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Mir-204 regulates the biological behavior of childhood leukemia cells by binding to 3'UTR end of target gene and reducing the level of the gene


Jia Wang
Hong Kou
Ting Kong
Wei Lu

Abstract

Purpose: To study the regulatory impact of mir-204 on the biological behavior of childhood leukemia cells and to elucidate its mechanism of action.


Methods: A total of 112 children with leukemia who were treated in Three Gorges University Yichang Central People's Hospital, Yichang,  China from July 2018 to June 2020 were randomly divided into study and control groups (n = 56 each). The expression levels of mir-204  and hepatocyte growth factor (HGF) were determined using real-time polymerase chain chain reaction (RT-PCR) while the cell proliferation potential was determined using the CCK-8 method. Apoptosis and cell cycle progression of each group were evaluated using  flow cytometry while changes in cell invasion and migration were assessed by Transwell assay. Luciferase reporter assay was used  to determine the binding of mir-204 and HGF to 3'UTR.


Results: The expression level of mir-204 in study group was significantly lower  than that in control group, while expression level of HGF was significantly higher (p < 0.01) compared to control group. There was no  significant change in cell proliferation capacity at 24 h. The expression level of mir-204 was significantly decreased, while the expression  level of HGF was significantly increased (p < 0.05). Luciferase activity of wild-type HGF 3'UTR in mir-204 overexpression group was  significantly decreased, relative to mir-204 negative control group (p < 0.01). There was no significant difference in luciferase activity in  mutant HGF gene between the two groups (p > 0.05).


Conclusion: Mir-204 reduces HGF expression level via HGF 3'UTR end, thereby  inhibiting cell proliferation, invasion and migration, while promoting apoptosis, blocking cell cycle and regulating biological behavior of  childhood leukemia cells.        


Journal Identifiers


eISSN: 1596-9827
print ISSN: 1596-5996