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高莉, 李晓明, 杨波, 秦英, 程冬, 郑丽飞, 李里. 组蛋白去甲基化酶KDM5A通过LncRNA TRIM52-AS1调控急性髓系白血病的发生和发展[J]. 实用临床医药杂志, 2023, 27(17): 23-28. DOI: 10.7619/jcmp.20230763
引用本文: 高莉, 李晓明, 杨波, 秦英, 程冬, 郑丽飞, 李里. 组蛋白去甲基化酶KDM5A通过LncRNA TRIM52-AS1调控急性髓系白血病的发生和发展[J]. 实用临床医药杂志, 2023, 27(17): 23-28. DOI: 10.7619/jcmp.20230763
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GAO Li, LI Xiaoming, YANG Bo, QIN Ying, CHENG Dong, ZHENG Lifei, LI Li. Histone demethylase KDM5A regulates the occurrence and development of acute myeloid leukemia through LncRNA TRIM52-AS1[J]. Journal of Clinical Medicine in Practice, 2023, 27(17): 23-28. DOI: 10.7619/jcmp.20230763
Citation: GAO Li, LI Xiaoming, YANG Bo, QIN Ying, CHENG Dong, ZHENG Lifei, LI Li. Histone demethylase KDM5A regulates the occurrence and development of acute myeloid leukemia through LncRNA TRIM52-AS1[J]. Journal of Clinical Medicine in Practice, 2023, 27(17): 23-28. DOI: 10.7619/jcmp.20230763
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组蛋白去甲基化酶KDM5A通过LncRNA TRIM52-AS1调控急性髓系白血病的发生和发展

Histone demethylase KDM5A regulates the occurrence and development of acute myeloid leukemia through LncRNA TRIM52-AS1

    摘要
  • 摘要:
    目的 初步探索组蛋白去甲基化酶赖氨酸特异性去甲基化酶5(KDM5A)通过长链非编码RNA(LncRNA) TRIM52-AS1调控急性髓系白血病(AML)发生、发展的机制。
    方法 通过逆转录定量聚合酶链式反应(qRT-PCR)和蛋白质印迹(Western blot)检测白血病患者血清和各种白血病细胞中的KDM5A、TRIM52-AS1的表达。采用双荧光素酶报告实验检测KDM5A和TRIM52-AS1的靶向关系。通过CCK8实验检测KDM5A和TRIM52-AS1对HL-60细胞增殖的影响。通过Transwell实验检测KDM5A和TRIM52-AS1对HL-60细胞迁移的影响。
    结果 KDM5A在白血病患者血清和各种白血病细胞中高表达, TRIM52-AS1在白血病患者血清和各种白血病细胞中低表达(P < 0.05)。KDM5A可以靶向抑制TRIM52-AS1。过表达TRIM52-AS1可以抑制白血病细胞的增殖和迁移, KDM5A可以通过抑制TRIM52-AS1进而抑制白血病细胞的增殖和迁移(P < 0.05)。
    结论 组蛋白去甲基化酶KDM5A可通过抑制LncRNA TRIM52-AS1进而抑制AML的发生、发展。

     

    Abstract:
    Objective To preliminarily explore the mechanism histone demethylase KDM5A in regulating the occurrence and development of acute myeloid leukemia (AML) through long non-coding RNA (LncRNA) TRIM52-AS1.
    Methods The levels of KDM5A and TRIM52-AS1 were detected by real-time quantitative polymerase chain reaction (qRT-PCR) and Western blot in the serum and various leukemia cells of AML patients. The targeting relationship between KDM5A and TRIM52-AS1 was detected by dual luciferase reporter assay. The effects of KDM5A and TRIM52-AS1 on HL-60 cell proliferation were detected by CCK8 assay. The effects ofKDM5A and TRIM52-AS1 on HL-60 cell migration were detected by Transwell assay.
    Results KDM5A was highly expressed in the serum and various leukemia cells of AML patients, while TRIM52-AS1 was lowly expressed (P < 0.05). KDM5A could targetedly inhibit TRIM52-AS1. Overexpression of TRIM52-AS1 could targetedly inhibit leukemia cell proliferation and migration, and KDM5A could inhibit leukemia cell proliferation and migration by inhibiting TRIM52-AS1 (P < 0.05).
    Conclusion Histone demethylase KDM5A can inhibit the occurrence and developmen of AML by inhibiting LncRNA TRIM52-AS1.

     

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