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. 2023 Feb;31(1):8-16.
doi: 10.19746/j.cnki.issn.1009-2137.2023.01.002.

[Study on the Relationship between Integrin 2A and Drug Resistance in Chronic Myeloid Leukemia]

[Article in Chinese]
Nai-Qin Zhao  1 , Cheng-Yun Pan  2 , Tian-Zhuo Zhang  3 , Ping Liu  2 , Tian-Zhen Hu  3 , Qin Shang  3 , Hong Luo  1 , Qin Fang  4 , Ji-Shi Wang  5
Affiliations

[Study on the Relationship between Integrin 2A and Drug Resistance in Chronic Myeloid Leukemia]

[Article in Chinese]
Nai-Qin Zhao et al. Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2023 Feb.

Abstract
in English, Chinese

Objective: To explore the expression pattern and clinical significance of Integral membrane protein 2A（ITM2A） in drug resistant patients with chronic myeloid leukemia (CML).

Methods: The expression of ITM2A in CML was evaluated by qRT-PCR, Western blot and immunocytochemistry. In order to understand the possible biological effects of ITM2A, apoptosis, cell cycle and myeloid differentiation antigen expression of CML cells were detected by flow cytometry after over-expression of ITM2A. The nuderlying molecular mechanism of its biological effect was explored.

Results: The expression of ITM2A in bone marrow of CML resistant patients was significantly lower than that of sensitive patients and healthy donors（P<0.05）. The CML resistant strain cell K562R was successfully constructed in vitro. The expression of ITM2A in the resistant strain was significantly lower than that in the sensitive strain(P<0.05). Overexpression of ITM2A in K562R cells increased the sensitivity of K562R cells to imatinib and blocked the cell cycle in G2 phase(P<0.05), but did not affect myeloid differentiation. Mechanistically, up-regulation of ITM2A reduced phosphorylation in ERK signaling (P<0.05).

Conclusion: The expression of ITM2A was low in patients with drug resistance of CML, and the low expression of ITM2A may be the key factor of imatinib resistance in CML.

题目: 整合膜蛋白2A与慢性粒细胞白血病耐药的相关性研究.

目的: 探索整合膜蛋白2A(ITM2A)在慢性粒细胞白血病(CML)耐药患者中的表达模式及临床意义.

方法: 采用qRT-PCR、Western blot、免疫细胞化学检测ITM2A在CML中的表达情况。为了解ITM2A可能介导的生物学效应，过表达ITM2A后流式细胞术检测CML细胞凋亡、细胞周期、髓系分化抗原表达变化。并初步探索其发挥生物学效应的潜在分子机制.

结果: ITM2A在CML耐药患者骨髓中的表达明显低于敏感患者及健康供者(P<005)；体外细胞实验成功构建CML耐药细胞株K562R，耐药株中ITM2A的表达明显低于敏感株(P<0.05)；过表达K562R细胞中的ITM2A能够使K562R细胞对伊马替尼的敏感性增加(P<0.05)，且阻滞细胞周期在G2期，但不影响髓系分化。上调ITM2A能够使ERK信号通路的磷酸化水平降低 (P<0.05).

结论: ITM2A在CML耐药患者中呈低表达，低表达ITM2A可能是CML对伊马替尼耐药的关键因子.

Keywords: ITM2A; K562R cells; chronic myeloid leukemia; imatinib; resistance.

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