Linc01094 Accelerates the Growth and Metastatic-Related Traits of Glioblastoma by Sponging miR-126-5p.
Linc01094 Accelerates the Growth and Metastatic-Related Traits of Glioblastoma by Sponging miR-126-5p.
复制标题
DOI：
10.2147/ott.s263091
复制
发表时间：
2020
影响因子：
4
通讯作者：
Yu Q
中科院分区：
文献类型：
--
作者：
Li XX;Yu Q
长基因间非编码RNA（lincRNA）与胶质母细胞瘤（GBM）的进展相关。然而，linc 01094如何促进GBM的生长和转移表型仍然没有完全研究。使用qRT-PCR分析GBM组织和细胞系中linc 01094和miR-126- 5 p的表达水平。进行功能丧失实验以检测linc 01094在GBM中的生物活性。构建胶质母细胞瘤模型以探讨linc 01094对体内GBM细胞生长的影响。Linc 01094海绵状miR-126- 5 p通过荧光素酶报告基因测定和RNA免疫沉淀（RIP）进行验证。Western blotting检测miRNA靶基因dynactin亚基4（DCTN 4）的蛋白表达。在此，我们观察到linc 01094的水平在GBM组织中更高。linc 01094基因的沉默抑制了GBM细胞的生长和侵袭能力。此外，linc 01094水平与GBM中的miR-126- 5 p水平负相关，linc 01094充当miR-126- 5 p的“海绵”。linc 01094的重新引入逆转了miR-126- 5 p在GBM中的肿瘤抑制作用。总之，linc 01094通过调节miR-1126- 5 p/DCTN 4信号轴促进GBM细胞的成瘤和转移表型。
Long intergenic non-coding RNAs (lincRNAs) are associated with the progression of glioblastoma (GBM). However, how linc01094 contributes to the growth and metastatic phenotypes of GBM remains not fully studied. The expression levels of linc01094 and miR-126-5p in GBM tissues and cell lines were analyzed using qRT-PCR. Loss-of-function experiments were performed to detect the biological activity of linc01094 in GBM. Glioblastoma tumor model was constructed to explore the impact of linc01094 on GBM cell growth in vivo. Linc01094-sponged miR-126-5p was certified by luciferase reporter assay and RNA immunoprecipitation (RIP). The protein expression of miRNA target gene, dynactin subunit 4 (DCTN4) was detected using Western blotting assay. Herein, we observed that the level of linc01094 was higher in GBM tissues. Silencing of linc01094 restrained the growth and invasive abilities of GBM cell. Moreover, linc01094 level was negatively associated with miR-126-5p level in GBM and linc01094 acted as a “sponge” for miR-126-5p. Reintroduction of linc01094 reversed the tumor-inhibiting effects of miR-126-5p in GBM. Altogether, linc01094 promoted the tumorigenesis and metastatic phenotypes of GBM cell by modulating of miR-1126-5p/DCTN4 signaling axis.