Notch信号通路
腺癌
癌症研究
生物
竞争性内源性RNA
细胞生物学
机制(生物学)
细胞生长
转录因子
功能(生物学)
小RNA
长非编码RNA
信号转导
核糖核酸
基因
遗传学
癌症
认识论
哲学
作者
Yanchao Deng,Liwei Zhang
标识
DOI:10.1016/j.prp.2022.153849
摘要
Numerous researches have emphasized that long non-coding RNAs (lncRNAs) have a close association with the biological process in multiple cancers including lung adenocarcinoma (LUAD). Nevertheless, the detailed function and potential mechanism of Small nucleolar RNA Host Gene 11 (SNHG11) in LUAD keep unknown.Quantitative reverse transcription polymerase chain reaction (RT-qPCR) tested SNHG11, miR-193a-5p and notch receptor 3 (Notch3) expression. Functional assays tested the function of SNHG11 in LUAD cells. The relationship among SNHG11, miR-193a-5p and Notch3 was verified by mechanism assays. In vivo assays were implemented to reveal the role of SNHG11 in LUAD tumor growth.SNHG11 was evidently high expressed in LUAD cells in comparison to normal lung epithelial cells. Moreover, down-regulation of SNHG11 hindered viability, proliferation and migration of LUAD cells as well as tumor growth. As for the mechanisms, SNHG11 activated Notch pathway via regulating Notch3. In addition, SNHG11 competitively bound with miR-193a-5p to up-regulate Notch3. The last rescue assays displayed that SNHG11 affecting LUAD cell malignant behaviors via regulating miR-193a-5p/SNHG11.SNHG11 regulated miR-193a-5p/Notch3 axis to activate Notch pathway, consequently facilitating the proliferation and migration in LUAD.
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