医学分子生物学杂志2026，Vol.23Issue(4)：375-381,388,8.DOI:10.3870/j.issn.1672-8009.2026.04.001
miR-133a-3p靶向TGIF2调节急性髓系白血病细胞系OCI-AML3细胞凋亡与线粒体功能
miR-133a-3p Regulates Apoptosis and Mitochondrial Function of OCI-AML3 Acute Myeloid Leukemia Cells via Targeting TGIF2
摘要
Abstract
Objective To analyze the effect of miR-133a-3p and its potential target transfor-ming growth factor-β-induced factor 2(TGIF2)on the apoptosis and mitochondrial function of a-cute myeloid leukemia cells OCI-AML3.Methods OCI-AML3 cells were transfected with miR-133a-3p mimic or/and pcDNA-TGIF2.Transfection efficiency was detected by RT-qPCR.The target sites of miR-133a-3p and TGIF2 were predicted by bioinformatics,and the targeting relationship was verified by dual-luciferase reporter gene assay.Cell proliferation was detected by CCK-8 assay and EdU staining.Flow cytometry was applied to detect the apoptosis and mitochondrial membrane potential.ROS level was measured by associated kit.Western blot was used to detect the expression levels of Caspase-3,Caspase-9,TGIF2,Bcl-2,Bax and c-Myc proteins.Results In OCI-AML3 cells,the miR-133a-3p expression was negatively correlated with TGIF2 expression,and miR-133a-3p targetly binded with TGIF2.Compared with those in the control group,the cell viability in the TGIF2 group was significantly enhanced(P＜0.05),the number of EdU positive cells was in-creased significantly,while the apoptosis rate was significantly reduced(P＜0.05);the expres-sions of Bax/Bcl-2,Caspase-3 and Caspase-9 were significantly down-regulated(P＜0.05),while the expression level of c-Myc was significantly up-regulated(P＜0.05);the mitochondrial mem-brane potential showed no significant change,whereas ROS content demonstrated a marked decrease(P＜0.05).The overexpression of miR-133a-3p reversed the above results.Compared with those in the TGIF2 group,the mimic+TGIF2 group exhibited significantly reduced cell viability(P＜0.05),the number of EdU positive cells was significantly declined,and the apoptosis rate was sig-nificantly increased(P＜0.05);The expression levels of Bax/Bcl-2,Caspase-3 and Caspase-9 were significantly up-regulated(P＜0.05),while the expression level of C-MYC was significantly down-regulated(P＜0.05);the mitochondrial membrane potential was significantly changed,and ROS level was significantly increased(P＜0.05).Conclusion miR-133a-3p inhibits OCI-AML3 cell viability and proliferation,up-regulates ROS level,induces mitochondrial membrane potential depolarization,and promotes apoptosis by targeting TGIF2.关键词
miR-133a-3p/转化生长因子-β诱导因子2/急性髓系白血病/细胞凋亡/活性氧Key words
miR-133a-3p/transforming growth factor-β-induced factor 2/acute myeloid leu-kemia/apoptosis/reactive oxygen species分类
医药卫生引用本文复制引用
郭丽,祝俊玲,卫雷,郭巧伟,龚艳玲..miR-133a-3p靶向TGIF2调节急性髓系白血病细胞系OCI-AML3细胞凋亡与线粒体功能[J].医学分子生物学杂志,2026,23(4):375-381,388,8.基金项目
河北省医学科学研究课题(No.20242351) This work was supported by a grant from the Medical Science Research Project of Hebei Province(No.20242351). （No.20242351）
