自噬
PI3K/AKT/mTOR通路
ULK1
细胞生物学
RPTOR公司
胶质瘤
信号转导
细胞生长
癌症研究
磷酸化
雷帕霉素的作用靶点
生物
长非编码RNA
mTORC2型
化学
核糖核酸
蛋白激酶A
mTORC1型
细胞凋亡
安普克
生物化学
基因
作者
Wei Zhao,Xiaoyan Lin,Han Han,Hongxu Zhang,Xiaoli Li,Chunming Jiang,Mei Feng
出处
期刊:Neuroreport
[Ovid Technologies (Wolters Kluwer)]
日期:2021-02-18
卷期号:32 (5): 352-358
被引量:18
标识
DOI:10.1097/wnr.0000000000001602
摘要
Long noncoding RNA (LncRNA) H19 has been proven to be involved in many kinds of cancers including glioma, and a previous study has shown an autophagy regulation of H19. The mammalian target of rapamycin (mTOR) signaling pathway plays a key role in autophagy and Unc-51 like autophagy activating kinase 1 (ULK1) is also thought to be involved in autophagy signaling. In our study, we investigated the role of mTOR/ULK1 autophagy signaling in the H19-mediated promotion of glioma proliferation. Human glioma cells U87 and U251 and normal human astrocytes HA1800 were used in the study. First, the expression of H19 was determined in U87, U251, and HA1800 cells. Then, the cell proliferation and migration of glioma cells were detected, while the protein levels of main molecules of the mTOR/ULK1 pathway and autophagy-related proteins were also examined. Rapamycin, an inhibitor of mTOR, was used to further study the role of H19 in autophagy. We observed that overexpressed H19 promoted the proliferation and migration in glioma cells. The autophagy of U87 cells was suppressed when H19 was overexpressed and enhanced when H19 was silenced. H19 overexpression inhibited mTOR phosphorylation and promoted ULK1 phosphorylation. H19 promoted proliferation, migration, and autophagy by regulating mTOR signaling. In conclusion, we validate that H19 contributes to the proliferation and autophagy of glioma cells through the mTOR/ULK1 pathway.
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