Found programs: Natural Science Foundation of Anhui Province(No.2008085MH296);Scientific Research Project of Anhui Medical University(No.2020xkj186);Natural Science Research Project of Anhui Educational Committee(No.2022AH051178)
Authors:Xu Han; Xu Tingting; Wang Wanjie; Bao Jing
Keywords:chronic myeloid leukemia;miR-141-5p;imatinib;ABCG1;drug resistance;K562
DOI:10.19405/j.cnki.issn1000-1492.2024.11.001
〔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.