Open AccessMicroRNA-124 regulates apoptosis in sevoflurane anesthesia-induced neuroblastoma cells by targeting enhancer of zeste homolog 2
Author(s) -
Lingyun Wei,
Jing-Xian Fang,
Yiqi Fang,
Chengnv Li
Publication year - 2021
Publication title -
tropical journal of pharmaceutical research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.209
H-Index - 36
eISSN - 1596-5996
pISSN - 1596-9827
DOI - 10.4314/tjpr.v18i3.7
Subject(s) - apoptosis , transfection , neuroblastoma , flow cytometry , gene knockdown , microrna , chemistry , microbiology and biotechnology , western blot , cancer research , cell growth , cell culture , sevoflurane , mtt assay , biology , pharmacology , gene , biochemistry , genetics
Purpose: To investigate the mechanism of microRNA-124 action on neuroblastoma apoptosis induced by sevoflurane.
Methods: MiR-124 expression was assessed in a neuroblastoma cell line (SMS-KAN) using quantitative reverse transcription polymerase chain reaction (qRT-PCR). The role of miR-124 in sevoflurane anesthesia-induced neuroblastoma was studied by cell activity and apoptosis analysis using 3-(4, 5-dimethylthiazolyl-2-yl)-2-5 diphenyl tetrazolium bromide (MTT) assay and flow cytometry, respectively. MiR-124 target protein genes were confirmed via luciferase reporter activity, qRT-PCR, and western blot analysis.
Results: miR-124 was upregulated in sevoflurane anesthesia-induced neuroblastoma (p < 0.05). After miR-124 knockdown, apoptosis was significantly reduced and cell viability was enhanced in sevoflurane anesthesia-induced SMS-KAN nerve cells (p < 0.05). Furthermore, a significant reduction of luciferase activity was observed in 293T cells co-transfected with miR-124 mimics and EZH2-wild type (EZH2-WT) (p < 0.05). The mRNA and protein expression levels of EZH2 decreased in SMS-KAN nerve cells transfected with miR-124 mimics (p < 0.05). Overexpression of EZH2 inhibited the apoptosis of SMSKAN cells induced by sevoflurane (p < 0.05). Furthermore, the apoptosis of SMS-KAN cells transfected with miR-124 inhibitor were offset by transfected siEZH2.
Conclusion: The results suggest that overexpression of miR-124 suppresses cell proliferation by targeting EZH2 in SMS-KAN cells. Therefore, miR-124 represents a potential target for neuroblastoma therapy