Xiao Shishan, Zha Yan, Zhu Hongqian
Department of Hematology, Guizhou Provincial People's Hospital, Guiyang City, Guizhou Province 550002, People's Republic of China.
Department of Nephrology, Guizhou Provincial People's Hospital, Guiyang City, Guizhou Province 550002, People's Republic of China.
Cancer Manag Res. 2021 Mar 2;13:2117-2123. doi: 10.2147/CMAR.S269528. eCollection 2021.
It has been reported that lncRNA SNHG10 (SNHG10) promotes the progression of liver cancer and osteosarcoma; however, the role of SNHG10 in acute myeloid leukemia (AML) remains unknown. This study was to explore the role of SNHG10 in AML.
The expression of SNHG10 and miR-621 in BM mononuclear cells (BMMNCs) isolated from 60 AML patients and 60 healthy controls were determined by RT-qPCR. Correlation between SNHG10 and miR-621 was analyzed by Pearson correlation coefficient. The overexpression of SNHG10 and miR-621 in transfected AML cells was detected by RT-qPCR, and the regulatory relationship between them was explored. Methylation-specific PCR (MSP) was applied to detect the methylation of miR-621 induced by the overexpression of SNHG10. CCK-8 assay was conducted to evaluate cell proliferation.
In this study, we found that the expression of SNHG10 was upregulated and the expression of miR-621 was downregulated in AML samples. Moreover, SNHG10 and miR-621 were inversely correlated across AML samples, and a high level of SNHG10 predicted poor survival of AML patients. Bioinformatics analysis showed that SNHG10 could be targeted by miR-621. In AML cells, miR-621 overexpression downregulated the expression of SNHG10, while SNHG10 overexpression could not affect the expression of miR-621. However, it was found that the reduction of miR-621 caused by SNHG10 overexpression might be due to the increase of miR-621 methylation. In addition, SNHG10 overexpression significantly promoted BMMNC proliferation, whereas miR-621 overexpression inhibited BMMNC proliferation and abolished the effect of SNHG10 overexpression on BMMNC proliferation.
miR-621 targets SNHG10 to suppress cell proliferation in AML.
据报道，长链非编码RNA SNHG10（SNHG10）促进肝癌和骨肉瘤的进展；然而，SNHG10在急性髓系白血病（AML）中的作用仍不清楚。本研究旨在探讨SNHG10在AML中的作用。
采用RT-qPCR检测60例AML患者和60例健康对照者骨髓单个核细胞（BMMNCs）中SNHG10和miR-621的表达。采用Pearson相关系数分析SNHG10与miR-621的相关性。通过RT-qPCR检测转染AML细胞中SNHG10和miR-621的过表达情况，并探讨它们之间的调控关系。应用甲基化特异性PCR（MSP）检测SNHG10过表达诱导的miR-621甲基化。采用CCK-8法评估细胞增殖。
在本研究中，我们发现AML样本中SNHG10的表达上调，miR-621的表达下调。此外，AML样本中SNHG10与miR-621呈负相关，高水平的SNHG10预示着AML患者的不良生存。生物信息学分析表明，SNHG10可能是miR-621的靶标。在AML细胞中miR-621过表达下调SNHG10的表达，而SNHG10过表达不影响miR-621的表达。然而，发现SNHG10过表达导致的miR-621减少可能是由于miR-621甲基化增加所致。此外，SNHG10过表达显著促进BMMNC增殖，而miR-621过表达抑制BMMNC增殖并消除SNHG10过表达对BMMNC增殖的影响。
miR-621靶向SNHG10抑制AML细胞增殖。
