The m<sup>6</sup>A reader IGF2BP2 promotes the progression of myelodysplastic syndromes by inhibiting ferroptosis through stabilizing GPX4 mRNA, which can be reversed by CWI1-2

Wei Yujie; Wang Liye; Chang Qing; Liu Shaomei; Pan Yuling; Liu Gaixia; Wang Chi; Li Mianyang

doi:10.16016/j.2097-0927.202606096

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The m⁶A reader IGF2BP2 promotes the progression of myelodysplastic syndromes by inhibiting ferroptosis through stabilizing GPX4 mRNA, which can be reversed by CWI1-2

Basic Medicine | 更新时间：2026-10-30

- The m⁶A reader IGF2BP2 promotes the progression of myelodysplastic syndromes by inhibiting ferroptosis through stabilizing GPX4 mRNA, which can be reversed by CWI1-2
- Journal of Army Medical University Vol. 48, Issue 20, Pages: 2877-2896(2026)
- 作者机构：
  
  1.中国人民解放军总医院第一医学中心检验科，北京
  2.中国人民解放军医学院，北京
- 作者简介：
  
  Wang Chi， E-mail： wangchi2018@126.com
  Li Mianyang， E-mail： limianyang301@126.com
- 基金信息：
  
  the General Program of National Natural Science Foundation of China(61971443)
- DOI：10.16016/j.2097-0927.202606096
  CLC： R341;R394.3;R551.3
- Received：25 June 2026，
  
  Revised：2026-09-04，
  
  Accepted：07 September 2026，
  
  Published：30 October 2026
- 稿件说明：
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韦玉洁，王立烨，常青，等.m⁶A阅读蛋白IGF2BP2通过稳定GPX4 mRNA抑制铁死亡促进骨髓增生异常综合征进展而CWI1-2可逆转该效应［J］.陆军军医大学学报，2026，48（20）：2877-2896.DOI：10.16016/j.2097-0927.202606096.

Wei Y J，Wang L Y，Chang Q，et al.The m⁶A reader IGF2BP2 promotes the progression of myelodysplastic syndromes by inhibiting ferroptosis through stabilizing GPX4 mRNA， which can be reversed by CWI1-2［J］.J Army Med Univ，2026，48（20）：2877-2896.DOI：10.16016/j.2097-0927.202606096.
韦玉洁，王立烨，常青，等.m⁶A阅读蛋白IGF2BP2通过稳定GPX4 mRNA抑制铁死亡促进骨髓增生异常综合征进展而CWI1-2可逆转该效应［J］.陆军军医大学学报，2026，48（20）：2877-2896.DOI：10.16016/j.2097-0927.202606096. DOI：

Wei Y J，Wang L Y，Chang Q，et al.The m⁶A reader IGF2BP2 promotes the progression of myelodysplastic syndromes by inhibiting ferroptosis through stabilizing GPX4 mRNA， which can be reversed by CWI1-2［J］.J Army Med Univ，2026，48（20）：2877-2896.DOI：10.16016/j.2097-0927.202606096. DOI：

摘要

目的

胰岛素样生长因子2 mRNA结合蛋白2（insulin like growth factor 2 mRNA-binding protein 2，IGF2BP2）作为N

-甲基腺苷（N

-methyladenosine，m

A）阅读蛋白在多种血液系统恶性肿瘤中发挥作用，本研究旨在阐明IGF2BP2对骨髓增生异常综合征（myelodysplastic syndromes，MDS）中氧化应激和铁死亡的影响及其可能的机制。

方法

通过GEO数据库生物信息学分析筛选健康对照（healthy control，HC）人群与MDS患者间差异表达的m⁶A基因。同时收集2023年1—12月在中国人民解放军总医院第一医学中心血液科初次确诊的MDS患者骨髓样本15例作为MDS组，另收集同期12例健康供者骨髓样本作为HC组，进一步在临床样本及MDS细胞系SKM-1、MUTZ-1中验证锁定的IGF2BP2这一靶点；采用斑点杂交检测MDS患者及SKM-1、MUTZ-1细胞中的m⁶A修饰水平。利用siRNA构建SKM-1细胞IGF2BP2敲低（IGF2BP2-KD）组与对照（IGF2BP2-NC）组，并通过EdU荧光染色、CCK-8和细胞周期实验检测细胞增殖情况。通过Western blotting和RT-qPCR检测IGF2BP2敲低效率及谷胱甘肽过氧化物酶4（glutathione peroxidase 4，GPX4）表达变化；采用RNA结合蛋白免疫沉淀-实时荧光定量PCR（RNA immunoprecipitation-quantitative PCR，RIP-qPCR）实验验证IGF2BP2与GPX4 mRNA的相互作用，并利用放线菌素D处理IGF2BP2-NC与IGF2BP2-KD组细胞进行GPX4 mRNA稳定性分析。围绕GPX4轴检测细胞内氧化应激水平：流式细胞术检测活性氧（reactive oxygen species，ROS）、脂质过氧化BODIPY 581/591 C11及髓系分化标志物CD14、CD11b水平，通过透射电子显微镜观察线粒体超微结构变化，可见分光光度法测定谷胱甘肽（glutathione，GSH）、丙二醛（malondialdehyde，MDA）含量及超氧化物歧化酶（superoxide dismutase，SOD）活性；利用GPX4过表达进行回复实验，设置IGF2BP2-NC、NC+oeGPX4、IGF2BP2-KD和KD+oeGPX4组，验证IGF2BP2是否通过GPX4参与MDS的发展；使用IGF2BP2特异性抑制剂CWI1-2处理SKM-1细胞（CWI1-2）组与对照（CON）组，观察其对SKM-1细胞增殖、分化及氧化应激状态的影响。

