What question did this study set out to answer?

To examine the role of LncRNA SNHG25 in enhancing the function of acute myeloid leukemia cells by binding to miR-205-5p.

March 24, 2026Open Access

LncRNA SNHG25 promotes proliferation, migration, and invasion of acute myeloid leukemia by competitively binding to miR-205-5p

Key Points

To examine the role of LncRNA SNHG25 in enhancing the function of acute myeloid leukemia cells by binding to miR-205-5p.
RT-qPCR for measuring SNHG25 and miR-205-5p levels.
ROC analysis to assess SNHG25's diagnostic capability for AML.
CCK8 and Transwell assays for evaluating cell proliferation, migration, and invasion.
Dual-luciferase reporter system to study the interaction of SNHG25 and miR-205-5p.
SNHG25 was found to be upregulated in the serum of AML patients and AML cell lines.
High SNHG25 levels accurately differentiated AML patients from healthy controls.
Overexpression of SNHG25 resulted in increased AML cell proliferation, migration, and invasion.
Silencing SNHG25 led to decreased malignant functions in AML cells.

Abstract

As a hematological malignancy, acute myeloid leukemia (AML) demonstrates considerable heterogeneity. The pathogenesis and progression are associated with aberrant long non-coding RNA (lncRNA) expression. Research indicates that lncRNA SNHG25 exerts a pro-cancerous role in various tumors, but its function in AML remains unclear. The aim was to investigate whether SNHG25 regulates AML cells function by competitive binding to miR-205-5p, thereby promoting disease progression. RT-qPCR was utilized to detect SNHG25 and miR-205-5p expression. ROC analysis was applied to evaluate diagnostic capability of SNHG25 for AML. CCK8 and Transwell assays were employed to assess proliferation, migration, and invasion of AML cells. Dual-luciferase reporter system was applied to examine interaction between SNHG25 and miR-205-5p. SNHG25 was upregulated in AML patient serum and AML cell lines. SNHG25 demonstrated a remarkable ability to distinguish AML patients from healthy controls. Overexpression of SNHG25 enhanced AML cell proliferation and accelerated migration and invasion, while silencing SNHG25 showed the opposite trend. Additionally, SNHG25 directly targets miR-205-5p, and co-suppression of SNHG25 and miR-205-5p counteracted functional consequences of silencing SNHG25 on AML cells. SNHG25 promoted malignant phenotypes of AML by adsorbing miR-205-5p, which provides a potential new target for therapy of AML.

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