Abstract
BackgroundNumerous 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. MethodsQuantitative 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. ResultsSNHG11 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. ConclusionSNHG11 regulated miR-193a-5p/Notch3 axis to activate Notch pathway, consequently facilitating the proliferation and migration in LUAD.
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