结果

GSE19429与GSE58831数据库取交集后共获得8个差异因子（上调7个、下调1个），与HC相比，MDS的m⁶A修饰水平升高，IGF2BP2 mRNA和蛋白表达明显升高（

0.01）；SKM-1和MUTZ-1细胞中m⁶A修饰水平升高，IGF2BP2 mRNA和蛋白水平亦呈高表达（

0.05）。EdU和CCK-8结果显示，与IGF2BP2-NC组相比，IGF2BP2-KD组显著抑制SKM-1细胞增殖（

0.05），细胞周期结果显示IGF2BP2-KD组细胞G0/G1期阻滞（

=0.025 7）。Western blotting和RT-qPCR结果表明，IGF2BP2敲低显著抑制GPX4的表达（

0.01）；RIP-qPCR实验结果显示，与IgG组相比，IGF2BP2组免疫沉淀产物中GPX4 mRNA的RIP-input比例显著升高（

0.000 1），5 μg/mL放线菌素D处理后结果显示IGF2BP2-KD组GPX4 mRNA相对表达水平下降幅度大于IGF2BP2-NC组（

0.000 1）。流式细胞术结果显示，与IGF2BP2-NC组相比，IGF2BP2-KD组细胞内ROS和脂质过氧化BODIPY 581/591 C11明显增加（

0.000 1，

0.000 1），GSH含量和总SOD活力明显降低（

0.05），MDA含量升高（

=0.011 7）；透射电镜观察到IGF2BP2-KD组线粒体嵴减少甚至消失、膜密度增高等形态学特征。GPX4过表达回复实验中，KD+oeGPX4组可部分逆转IGF2BP2-KD组引起的ROS升高、脂质过氧化BODIPY 581/591 C11加剧及GSH/SOD下降、MDA升高（

0.05）。经1 μmol/L CWI1-2处理后，IGF2BP2的m

A修饰作用被有效抑制，IGF2BP2蛋白水平补偿增加（

=0.001 1），但IGF2BP2 mRNA表达水平不受影响（

=0.120 8），GPX4的蛋白与mRNA水平均降低（

0.05）；EdU结果提示CWI1-2抑制MDS细胞增殖（

=0.003 8），髓系分化标志物CD14、CD11b水平明显升高（

0.01）；同时，流式细胞术结果显示，CWI1-2处理后ROS和脂质过氧化BODIPY 581/591 C11水平明显增加（

0.000 1，

0.000 1），GSH含量和总SOD活力明显降低（

0.001），MDA含量升高（

=0.001 4）。

结论

IGF2BP2通过调控GPX4的表达和mRNA稳定性，抑制细胞内的氧化应激，从而促进MDS细胞增殖；CWI1-2作为IGF2BP2抑制剂能够通过IGF2BP2/GPX4轴促进细胞铁死亡，具备抗MDS治疗潜力。

Abstract

Objective

Insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2)

as an N

-methyladenosine (m

A) reader protein

plays a role in various hematological malignancies. This study aimed to determine the effects of IGF2BP2 on oxidative stress and ferroptosis in myelodysplastic syndromes (MDS) and its underlying mechanism.

Methods

Bioinformatics analysis of Gene Expression Omnibus (GEO) datasets was performed to screen differentially expressed m⁶A-related genes between healthy control (HC) and MDS patients. Meanwhile

bone marrow samples from 15 MDS patients newly diagnosed in Department of Hematology

