Department of Neurosurgery, The First People's Hospital of Wenling, Wenling, Zhejiang, China.
Eur Rev Med Pharmacol Sci. 2019 Jan;23(1):262-270. doi: 10.26355/eurrev_201901_16772.
Recent evidence shows that gastric adenocarcinoma predictive long intergenic noncoding RNA (GAPLINC) acts as a critical role in the proliferation and metastasis in several tumors. We aimed to explore the expression pattern, function, and potential mechanism of GAPLINC in glioblastoma multiforme (GBM).
The expression levels of GAPLINC and its clinical significance were determined by analyzing TCGA datasets. RT-PCR was performed to detect the levels of GAPLINC and miR-331-3p. CCK-8, colony formation, EdU assays, wound healing assay and transwell invasion assay were performed to analyze the effect of GAPLINC on GBM behaviors. MiRNAs that may interact with GAPLINC were predicted using StarBase and RegRNA 2.0. A luciferase reporter assay was used to detect the targeting effect of GAPLINC on miR-331-3p.
We found that GAPLINC expression was significantly up-regulated in both GBM tissues and cell lines. The overexpression of GAPLINC was associated with shorter overall survival and disease-free survival. Functional assays indicated that GAPLINC silencing suppressed GBM cells proliferation, migration, and invasion, and promoted apoptosis. In the mechanism, we found that GAPLINC acted as a competing endogenous RNA to sponge miR-331-3p and knockdown of GAPLINC promoted the expression of miR-331-3p.
Our findings suggested that GAPLINC served as an oncogenic lncRNA in GBM through negative modulation of miR-331-3p, providing a novel treatment targeting for GBM.
最近的证据表明，胃腺癌预测长非编码 RNA（GAPLINC）在几种肿瘤的增殖和转移中发挥关键作用。我们旨在探讨 GAPLINC 在多形性胶质母细胞瘤（GBM）中的表达模式、功能和潜在机制。
通过分析 TCGA 数据集确定 GAPLINC 的表达水平及其临床意义。通过 RT-PCR 检测 GAPLINC 和 miR-331-3p 的水平。通过 CCK-8、集落形成、EdU 测定、划痕愈合测定和 Transwell 侵袭测定分析 GAPLINC 对 GBM 行为的影响。使用 StarBase 和 RegRNA 2.0 预测可能与 GAPLINC 相互作用的 miRNAs。使用荧光素酶报告基因测定检测 GAPLINC 对 miR-331-3p 的靶向作用。
我们发现 GAPLINC 在 GBM 组织和细胞系中均明显上调。GAPLINC 的过表达与总生存期和无病生存期缩短有关。功能测定表明，GAPLINC 沉默抑制 GBM 细胞增殖、迁移和侵袭，并促进细胞凋亡。在机制方面，我们发现 GAPLINC 作为竞争性内源性 RNA 与 miR-331-3p 结合，敲低 GAPLINC 可促进 miR-331-3p 的表达。
我们的研究结果表明，GAPLINC 通过负调控 miR-331-3p 在 GBM 中发挥致癌 lncRNA 的作用，为 GBM 提供了一种新的治疗靶点。
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