测定用于研究 MYCNOS、miR-216b 和 FOXM1 在调节 GBM 细胞增殖中的作用。与配对的非肿瘤组织相比,GBM 组织中 MYCNOS 上调。预测 MYCNOS 与 miR-216b 相互作用,但过表达 MYCNOS 和 miR-216b 并未显著影响彼此的表达。双荧光素酶活性测定表明 MYCNOS 和 miR-216b 可以直接相互作用。MYCNOS 过表达增加了 FOXM1 的表达,FOXM1 是 miR-216b 的直接靶标。细胞增殖测定表明,MYCNOS 和 FOXM1 过表达导致 GBM 细胞增殖率增加,而 miR-216b 过表达抑制细胞增殖。此外,MYCNOS 过表达抑制了 miR-216b 的作用。MYCNOS 可能通过作为 miR-216b 轴的内源性海绵来调节 FOXM1 的表达,从而促进 GBM 细胞的增殖。

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