Function of MEIS1 and miR-425 to the Regulating of Chronic Myeloid Leukemia Cell Proliferation.
10.19746/j.cnki.issn.1009-2137.2020.03.014
- Author:
Xu-Hong ZHAO
1
;
Gui-Hua YANG
2
;
Dan-Dan LI
3
,
4
Author Information
1. Department of Clinical Laboratorial Examination, Beijing Geneplus, Beijing 102206, China.
2. Department of Clinical Laboratorial Examination, Beijing Giantmed Medical Dignostics Lab, Beijing 101300, China.
3. Department of Hematology, the Beijing Shijitan Hospital Affiliated to Capital Medical University, Beijing 100038, China ,E-mail: lidan533@
4. com.
- Publication Type:Journal Article
- MeSH:
Apoptosis;
Cell Proliferation;
Humans;
K562 Cells;
Leukemia, Myelogenous, Chronic, BCR-ABL Positive;
genetics;
MicroRNAs;
genetics;
Myeloid Ecotropic Viral Integration Site 1 Protein;
genetics
- From:
Journal of Experimental Hematology
2020;28(3):802-807
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To investigate the function and mechanism of transcription factor of MEIS1 and miR-425 to the proliferation of chronic myeloid leukemia cell K562.
METHODS:Bioinformatic prediction was used to analyze the binding of MEIS1 in miR-425 promoter region. ChIP-qPCR coupled with dual luciferase assay was used to detect the combination of MEIS1 and the transcription activity of miR-425, and its regulative role in the transcription activity miR-425. CCK-8 was used to detect the effect of MEIS1 and miR-425 on cell proliferation. Flow cytometry with PI staining was used to detected the effect of MEIS1 and miR-425 on K562 cell cycle progression. Western blot was used to examine the effect of miR-452 on the expression level of MEIS1.
RESULTS:MEIS1 could bind the promoter of miR-425 and repressed its transcription. After K562 was transfected by shRNA, the K562 cell proliferation and cell cycle progression was significantly inhibitied. Moreover, after K562 cells were transfected by miR-425 mimic, cell proliferation and cell cycle was inhibited. The expression level of MEIS1 could be inhibited by the combination of miR-425 and MEIS1 3'UTR.
CONCLUSION:MEIS1 can inhibit the activity of miR-425 in transcriptional level, while the miR-425 can suppress the expression of MEIS1 protein in post-transnational level. Therefore, a regulatory circuit comprising from MEIS1 and miR-425 regulates K562 cell proliferation.