ArticleTranslational oncology2022
Overexpression miR-520a-3p inhibits acute myeloid leukemia progression via targeting MUC1.
Article in Translational oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- miR-378, miR-20a, and miR-520a-3p can be used in a novel serum prognostic panel for cervical cancer.Scientific reports · 2025Article
- miR-128-3p Reduces Proliferation and Immune Escape in Acute Myeloid Leukemia Through Targeted Regulation of ZEB1.Applied biochemistry and biotechnology · 2025Article
- Role of MicroRNAs in Acute Myeloid Leukemia.Genes · 2025Review
- MYO19 is associated with tumor progression, immune evasion, ferroptosis-related signatures in lung squamous cell carcinoma.Frontiers in oncology · 2025Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAcute myeloid leukemia (AML) is one of the familiar malignant tumors in the hematological system. miR-520a-3p is reported to be involved in several cancers' progression. However, miR-520a-3p role in AML remains unclear. In this study, we aimed to clarify the role and potential mechanism of miR-520a-3p in AML.
methodsCell viability, proliferation, cycle and apoptosis were detected by MTT assay, colony formation assay, flow cytometry, respectively. The levels of PNCA, Bcl-2, Cleaved caspase 3, Cleaved caspase 9 and β-catenin protein were detected by Western blot. Dual-luciferase reported assay was performed to detect the regulation between miR-520a-3p and MUC1. To verify the effect of miR-520a-3p on tumor proliferation in vivo, a non-homogenous transplant model of tumors was established.
resultsmiR-520a-3p expression was down-regulated, and MUC1 expression was up-regulated in AML patients. miR-520a-3p overexpression suppressed THP-1 cell proliferation, induced cell cycle G0/G1 inhibition and promoted apoptosis. miR-520a-3p targeted MUC1 and negatively regulated its expression. MUC1 knockdown inhibited THP-1 cell proliferation and promoted apoptosis. miR-520a-3p overexpression inhibited AML tumors growth.
conclusionOverexpression miR-520a-3p inhibited AML cell proliferation, and promoted apoptosis via inhibiting MUC1 expression and repressing Wnt/β-catenin pathway activation.
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