First Medical Center of Chinese PLA General Hospital from January 2023 to December 2023 were collected as the MDS group

and bone marrow samples from 12 healthy donors during the same period were collected as HC group. The identified target IGF2BP2 was further verified in clinical samples and the MDS cell lines SKM-1 and MUTZ-1. Dot blot assay was performed to determine m⁶A modification levels in the MDS group and in SKM-1 and MUTZ-1 cells. Small interfering RNA (siRNA) was used to establish an IGF2BP2-knockdown group (IGF2BP2-KD) and a negative control group (IGF2BP2-NC) in SKM-1 cells

and cell proliferation was detected using EdU fluorescence staining

CCK-8 assay

and cell cycle analysis. Western blotting and RT-qPCR were employed to detect the knockdown efficiency of IGF2BP2 and changes in the expression of glutathione peroxidase 4 (GPX4). RNA immunoprecipitation-quantitative PCR (RIP-qPCR) was performed to verify the interaction between IGF2BP2 and GPX4 mRNA

and GPX4 mRNA stability was assessed in IGF2BP2-NC and IGF2BP2-KD cells after actinomycin D treatment. To evaluate the intracellular oxidative stress levels associated with the GPX4 axis

flow cytometry was applied to measure reactive oxygen species (ROS)

lipid peroxidation using BODIPY 581/591 C11

and myeloid differentiation markers CD14 and CD11b. Mitochondrial ultrastructural changes were observed with transmission electron microscopy (TEM)

while glutathione (GSH) and malondialdehyde (MDA) contents and superoxide dismutase (SOD) activity were measured by visible spectrophotometry. A GPX4 overexpression rescue experiment was performed

with 4 groups set up: IGF2BP2-NC

NC+oeGPX4

IGF2BP2-KD

and KD+oeGPX4

to verify whether GPX4 mediates the effects of IGF2BP2 in MDS. In addition

SKM-1 cells were treated with the IGF2BP2-specific inhibitor CWI1-2 (CWI1-2 group) or vehicle control (CON group)

and its effects on SKM-1 cell proliferation

differentiation

and oxidative stress were evaluated.

Results

Intersection analysis of the GSE19429 and GSE58831 datasets identified 8 differentially ex

pressed factors (including 7 upregulated and 1 downregulated). Compared with the HC group

the m⁶A modification level improved

and the IGF2BP2 expression at mRNA and protein levels were significantly increased in the MDS group (

0.01); same increases were also observed in SKM-1 and MUTZ-1 cells (

0.05). EdU and CCK-8 assays showed that the IGF2BP2-KD group exhibited significantly inhibited SKM-1 cell proliferation (

0.05) and G0/G1 cell cycle arrest (

=0.025 7) compared with the IGF2BP2-NC group. Western blotting and RT-qPCR demonstrated that IGF2BP2 knockdown significantly reduced GPX4 expression (

0.01). RIP-qPCR indicated that the RIP-input ratio of GPX4 mRNA in the immunoprecipitates was significantly higher in the IGF2BP2 group than the IgG control group (

0.000 1). Treatment with 5 μg/mL actinomycin D resulted in markedly decreased GPX4 mRNA level in the IGF2BP2-KD group than the IGF2BP2-NC group (

0.000 1). The results of the flow cytometry analysis showed that compared with the IGF2BP2-NC group

the IGF2BP2-KD group showed significantly increased intracellular ROS levels and BODIPY 581/591 C11-detected lipid peroxidation(

0.000 1

0.000 1)

accompanied by decreased GSH content and total SOD activity (

0.05) and increased MDA content (

=0.011 7). TEM revealed morphological alterations in the IGF2BP2-KD group

such as reduced or even absent mitochondrial cristae and increased mitochondrial membrane density. In the GPX4 overexpression rescue experiment

the KD+oeGPX4 group partially reversed the increases in ROS level and BODIPY 581/591 C11-detected lipid peroxidation

as well as the decreases in GSH content and SOD activity and the increment of MDA content in the IGF2BP2-KD group (

0.05). After treatment with 1 μmol/L CWI1-2

the m⁶A-related function of IGF2BP2 was

effectively inhibited

accompanied by a compensatory increase in IGF2BP2 protein level (

=0.001 1)

whereas unchanged IGF2BP2 mRNA expression level (

=0.120 8)

and decreased GPX4 protein and mRNA levels (

0.05). EdU assay showed that CWI1-2 inhibited SKM-1 cell proliferation (

=0.003 8)

while the expression levels of the myeloid differentiation markers CD14 and CD11b were significantly increased (

0.01). In addition

the results of the flow cytometry analysis showed that CWI1-2 treatment significantly increased ROS levels and BODIPY 581/591 C11-detected lipid peroxidation (

0.000 1

0.000 1)

decreased GSH content and total SOD activity (

0.001)

and increased MDA content (

=0.001 4).

Conclusion

IGF2BP2 inhibits intracellular oxidative stress by regulating GPX4 expression and mRNA stability

thereby promoting MDS cell proliferation. CWI1-2

as an IGF2BP2 inhibitor

can promote ferroptosis through the IGF2BP2/GPX4 axis and possesses anti-MDS therapeutic potential.

关键词

Keywords

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The m6A reader IGF2BP2 promotes the progression of myelodysplastic syndromes by inhibiting ferroptosis through stabilizing GPX4 mRNA, which can be reversed by CWI1-2

DOI：10.16016/j.2097-0927.202606096

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The m⁶A reader IGF2BP2 promotes the progression of myelodysplastic syndromes by inhibiting ferroptosis through stabilizing GPX4 mRNA, which can be reversed by CWI1-2