Assessment of mechanism of Ganoderma lucidum neutral triterpenes mediating bone marrow mesenchymal stem cells with high expression of miR-125b targeting Bak1 gene in leukemia cell proliferation and apoptosis

被引:0
|
作者
Shen, Yang [1 ]
Chen, Junyi [2 ]
Zhu, Ye [3 ]
机构
[1] Univ South China, Hengyang Med Coll, Postdoctoral Stn Basic Med, Hengyang 421001, Hunan, Peoples R China
[2] Brain Hosp Hunan Prov, Dept ICU, Changsha 410000, Hunan, Peoples R China
[3] Cent Hosp Hengyang, Dept Med Oncol, Hengyang 421001, Hunan, Peoples R China
关键词
miR-125b; BMSCs; Bak1; Leukemia; Proliferation; Apoptosis; CANCER; RESISTANCE; PROGNOSIS; PREDICT;
D O I
10.1166/mex.2023.2467
中图分类号
TB3 [工程材料学];
学科分类号
0805 ; 080502 ;
摘要
This study focused on assessing mechanism of bone marrow mesenchymal stem cells (BMSCs) with high Delivered by Ingenta miR-125b level on leukemia cells. Cultured MSC cells were identified, transfected with miR-125b, and miR125b level was tested by Reverse Transcription-Polymerase Chain Reaction (RT-PCR). After transfection, cells were divided into NC group, miR-125b mimics group, miR-125b inhibitor group, BMSC group and BMSCs group with high miR-125b expression. The miR-125b target gene was further explored by luciferase activity. Morphology of BMSC cell line P3 was stable, and CD90, CD71 and CD29 surface markers were positive, while CD45 was negative. miR-125b overexpression of BMSC in this study was successfully transfected, and the BMSCs with transfected miR-125b notably suppressed THP-1 cells proliferation, further enhancing cell apoptosis and levels of apoptosis-related proteins. Moreover, the BMSCs with miR-125b notably inhibited colony formation ability, and induced G1 phase arrest. miR-125b showed targeted relationship to Bak1, while the BMSCs with miR-125b targeted Bak1 gene, leading to up-regulation of Bakl, p53 and Puma protein expressions and inhibition of proliferation and apoptosis of leukemia THP-1 cells. miR-125b can therefore be used as a therapeutic target for acute myeloid leukemia.
引用
收藏
页码:1383 / 1391
页数:9
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