LINC01087 通过 miR-384/Bcl-2 轴抑制神经胶质瘤细胞增殖和迁移，并增加细胞凋亡。
LINC01087 inhibits glioma cell proliferation and migration, and increases cell apoptosis via miR-384/Bcl-2 axis.
机构信息
Department of Neurosurgery, Cangzhou Central Hospital, Cangzhou, Hebei Province, China.
出版信息
Aging (Albany NY). 2021 Aug 30;13(16):20808-20819. doi: 10.18632/aging.203478.
BACKGROUND
Long non-coding RNA (LncRNA) is associated with disease progression. It is reported that LINC01087 is highly expressed in cancer and participates in tumorigenesis. However, whether it regulates the development of glioma has not been studied. So, the goal of this research is to determine the role of LINC01087 in gliomas and to provide potential targets for clinical treatment.
METHODS
The gene expression was detected by quantitative reverse transcriptase polymerase chain reaction (QRT-PCR) and Western blotting (WB). Cell proliferation was analyzed by CCK8 and colony formation test, and apoptosis was detected by flow cytometry. Luciferase report experiment and RNA Binding Protein Immunoprecipitation confirmed the interaction between LINC01087, miR-384 and Bcl-2. The effect of regulating LINC01087 on the growth of glioma was confirmed .
RESULTS
The LINC01087 expression was up-regulated in clinical glioma samples ( = 35). Furthermore, LINC01087 silencing can obviously suppress the proliferation of glioma cells and induce apoptosis. Mechanically, we found that LINC01087 was the molecular sponge of miR-384. LINC01087 could inhibit the miR-384 expression and boost the Bcl-2 expression through sponge expression of miR-384. The repair of Bcl-2 effectively saved the proliferation and apoptosis of glioma cells lacking LINC01087.
CONCLUSION
LINC01087 is highly expressed in glioma and can participate in the growth of glioma through miR-384/Bcl-2 axis. So, it is a potential therapeutic target.
背景
长链非编码 RNA（LncRNA）与疾病进展有关。据报道，LINC01087 在癌症中高表达，并参与肿瘤发生。然而，它是否调节胶质瘤的发展尚未研究。因此，本研究旨在确定 LINC01087 在胶质瘤中的作用，并为临床治疗提供潜在靶点。
方法
通过定量逆转录聚合酶链反应（QRT-PCR）和 Western blot（WB）检测基因表达。通过 CCK8 和集落形成试验分析细胞增殖，通过流式细胞术检测细胞凋亡。荧光素酶报告实验和 RNA 结合蛋白免疫沉淀证实了 LINC01087、miR-384 和 Bcl-2 之间的相互作用。通过调节 LINC01087 对胶质瘤生长的影响来证实。
结果
LINC01087 在临床胶质瘤样本中表达上调（=35）。此外，LINC01087 沉默可明显抑制胶质瘤细胞的增殖并诱导细胞凋亡。从机制上讲，我们发现 LINC01087 是 miR-384 的分子海绵。LINC01087 通过海绵表达 miR-384 抑制 miR-384 的表达并上调 Bcl-2 的表达。Bcl-2 的修复有效挽救了缺乏 LINC01087 的胶质瘤细胞的增殖和凋亡。
结论
LINC01087 在胶质瘤中高表达，可通过 miR-384/Bcl-2 轴参与胶质瘤的生长。因此，它是一个潜在的治疗靶点。
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