Department of Neurosurgery, Affiliated Hospital of Southwest Medical University, Luzhou, China.
Hum Cell. 2022 Jan;35(1):214-225. doi: 10.1007/s13577-021-00637-6. Epub 2021 Oct 30.
Glioma serves as the most common malignancy influencing modern people and is associated with severe morbidity and high mortality. Long non-coding RNAs (lncRNAs) as crucial regulators participate in multiple cancer progression. However, the role of lncRNA LINC01094 in the development of glioma remains unclear. Here, we aimed to explore the effect of lncRNA LINC01094 on the glioma progression and the underlying mechanism. Significantly, we revealed that the expression levels of LINC01094 were elevated in the glioma patient tissues compared to adjacent normal tissues. The LINC01094 expression was enhanced in the glioma cell lines. The depletion of LINC01094 inhibited cell viability and colony formation in the glioma cells. Meanwhile, the migration and invasion of glioma cells were impaired by the depletion of LINC01094. Mechanically, we identified that LINC01094 was able to sponge the miR-224-5p in the glioma cells and miR-224-5p inhibitor could reverse the effect of LINC01094 on glioma progression. In addition, miR-224-5p targeted CHSY1 and LINC01094 up-regulated CHSY1 by targeting miR-224-5p in the glioma cells. LINC01094 promoted glioma progression by the positive regulation of CHSY1. Moreover, tumorigenicity analysis showed that LINC01094 enhanced tumor growth of glioma in vivo. Thus, we conclude that lncRNA LINC01094 promotes glioma progression by modulating miR-224-5p/CHSY1 axis. Our finding provides new insights into the mechanism by which lncRNA LINC01094 contributes to the development of glioma, improving the understanding of lncRNA LINC01094 and glioma. LncRNA LINC01094, miR-224-5p, and CHSY1 may serve as potential targets for glioma.
神经胶质瘤是影响现代人的最常见恶性肿瘤，与严重发病率和高死亡率相关。长链非编码 RNA（lncRNA）作为重要的调控因子参与多种癌症的进展。然而，lncRNA LINC01094 在神经胶质瘤发展中的作用尚不清楚。在这里，我们旨在探讨 lncRNA LINC01094 对神经胶质瘤进展的影响及其潜在机制。显著地，我们揭示了与相邻正常组织相比，神经胶质瘤患者组织中 LINC01094 的表达水平升高。LINC01094 在神经胶质瘤细胞系中表达增强。LINC01094 的耗竭抑制了神经胶质瘤细胞的活力和集落形成。同时，LINC01094 的耗竭削弱了神经胶质瘤细胞的迁移和侵袭。从机制上讲，我们发现 LINC01094 能够在神经胶质瘤细胞中吸附 miR-224-5p，而 miR-224-5p 抑制剂可以逆转 LINC01094 对神经胶质瘤进展的影响。此外，miR-224-5p 靶向 CHSY1，LINC01094 通过在神经胶质瘤细胞中靶向 miR-224-5p 上调 CHSY1。LINC01094 通过正向调节 CHSY1 促进神经胶质瘤的进展。此外，肿瘤发生分析表明，LINC01094 增强了体内神经胶质瘤的肿瘤生长。因此，我们得出结论，lncRNA LINC01094 通过调节 miR-224-5p/CHSY1 轴促进神经胶质瘤的进展。我们的发现为 lncRNA LINC01094 促进神经胶质瘤发展的机制提供了新的见解，提高了对 lncRNA LINC01094 和神经胶质瘤的认识。LncRNA LINC01094、miR-224-5p 和 CHSY1 可能成为神经胶质瘤的潜在靶点。
