[microRNA-30d can inhibit the proliferation, migration and invasion of human mesothelial cell MSTO-211H].
Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi
; 39(2): 99-104, 2021 Feb 20.
Article
em Zh
| MEDLINE
| ID: mdl-33691362
ABSTRACT
Objective:
To investigate the inhibitory effect and molecular mechanism of microRNA-30d (miR-30d) in the process of proliferation, migration and invasion of malignant mesothelioma cell line MSTO-211H.Methods:
In April 2017, the human MSTO-211H cells was used to establish miR-30d overexpressed MSTO-211H cell model by transfection of miR-30d mimics. The qRT-PCR was performed to detect the expression level of miR-30d in the cells transfected miR-30d mimics. The effects of miR-30d on the proliferation, apoptosis, migration and invasion of MSTO-211H cells were analyzed by CCK-8 experiment, flow cytometry, cell scratch experiment and Transwell method.Results:
After transfection of miR-30d, the expression level of miR-30d in the MSTO-211H+miR-30d cells group was significantly higher than MSTO-211H+miR NC cells group (P<0.01) . The cell activity of MSTO-211H+miR-30d group (105.13%±2.35%) was significantly lower than MSTO-211H+miR NC cells group (115.40%±1.35%) , and the level of apoptosis (3.97%±0.36%) was significantly higher than MSTO-211H+miR NC cells group (1.47%±0.10%) (P<0.01) . The relative migration areas at 12 and 24 h of MSTO-211H+miR-30d cells group (9.35±3.16 µm(2) and 58.19±1.82 µm(2)) were significantly lower than MSTO-211H+miR NC cells group (54.42±5.26 µm(2) and 88.32±1.96 µm(2)) (P<0.01) . Compared with the MSTO-211H+miR NC cells group, the numbers of cell migration and cell invasion were reduced in the MSTO-211H+miR-30d cells group (P<0.01) .Conclusion:
miR-30d can regulate the progression of malignant pleural mesothelioma by inhibiting the proliferation, apoptosis, migration and invasion of MSTO-211H cells.Palavras-chave
Texto completo:
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Base de dados:
MEDLINE
Assunto principal:
Regulação Neoplásica da Expressão Gênica
/
MicroRNAs
Idioma:
Zh
Ano de publicação:
2021
Tipo de documento:
Article