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

Sep 22, 2026

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Acute myeloid leukemia (AML) shows marked heterogeneity, and aberrant long non-coding RNA expression contributes to its pathogenesis and progression. This study investigates whether lncRNA SNHG25 modulates AML cell function through competitive binding to miR-205-5p, promoting disease progression. RT-qPCR, ROC analysis, and CCK8/Transwell assays assess expression, diagnostic potential, and malignant behaviors. Dual-luciferase reporter experiments validate SNHG25–miR-205-5p interaction, with SNHG25 upregulation in AML serum and cell lines.

LanguageEnglish

CategoryResearch & Report

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Pages8

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Abstract

Introduction

Clinical and Experimental Medicine (2026) 26:203 [https://doi.org/10.1007/s10238-026-02108-4](https://doi.org/10.1007/s10238-026-02108-4) RESEARCH LncRNA SNHG25 promotes proliferation, migration, and invasion of acute myeloid leukemia by competitively binding to miR-205-5p Jinfang Zeng1 · Lina Huang2,3 · Qiuhui Sun4 · Min Liang5 · Fangfang Guo6 Received: 13 November 2025 / Accepted: 13 February 2026 © The Author(s) 2026 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. Keywords Acute myeloid leukemia · SNHG25 · miR-205-5p · Proliferation · Migration and invasion Jinfang Zeng and Lina Huang should be considered joint first author. 􀀍 Min Liang [liangmin_dr@163.com](liangmin_dr@163.com) 􀀍 Fangfang Guo [Guofangfang25@163.com](Guofangfang25@163.com) 1 Department of Hematology, The Affiliated Hospital of Putian University, Putian 351100, Fujian Province, China 2 Department of Rehabilitation Medicine, The Affiliated Hospital of Youjiang Medical University for Nationalities, Baise 533000, China 3 Key Laboratory of Research and Development on Clinical Molecular Diagnosis for High-Incidence Diseases of Baise, Baise, Guangxi, China 4 Hematology and Chemotherapy Department, Yueqing People’s Hospital, Wenzhou City, Zhejiang Province, China 5 Liaocheng People’s Hospital, No.67 Dongchang West Road, Dongchangfu District, Liaocheng City 252000, Shandong Province, China 6 Department of Hematology, Ganzhou Hospital-Nanfang Hospital, Southern Medical University (Ganzhou People’s Hospital), No.16, Meiguan Avenue, Zhanggong District, Ganzhou City 341000, Jiangxi Province, China Introduction Acute myeloid leukemia (AML) features abnormal proliferation and impaired differentiation of myeloid progenitor cells, leading to failure of bone marrow hematopoiesis [1] . In recent years, chemotherapy, targeted therapy, and hematopoietic stem cell transplantation have achieved certain progress in treating AML [2] . However, long-term survival rates for AML patients remain suboptimal, particularly among elderly patients and those with relapsed or refractory disease [3]. Therefore, it is still one of the key research directions to explore the molecular mechanism of AML and find new therapeutic targets. The role of non-coding RNA in tumorigenesis and progression has garnered increasing attention [4] . Among these, long non-coding RNAs (lncRNAs) have emerged asa hotspot in tumor research due to their extensive involvement in gene expression regulation, cellular signaling transduction, and epigenetic modifications [5] . Increasing evidence indicates that lncRNAs play a critic

FAQs

What is the main purpose of the study on SNHG25 in AML?

To determine whether lncRNA SNHG25 regulates AML cell functions by competitively binding to miR-205-5p, thereby promoting disease progression.

How do the researchers measure SNHG25 and miR-205-5p and evaluate AML cell behavior?

RT-qPCR detects expression levels, ROC analysis evaluates diagnostic capability, and CCK8 and Transwell assays assess proliferation, migration, and invasion.

What experimental evidence supports that SNHG25 directly targets miR-205-5p?

A dual-luciferase reporter system examines the interaction between SNHG25 and miR-205-5p, and co-suppression of both counteracts the effects of SNHG25 knockdown on AML cells.

Sep 22, 2026

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