ArticleClinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico2026
Loss of miR-122 promotes cell migration and poor prognosis in triple-negative breast cancer treated by neoadjuvant chemotherapy.
Article in Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico, 2026. 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
backgroundMicroRNAs (miRNAs) are short non-coding RNAs that regulate gene expression post-transcriptionally. miR-122 is abnormally expressed in breast cancer, functioning as both a tumor suppressor and oncomiR, however, its role in triple-negative breast cancer (TNBC) remains unclear. PURPOSE: In this study we investigate the molecular mechanism of miR-122 in TNBC patients undergoing neoadjuvant chemotherapy (NAC).
methodsWe analyzed the expression of miR-122 and its clinical association in TNBC patients from TCGA and KM-plotter datasets. Functional analysis was performed by modulating miR-122 levels in TNBC cells through antagomiR transfections for knockdown assays, and mimic-miR-122 assays, followed by RT-qPCR, immunoblotting, cell viability and migration assays.
resultsDownregulation of miR-122 in TNBC patients is associated with tumor recurrence but not with pathologic complete response after NAC. Low miR-122 levels in rapid-relapse TNBC patients activate a gene co-expression network enriched in genes linked to migration, invasion, and cell differentiation. Among these, DNA-binding protein BORIS was identified as a target of miR-122. Overexpression of miR-122 inhibited cell migration and BORIS expression. Additionally, BORIS promoted a gene expression profile related to cell differentiation and cytoskeletal components in TNBC tumors deficient of miR-122.
conclusionThe loss of miR-122 in TNBC tumors is associated with rapid relapse after chemotherapy in patients and allows cell migration by promoting a metastatic-related transcriptomic landscape, including positive modulation of BORIS expression.
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