ArticleMolecular biology reports2026
miR-548as-5p promotes breast cancer cell apoptosis and improves tamoxifen resistance by downregulating NF-κB1.
Article in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Not yet cited in PubMed.
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Corrections and comments
- Erratum issued
Authors and funding
6 authors.
Funding
Abstract
backgroundTamoxifen (TAM) resistance limits favorable outcomes in patients with breast cancer. Bioinformatics results suggest that the miR-548as-5p/nuclear factor kappa B1 (NF-κB1) axis may regulate TAM resistance. The aim of this study was to investigate the role of the miR-548as-5p/NF-κB1 axis in TAM resistance. METHODS AND
resultsWe successfully established a TAM-resistant MCF-7 (MCF-7/TamR) breast cancer cell line and calculated its TAM resistance index. The expression levels of miR-548as-5p and NF-κB1 in MCF-7/TamR cells were analyzed. By regulating the expression levels of miR-548as-5p and NF-κB1, the apoptosis rate and TAM resistance of MCF-7/TamR cells were analyzed in vivo and in vitro. The expression level of miR-548as-5p was considerable decreased, whereas that of NF-κB1 was markedly increased in the MCF-7/TamR cell line. The knockdown of miR-548as-5p in MCF-7/TamR cells decreased apoptosis following TAM treatment, whereas overexpression increased apoptosis. Reduced expression of miR-548as-5p increased NF-κB1 expression, thereby enhancing the resistance to TAM. Overexpression of miR-548as-5p partially restored TAM sensitivity and markedly increased apoptosis of MCF-7/TamR cells, whereas additional overexpression of NF-κB1 reversed these effects. These results were validated in vivo using a mouse model.
conclusionsThe miR-548as-5p/NF-κB1 axis may represent a novel therapeutic target for reducing TAM resistance in breast cancer.
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