LncRNA SNHG1 contributes to the regulation of acute myeloid leukemia cell growth by modulating miR-489-3p/SOX12/Wnt/β-catenin signaling.

Abstract

The long noncoding RNA (lncRNA) small nucleolar RNA host gene 1 (SNHG1) is a critical regulator for the development and progression of multiple tumors. Yet, the role of SNHG1 in acute myeloid leukemia (AML) is unknown. The present study demonstrated that SNHG1 expression was upregulated in AML. SNHG1 silencing markedly repressed AML cell growth, whereas SNHG1 overexpression had the opposite effect. MicroRNA-489-3p (miR-489-3p) was identified as a SNHG1-targeting miRNA. SNHG1 knockdown increased miR-489-3p expression. Low expression of miR-489-3p was correlated with high expression of SNHG1 in AML tissues. miR-489-3p overexpression restricted AML cell growth, and SRY-related high-mobility-group box 12 (SOX12) was identified as a miR-489-3p-targeting gene. SNHG1 inhibition or miR-489-3p overexpression inactivated Wnt/β-catenin signaling through downregulation of SOX12. SOX12 overexpression partially reversed the SNHG1 knockdown- or miR-489-3p overexpression-mediated effects. Taken together, these data indicate that suppression of SNHG1 downregulates AML cell growth by inactivating SOX12/Wnt/β-catenin signaling via upregulating miR-489-3p.