| Literature DB >> 31452816 |
Chan Li1, Hua Yan2, Jie Yin2, Jian Ma2, Ang Liao2, Shengyou Yang2, Lijuan Wang2, Yongxiang Huang2, Chon Lin2, Zhiqiang Dong2, Bo Yang2, Ting Cao2, Guo Liu2, Lv Wang2.
Abstract
Abnormal expression of microRNA (miR)-21 has been reported in various types of cancers. However, the role and mechanism of miR-21 remain to be elucidated in acute myeloid leukemia (AML). In the present study, it was observed that miR-21 was upregulated and Krüppel-like factor 5 (KLF5) was downregulated in AML cells compared with normal bone marrow cells. Dual luciferase reporter assays revealed that KLF5 was a direct target of miR-21. Indeed, miR-21 overexpression resulted in a downregulation of KLF5 expression, while miR-21 inhibition had the opposite effect in AML cells. In addition, miR-21 overexpression promoted the proliferation of AML cells in vitro. Notably, using a mouse xenograft model, miR-21 overexpression was demonstrated to result in enhanced tumor growth and suppressed KLF5 expression in the xenograft tumors in vivo. In conclusion, the present results indicated that miR-21 promoted proliferation through directly regulating KLF5 expression in AML cells. miR-21 may thus serve as an oncogene in AML, providing a potential target for AML therapy.Entities:
Keywords: Krüppel-like factor 5; acute myeloid leukemia; microRNA-21; proliferation
Year: 2019 PMID: 31452816 PMCID: PMC6704287 DOI: 10.3892/ol.2019.10667
Source DB: PubMed Journal: Oncol Lett ISSN: 1792-1074 Impact factor: 2.967