ArticleBiochemical genetics2026
miR-486-3p Suppresses Osteosarcoma Proliferation and Migration by Targeting the SPRED1-MAPK/ERK Pathway.
Article in Biochemical genetics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
2 citing papers in PubMed.
- MiR-18b-3p promotes cell proliferation and metastasis by directly inhibiting PTEN expression in osteosarcoma.Journal of orthopaedic surgery and research · 2025Article
- Enhancing the sensitivity of lung adenocarcinoma to immune therapeutic agents throughTranslational lung cancer research · 2025Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Osteosarcoma (OS) is a common malignancy of the bone that originates from stromal cell lines. One of the key cellular pathways extensively studied in OS is the mitogen-activated protein kinase (MAPK) pathway, particularly ERK1/2, whose activation is closely associated with tumor growth and metastasis. MicroRNA (miRNA)-based detection and targeted therapies offer promising new strategies for the treatment of OS. In this study, we investigated the role of miR‑486‑3p in the regulation of the ERK1/2 pathway in OS. We examined the expression level of miR‑486‑3p in the GEO dataset (GSE65071) and clinical samples, and analyzed its regulation of the target gene SPRED1 in OS cells and tumor-bearing mice. Downregulation of miR‑486‑3p was confirmed in OS tissues, with its expression decreasing in line with the progression of clinical stages. Furthermore, the exogenous introduction of a miR-486-3p mimic attenuated the malignant behavior of OS cells, inhibiting their proliferation, migration, and invasion. Bioinformatic analysis revealed that miR‑486‑3p directly targets SPRED1 in OS, leading to alterations in epithelial-to-mesenchymal transition (EMT) markers, including E-cadherin, N-cadherin, and Vimentin. Functional loss- and gain-of-function experiments confirmed that miR‑486‑3p directly targets SPRED1 and inactivates the ERK1/2 pathway in both OS cells and tumor-bearing mice. This review demonstrates that downregulation of miR-486-3p leads to increased SPRED1 expression, which activates the ERK1/2 pathway in OS. Targeting miR-486-3p and SPRED1 could offer potential therapeutic benefits.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.