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LINC02308 promotes the progression of glioma through activating mTOR/AKT-signaling pathway by targeting miR-30e-3p/TM4SF1 axis
Cell Biology and Toxicology ( IF 5.3 ) Pub Date : 2021-05-04 , DOI: 10.1007/s10565-021-09604-1
Xianfeng Gao 1 , Xiaoya Wang 2 , Huaiqiang He 3 , Yang Cao 4, 5
Affiliation  

Background

Glioma is a common brain malignancy, and the purpose of this study is to investigate the function of LINC02308 in glioma.

Methods

The differentially expressed lncRNAs were screened by microarray. The expression of LINC02308 in glioma tissues and cells was evaluated. The interaction among LINC02308, miR-30e-3p, and TM4SF1 was determined. Cell proliferation and apoptosis were evaluated. The expression of mTOR/AKT-signaling and apoptosis-related markers was detected by Western blot. A xenograft tumor mouse model was constructed to investigate the roles of LINC02308.

Results

LINC02308 was significantly overexpressed in glioma, and a high LINC02308 level was correlated with a poor prognosis. LINC02308 silencing markedly inhibited proliferation and reduced apoptosis of glioma cells and also suppressed tumor growth in the xenograft tumor mouse model. Finally, we demonstrated that LINC02308 played its oncogenic role through binding to miR-30e-3p so as to relieve miR-30e-3p-induced suppression of TM4SF1.

Conclusions

LINC02308 promoted glioma tumorigenesis as a sponge of miR-30e-3p to upregulate TM4SF1 and activate AKT/mTOR pathway.



中文翻译:

LINC02308通过靶向miR-30e-3p/TM4SF1轴激活mTOR/AKT信号通路促进胶质瘤进展

背景

胶质瘤是一种常见的脑部恶性肿瘤,本研究旨在探讨LINC02308在胶质瘤中的作用。

方法

通过微阵列筛选差异表达的lncRNA。评估了 LINC02308 在胶质瘤组织和细胞中的表达。确定了 LINC02308、miR-30e-3p 和 TM4SF1 之间的相互作用。评估细胞增殖和凋亡。Western blot检测mTOR/AKT信号及凋亡相关标志物的表达。构建了异种移植肿瘤小鼠模型以研究 LINC02308 的作用。

结果

LINC02308 在胶质瘤中显着过表达,高水平的 LINC02308 与不良预后相关。在异种移植肿瘤小鼠模型中,LINC02308 沉默显着抑制了胶质瘤细胞的增殖并减少了细胞凋亡,并且还抑制了肿瘤的生长。最后,我们证明LINC02308通过与miR-30e-3p结合发挥其致癌作用,从而缓解miR-30e-3p诱导的TM4SF1抑制。

结论

LINC02308 作为 miR-30e-3p 的海绵促进神经胶质瘤的发生,以上调 TM4SF1 并激活 AKT/mTOR 通路。

更新日期:2021-05-04
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