Long noncoding RNA MIAT promotes the progression of acute myeloid leukemia by negatively regulating miR-495.

• MIAT is highly expressed in AML patients than healthy controls. • High MIAT expression can predict poor over survival in AML patients. • MIAT promotes the proliferation and inhibits the apoptosis of AML cells. • MIAT acts as a sponge to negatively regulate miR-495 in AML cells. Acute myeloid leukemia (AML) is a malignant myeloid hematopoietic stem and progenitor cell disease. Studies have shown that the long noncoding RNA (lncRNA) myocardial infarction associated transcript (MIAT) is abundantly expressed in multiple human solid tumors. However, the expression and role of MIAT in AML has not been explored previously. In this study, we find that MIAT is overexpressed in AML patient specimens and AML cell lines. Importantly, upregulation of MIAT is closely related with poor clinical outcome. Further investigations reveal that knockdown of MIAT inhibits the colony formation and proliferation, meanwhile, accelerates the apoptosis of AML cells in vitro. Consistently, MIAT knockdown slows AML progression in immunodeficient mice. Mechanistically, we confirm that MIAT can function as a sponge to inhibit microRNA-495 (miR-495), a tumor suppressor, in AML cells. Collectively, our results demonstrate that MIAT is involved in promoting the progression of AML, at least partly, through negative regulation of miR-495, and therefore provide a promising target for treatment of AML. [ABSTRACT FROM AUTHOR]