lncRNA SNHG3 facilitates acute myeloid leukemia cell growth via the regulation of miR‐758‐3p/SRGN axis

Small nucleolar RNA host gene 3 (SNHG3) is a newly identified long non‐coding RNA whose dysregulation has been reported in several cancers. However, the details about clinical significances and biological functions of SNHG3 on acute myeloid leukemia (AML) remain covered. In this study, we revealed increased SNHG3 expression in AML samples and cells and its high potential as a prognostic biomarker for AML patients. Likewise, serglycin (SRGN), which plays an important role in granule‐mediated apoptosis, was previously verified to be upregulated in AML and confirmed again by the present study, and its upregulation predicted poor outcomes in AML. Furthermore, knockdown of SNHG3 or SRGN inhibited cell proliferation and induced cell apoptosis. Besides, silencing SNHG3 noticeably decreased the expression of SRGN in AML cells. Moreover, we uncovered that SNHG3 modulated SRGN expression by competitively binding with miR‐758‐3p. Importantly, both miR‐758‐3p suppression and SRGN overexpression could mitigate the inhibitory effects of SNHG3 depletion on AML cell growth. Intriguingly, the higher SRGN expression in AML samples with a higher SNHG3 level exhibited an enhanced Ki67 level but a reduced caspase 3 level. To sum up, SNHG3 elicits a growth‐promoting function in AML via sponging miR‐758‐3p to regulate SRGN expression, providing a new therapeutic road for AML patients. Upregulated small nucleolar RNA host gene 3 (SNHG3) and serglycin (SRGN) predict poor outcome in adult acute myeloid leukemia (AML) patients. Silencing SNHG3 or SRGN results in suppressed cell growth in AML cells. SNHG3 modulates SRGN expression via sponging miR‐758‐3p. SNHG3 modulates AML cell growth through regulating the miR‐758‐3p/SRGN axis.