ArticleInternational journal of molecular sciences2025
Identification of the EBF1/ETS2/KLF2-miR-126-Gene Feed-Forward Loop in Breast Carcinogenesis and Stemness.
Article in International journal of molecular sciences, 2025. 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.
- Bioinformatics Strategies in Breast Cancer Research.Biomolecules · 2025Review
- The Role of Non-Coding Regions in Breast Cancer: From Gene Regulation to Therapeutic Implications.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Decoding the Epigenome of Breast Cancer.International journal of molecular sciences · 2025Review
- The Emerging Role of MicroRNAs in Nasal Inflammatory Diseases and Tumors: From Bench to Bedside.Genes · 2025Review
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Authors and funding
6 authors.
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Abstract
MicroRNA (miR)-126 is frequently downregulated in malignancies, including breast cancer (BC). Despite its tumor-suppressive role, the mechanisms underlying miR-126 deregulation in BC remain elusive. Through silencing experiments, we identified Early B Cell Factor 1 (EBF1), ETS Proto-Oncogene 2 (ETS2), and Krüppel-Like Factor 2 (KLF2) as pivotal regulators of miR-126 expression. These transcription factors were found to be downregulated in BC due to epigenetic silencing or a "poised but not transcribed" promoter state, impairing miR-126 expression. Gene Ontology analysis of differentially expressed miR-126 target genes in the Cancer Genome Atlas: Breast Invasive Carcinoma (TCGA-BRCA) cohort revealed their involvement in cancer-related pathways, primarily signal transduction, chromatin remodeling/transcription, and differentiation/development. Furthermore, we defined interconnections among transcription factors, miR-126, and target genes, identifying a potential feed-forward loop (FFL) crucial in maintaining cellular identity and preventing the acquisition of stemness properties associated with cancer progression. Our findings propose that the dysregulation of the EBF1/ETS2/KLF2/miR-126 axis disrupts this FFL, promoting oncogenic transformation and progression in BC. This study provides new insights into the molecular mechanisms of miR-126 downregulation in BC and highlights potential targets for therapeutic intervention. Further research is warranted to clarify the role of this FFL in BC, and to identify novel therapeutic strategies aimed at modulating this network as a whole, rather than targeting individual signals, for cancer management.
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