ArticleAdvanced pharmaceutical bulletin2025
Continuous Uptake of MiR-181a-2 Mimetic Induces Constitutive Overexpression of Cellular MiR-181a-2 in MCF-7 Breast Cancer Cells: Links with Progression of Drug Resistance.
Article in Advanced pharmaceutical bulletin, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Purpose: The aim of this study was to elucidate the mechanisms underlying the formation and maintenance of drug resistance in cancer cells. Previously, we demonstrated that prolonged treatment of estrogen-dependent MCF-7 breast cancer cells with exosomes derived from estrogen-resistant MCF-7/T cells leads to a partial loss of estrogen sensitivity in MCF-7 cells. Moreover, repeated transfection with one of the exosomal microRNAs-microRNA-181a-2-induced an irreversible decrease in hormonal sensitivity in the recipient cells. In the present work, to further investigate the possible mechanism of miR-181a-2-induced acquired resistance, we analyzed the effect of multiple miR-181a-2 transfections on the expression of cellular miR-181a-2 and related signaling proteins. Methods: miR-181a-2 was ectopically expressed by mimetic transfection or suppressed by antisense oligonucleotides. miR-181a-2 precursor/MIR181A2HG expression (qRT-PCR) and MIR181A2 locus copy number (qPCR) were assessed. wtSnail was expressed via transient transfection. Tamoxifen sensitivity was measured by MTT assay. Protein expression was studied by immunoblotting, estrogen receptor α/Snail transcriptional activity was evaluated by reporter analysis. Results: We found that multiple transfections with miR-181a-2 resulted in a marked increase in cellular miR-181a-2 precursor levels, whereas single transfection had no such effect. Similarly, stable transfection with miR-181a-2 led to increased levels of cellular miR-181a-2 and its host gene, MIR181A2HG, which was associated with partial resistance to tamoxifen. Analysis of the genomic DNA encoding miR-181a-2 revealed no changes in copy number in transfected cells. Furthermore, we identified the transcription factor Snail as a key mediator of miR-181a-2-induced resistance and demonstrated its role in the formation of an autoregulatory loop of miR181a-2 and the maintenance of cell resistance. Conclusion: Overall, these results reveal a novel mechanism of resistance-associated signaling pathway rearrangement based on the formation of a miR-181a-2 autoregulatory loop.
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