ArticleMolecular therapy. Oncology2025
hsa-miR-5688 inhibits FOXC1-OCT4/SOX2 feedforward loop that drives chemoresistance in breast cancer stem cells.
Article in Molecular therapy. Oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Cancer Stem Cells Decide the Fate of Cancer Immunotherapy by Remodeling Tumor Microenvironment.Cancer control : journal of the Moffitt Cancer CenterReview
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Authors and funding
14 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Inherently chemotherapy-resistant breast cancer stem cells (CSCs) are responsible for tumor initiation, metastasis, and relapse. CSCs "acquire" more resistance and stemness upon chemotherapy, thereby making relapse-free survival extremely challenging. Here, we describe a novel role of FOXC1 in "acquired resistance" of breast CSCs during chemotherapy. Putative binding sites of pluripotency factors OCT4 and SOX2, but not NANOG, on FOXC1 promoter, were demonstrated by JASPAR and validated by a docking experiment. Significant decline in FOXC1 expression was noticed after OCT4 or SOX2 ablation in breast CSCs. Contrastingly, presence of putative FOXC1 binding sites on the promoters of stemness genes and drug-resistance marker ABCG2, along with downregulation of OCT4 and SOX2 in FOXC1-ablated CSCs, indicated the existence of a feedforward FOXC1-OCT4/SOX2 transactivation loop in CSCs. Chemotherapy-induced upregulation of FOXC1, stemness, as well as drug resistance in CSCs, and downregulation of the same by prior FOXC1-ablation in
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