Dexmedetomidine upregulates the expression of miR-493-5p, inhibiting growth and inducing the apoptosis of lung adenocarcinoma cells by targeting RASL11B.

Abstract	Numerous studies have indicated that microRNAs (miRNAs) play critical roles in the development and progression of cancer. However, how changes to the expression levels of miRNAs in response to dexmedetomidine affects the progression of lung cancer remains poorly understood. In this study, we treated the lung adenocarcinoma cell line-A549 with dexmedetomidine and then examined the changes to the expression levels of miRNAs. We found that one of the most significantly upregulated miRNAs was miR-493-5p, which has an important role in the growth and apoptosis of lung adenocarcinoma (LUAD) cells. In addition, bioinformatics searches and luciferase reporter assays revealed that miR-493-5p targets RASL11B, which has a high degree of similarity to RAS. Finally, database searches revealed that RASL11B is associated with survival of LUAD cells. In conclusion, dexmedetomidine causes changes to the expression levels of miRNAs in LUAD, including significant upregulation of miR-493-5p. MiR-493-5p targets RASL11B, thereby inhibiting cell growth and inducing apoptosis in LUAD.
Authors	Bo Xu, Yiling Qian, Chunxiao Hu, Yongsheng Wang, Hong Gao, Jianping Yang
Journal	Biochemistry and cell biology = Biochimie et biologie cellulaire (Biochem Cell Biol) Vol. 99 Issue 4 Pg. 457-464 (08 2021) ISSN: 1208-6002 [Electronic] Canada
PMID	34296954 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References	Adrenergic alpha-2 Receptor Agonists Biomarkers, Tumor MIRN493 microRNA, human MicroRNAs Dexmedetomidine Monomeric GTP-Binding Proteins RASL11B protein, human
Topics	Adenocarcinoma of Lung (drug therapy, genetics, metabolism, pathology) Adrenergic alpha-2 Receptor Agonists (pharmacology) Apoptosis Biomarkers, Tumor (genetics, metabolism) Cell Proliferation Dexmedetomidine (pharmacology) Gene Expression Regulation, Neoplastic (drug effects) Humans Lung Neoplasms (drug therapy, genetics, metabolism, pathology) MicroRNAs (genetics) Monomeric GTP-Binding Proteins (genetics, metabolism) Tumor Cells, Cultured

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