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Copyright (c) 2023 Yan Li, Ying Zhang, Lei Guan
This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
The undersigned hereby assign all rights, included but not limited to copyright, for this manuscript to CMB Association upon its submission for consideration to publication on Cellular and Molecular Biology. The rights assigned include, but are not limited to, the sole and exclusive rights to license, sell, subsequently assign, derive, distribute, display and reproduce this manuscript, in whole or in part, in any format, electronic or otherwise, including those in existence at the time this agreement was signed. The authors hereby warrant that they have not granted or assigned, and shall not grant or assign, the aforementioned rights to any other person, firm, organization, or other entity. All rights are automatically restored to authors if this manuscript is not accepted for publication.MiR-708 regulates the biological behavior of childhood leukemia cells by binding to the 3'utr end of the target gene and reducing the level of the target gene
Corresponding Author(s) : Yan Li
Cellular and Molecular Biology,
Vol. 69 No. 2: Issue 2
Abstract
This study was performed to analyze the biological behavior of childhood leukemia cells regulated by miR-708 by binding to the 3' UTR end of the target gene and reducing the level of the target gene. In this regard, human leukemia Jurkat cell lines were selected and divided into a control group, miR-708 overexpression group and miR-708 inhibition group. MTT assay was used to detect the cell proliferation inhibition rate, flow cytometry was used to detect the apoptosis rate and cell cycle change, the scratch test was used to detect the cell migration capacity, and Western Blot assay was used to detect the expression of CNTFR, apoptosis and JAK/STAT pathway related proteins. To verify the binding site of miR-708 and target gene CNTFR. The results showed that the cell proliferation inhibition rate, apoptosis rate, G1 phase ratio, Bax protein, and CNTFR protein in the miR-708 overexpression group were significantly lower than those in the control group at each time point, while the S phase ratio, Bcl-2 protein, cell migration ability, JAK3 and STAT3 protein were significantly higher than those in the control group (P<0.05). The results of the miR-708 inhibition group were contrary to those of the miR-708 overexpression group. The binding sites of miR-708 and CNTFR were predicted by TargetScan bioinformatics software. It was found that there were two binding sites of miR-708 and CNTFR, 394-400 bp and 497-503 bp respectively. In conclusion, miR-708 can reduce the expression of CNTFR by binding to the target gene CNTFR3' UTR, activate the JAK/STAT pathway to regulate apoptosis-related proteins, reduce apoptosis, and enhance the migration ability of leukemia cells.
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