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长链非编码RNA SNHG4通过调控miR-10a/PTEN抑制急性髓系白血病细胞的增殖。

LncRNA SNHG4 regulates miR-10a/PTEN to inhibit the proliferation of acute myeloid leukemia cells.

作者信息

Yuan Zhongtao, Wang Wei

机构信息

Department of Hematology, The 920 Hospital of People's Liberation Army, Kunming City, People's Republic of China.

Department of Rheumatology and Immunology, First Affiliated Hospital of Kunming Medical University, Kunming City, People's Republic of China.

出版信息

Hematology. 2020 Dec;25(1):160-164. doi: 10.1080/16078454.2020.1754636.

Abstract

Long non-coding RNA (lncRNA) small nucleolar RNA host gene 4 (SNHG4) is a characterized oncogenic lncRNA in osteosarcoma. The analysis of the TCGA dataset suggested the downregulation of SNHG4 in acute myeloid leukemia (AML), indicating its possible involvement in this disease. Therefore, this study was performed to analyze the interaction between SNHG4 and miR-10a in AML. We included 60 patients with AML and 60 healthy participants. Transient transfections, luciferase activity assay, RT-qPCR, CCK-8, and Western blot were used to carry out the research. In this study, we found that SNHG4 was downregulated in AML patients compared to healthy participants. SNHG4 and miR-10a can interact with each other. However, overexpression of SNHG4 and miR-10a failed to affect the expression of each other. Instead, SNHG4 overexpression led to upregulated PTEN, a downstream target of miR-10a. Cell proliferation analysis showed that SNHG4 and PTEN overexpression led to decreased proliferation rates of AML cells and attenuated the enhancing effects of miR-10a on cell proliferation. In conclusion, SNHG4 may regulate miR-10a/PTEN to inhibit the proliferation of AML cells.

摘要

长链非编码RNA(lncRNA)小核仁RNA宿主基因4(SNHG4)是一种已明确的骨肉瘤致癌lncRNA。对TCGA数据集的分析表明,急性髓系白血病(AML)中SNHG4表达下调,提示其可能参与该疾病。因此,本研究旨在分析AML中SNHG4与miR-10a之间的相互作用。我们纳入了60例AML患者和60名健康参与者。采用瞬时转染、荧光素酶活性测定、RT-qPCR、CCK-8和蛋白质印迹法进行研究。在本研究中,我们发现与健康参与者相比,AML患者中SNHG4表达下调。SNHG4与miR-10a可相互作用。然而,SNHG4和miR-10a的过表达未能影响彼此的表达。相反,SNHG4过表达导致miR-10a的下游靶点PTEN表达上调。细胞增殖分析表明,SNHG4和PTEN过表达导致AML细胞增殖率降低,并减弱了miR-10a对细胞增殖的增强作用。总之,SNHG4可能通过调节miR-10a/PTEN来抑制AML细胞的增殖。

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