| lncRNA HOXB-AS3 通过激活 PI3K-AKT 通路加剧急性髓样白血病患者细胞的增殖、 凋亡、 迁移和侵袭 |
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| 引用本文： | 黄耘,于永洋,苏蕊,王思力. lncRNA HOXB-AS3 通过激活 PI3K-AKT 通路加剧急性髓样白血病患者细胞的增殖、 凋亡、 迁移和侵袭[J]. 医学分子生物学杂志, 2022, 19(5): 366-373. DOI: 10.3870/j.issn.1672-8009.2022.05.003 |
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| 作者姓名： | 黄耘 于永洋 苏蕊 王思力 |
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| 作者单位： | 厦门大学附属第一医院;1.血液科, ;2.普外科 福建省厦门市, 361003 |
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| 摘 要： | 目的 探究 lncRNA HOXB-AS3 对急性髓样白血病 (acute myeloid leukemia, AML) 的增殖、 凋亡和侵袭的影响和机制。 方法 RT-qPCR 检测 AML 患者骨髓单核细胞 (BMMCs) 和细胞系中 lncRNA HOXB-AS3 相对表达量。 慢病毒转染建立稳定表达 shRNA-HOXB-AS3-01, shRNA-HOXB-AS3-02 和 shRNA-HOXB-AS3-03 的 THP1 和 HL60 细胞系。 CCK-8 实验、 EdU 实验、 流式细胞术实验和 Transwell 实验分别检测 THP1和 HL60 细胞活力、 增殖、 凋亡和侵袭能力, Western 印迹检测蛋白相对表达量。 建立裸鼠 AML 移植瘤模型, 体内验证 HOXB-AS3 低表达对肿瘤生长的影响。 结果 lncRNA HOXB-AS3 在 AML 患者 BMMCs 和细胞系中的表达量显著增加。 在细胞实验中, HOXB-AS3 低表达显著抑制 THP1 和 HL60 细胞活力、 增殖和侵袭, 增加细胞凋亡率, 上调 cleaved caspase-3、 cleaved caspase-9 和 E-cadherin 蛋白的表达, 下调 N-cadherin、VEGF、 PI3Kp85α 和 p-AKT 蛋白的表达。 在体内实验中, HOXB-AS3 低表达显著抑制肿瘤生长, 下调PI3Kp85α 和 p-AKT 蛋白表达。 结论 lncRNA HOXB-AS3 通过激活 PI3K-AKT 通路加剧 AML 细胞的增殖、凋亡和侵袭。
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| 关 键 词： | lncRNA HOXB-AS3 急性髓样白血病 增殖 凋亡 侵袭 PI3K-AKT 通路 |
lncRNA HOXB-AS3 Aggravates the Proliferation,Apoptosis, Migration and Invasion of Acute Myeloid Leukemia Cells by Activatingthe PI3K-AKT Pathway |
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| HUANG Yun,YU Yongyang,SU Rui,WANG Sili. lncRNA HOXB-AS3 Aggravates the Proliferation,Apoptosis, Migration and Invasion of Acute Myeloid Leukemia Cells by Activatingthe PI3K-AKT Pathway[J]. Journal of Medical Molecular Biology, 2022, 19(5): 366-373. DOI: 10.3870/j.issn.1672-8009.2022.05.003 |
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| Authors: | HUANG Yun YU Yongyang SU Rui WANG Sili |
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| Affiliation: | 1 Department of Hematology, 2 Department of General Surgery, the First Affiliated Hospital of XiamenUniversity, Xiamen, Fujian, 361003, China |
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| Abstract: | Objective To investigate the effect of lncRNA HOXB-AS3 on cell proliferation,apoptosis and invasion in acute myeloid leukemia (AML) and the underlying mechanism. Methods The expression level of lncRNA HOXB-AS3 in bone marrow mononuclear cells ( BMMCs) ofAML patients and the AML cell lines were detected by RT-qPCR. THP1 and HL60 cell lines stablyexpressed shRNA-HOXB-AS3-01, shRNA-HOXB-AS3-02 or shRNA-HOXB-AS3-03 were established by lentivirus transfection. CCK-8 assay, EdU assay, flow cytometry, and transwell assaywere used to measure the cell viability, proliferation, apoptosis and invasion, Western blotting wasemployed to detect the protein levels. The AML nude mouse xenograft model was established to verifythe effect of low expression level of HOXB-AS3 on the tumor growth in vivo. Results The expressionlevel of lncRNA HOXB-AS3 in AML BMMCs and cell lines was increased significantly. The low expression of HOXB-AS3 significantly inhibited the cell viability, proliferation, and invasion of THP1and HL60 cells, enhanced the apoptosis, up-regulated the expression levels of cleaved caspase-3,cleaved caspase-9 and E-cadherin, and down-regulated the expression levels of N-cadherin,VEGF, PI3Kp85α and p-AKT. The low expression of HOXB-AS3 significantly inhibited the tumorgrowth, and down-regulated the expression level of PI3Kp85α and p-AKT In vivo. Conclusion lncRNA HOXB-AS3 aggravates the proliferation, apoptosis and invasion of AML cells by activatingthe PI3K-AKT pathway. |
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| Keywords: | lncRNA HOXB-AS3 acute myeloid leukemia proliferation apoptosis invasion PI3K-AKT pathway |
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