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Zhongguo Ying Yong Sheng Li Xue Za Zhi ; 37(6): 601-605, 2021 Nov.
Artigo em Chinês | MEDLINE | ID: mdl-34821091

RESUMO

Objective: To investigate the effects and mechanisms of miR-155-3p on the malignant behavior of human NK/T cell lymphoma cell line HANK1. Methods: Targetscan database was used to predict the target gene of miR-155-3p. HANK1 cells in logarithmic growth period were cultured, and the cells were divided into blank group, over-expressed group, control group and interference group, which were transfected with pENTER-puro vector, pENTER-miR-155-3p vector, GV248 control vector and GV248-miR-155-3p siRNA interference vector, respectively. Meanwhile, actinomycin D (ActD) was used to treat each group of cells, and the expressions of miR-155-3p, EAf1, ß-catenin and c-Myc in each group were detected by real-time fluorescence quantitative PCR (n=5). The degradation rate of EAF1 mRNA, the expressions of EAF1, ß-catenin and c-Myc protein were detected by Western blot (n=3), and the malignant proliferation abilities of cells were detected by CCK-8 (n=5). Results: Compared with the blank group, the expression levels of miR-155-3p, ß-catenin and c-Myc in the over-expressed group were significantly higher, the expression level of EAF1 was lower, the half-life of EAF1 mRNA was shortened, and the malignant proliferation ability of the cells was strengthened (P<0.05). Compared with the control group, the expression levels of miR-155-3p, ß-catenin and c-Myc in the interference group were significantly lower, and the expression level of EAF1 was increased, the half-life of mRNA was prolonged and the ability of cell proliferation was decreased (P<0.05). Conclusion: miR-155-3p can promote EAF1 mRNA degradation and proliferation in HANK1 cells.


Assuntos
Proliferação de Células , MicroRNAs , Fatores de Transcrição , Linhagem Celular Tumoral , Regulação Neoplásica da Expressão Gênica , Humanos , MicroRNAs/genética , Proteínas Proto-Oncogênicas c-myc/genética , Proteínas Proto-Oncogênicas c-myc/metabolismo , RNA Mensageiro/genética , Fatores de Transcrição/genética
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