MicroRNA-141-5p/ABCG1 reverses imatinib resistance in K562 chronic myeloid leukemia cells
10.19405/j.cnki.issn1000-1492.2024.11.001
- Author:
Han Xu
1
;
Tingting Xu
1
;
Wanjie Wang
1
;
Jing Bao
1
Author Information
1. Dept of Hematology , Afiliated Hospital of Anhui Medical University , Hefei 230022
- Publication Type:Journal Article
- Keywords:
chronic myeloid leukemia;
miR-141-5p;
imatinib;
ABCG1;
drug resistance;
K562
- From:
Acta Universitatis Medicinalis Anhui
2024;59(11):1887-1896
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To explore the mechanism of miR-141-5p and its effect on Imatinib(IM) resistance in CML.
Methods:qRT-PCR was used to detect miR-141-5p mRNA levels in IM resistant and sensitive patients.Western blot was used to detect the expression of proteins such as MMP-3,MMP-9,and Bcl-2 before and after transfection in K562 and K562/G01 cells.CCK-8 was used to detect of K562 and K562/G01 cell activity;Flow cytometry assay was used to detect the binding of miR-141-5p with ABCG1;Nude mice were used to validate the effect of miR-141-5p on tumors in vivo.
Results:The results showed that miR-141-5p was downregulated in IMresistant CML patients and IM-resistant CML cells and overexpression of miR-141-5p could inhibit the growth of IMresistant CML cells and promote their apoptosis.Research on tumor bearing mice had shown that miR-141-5p inhibits tumor growth in vivo.Finally,it was found that miR-141-5p could directly target ABCG1 in IM-resistant CML cells to regulate CML occurrence.
Conclusion:miR-141-5p and ABCG1 form a competing endogenous RNA(ceRNA) network to function in IM resistance,thus facilitating CML progression.
- Full text:2024122612280897066MicroRNA-141-...62细胞对伊马替尼的耐药性_许晗.pdf
