期刊
NAUNYN-SCHMIEDEBERGS ARCHIVES OF PHARMACOLOGY
卷 394, 期 1, 页码 177-187出版社
SPRINGER
DOI: 10.1007/s00210-020-01892-4
关键词
miR-486; Acute myeloid leukemia; SOCS2; JAK-STAT; Proliferation
The study revealed that miR-486 was upregulated in AML, and its enhancement of JAK-STAT3 pathway activity promoted cell proliferation, implicating the miR-486-SOCS2-STAT3 proliferation axis in the pathogenesis of AML.
Acute myeloid leukemia (AML) is a widely prevalent disease worldwide and poses a large threat to public health. Previous studies have shown that AML is associated with cytogenetic heterogeneity, complex subtypes, and different therapeutic approaches. In this study, we found that miR-486 was upregulated in AML using both The Cancer Genome Atlas (TCGA) database and patient tissues. After knockdown of miR-486 by short hairpin RNA (shRNA), we discovered that miR-486 was required for cell proliferation. Through miRNA profile analysis and a dual-luciferase reporter assay, suppressor of cytokine signaling 2 (SOCS2) was identified as a direct target of miR-486. Therefore, by silencing SOCS2, a negative regulator of the Janus kinase (JAK)-signal transducer and activator of transcription (STAT) pathway, miR-486 enhanced JAK-STAT3 activity and promoted cell proliferation. The miR-486-SOCS2-STAT3 proliferation axis is therefore involved in the pathogenesis of AML, providing a novel molecular mechanism and diagnostic and therapeutic clues for AML.
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