miR-621 May Suppress Cell Proliferation via Targeting lncRNA SNHG10 in Acute Myeloid Leukemia
Authors Xiao S, Zha Y, Zhu H
Received 26 June 2020
Accepted for publication 4 December 2020
Published 2 March 2021 Volume 2021:13 Pages 2117—2123
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Dr Antonella D'Anneo
Shishan Xiao,1,* Yan Zha,2,* Hongqian Zhu1
1Department of Hematology, Guizhou Provincial People’s Hospital, Guiyang City, Guizhou Province 550002, People’s Republic of China; 2Department of Nephrology, Guizhou Provincial People’s Hospital, Guiyang City, Guizhou Province 550002, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Hongqian Zhu
Guizhou Provincial People’s Hospital, No. 83 Zhongshan East Road, Guiyang City, Guizhou Province 550002, People’s Republic of China
Email [email protected]
Background: 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.
Methods: 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.
Results: 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.
Conclusion: miR-621 targets SNHG10 to suppress cell proliferation in AML.
Keywords: acute myeloid leukemia, miR-621, SNHG10, proliferation
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