ArticleCell death & disease2022
Activation of CD44 signaling in leader cells induced by tumor-associated macrophages drives collective detachment in luminal breast carcinomas.
Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- CD44 knockdown and TGF‑β inhibition modulate cell proliferation and invasion in claudin‑low breast cancer cells.Oncology reports · 2026Article
- Biomarkers, isolation methods, and therapeutic implications of breast cancer stem cells.Cancer pathogenesis and therapy · 2025Review
- TGF-β signaling redirects Sox11 gene regulatory activity to promote partial EMT and collective invasion of oncogenically transformed intestinal organoids.Oncogenesis · 2025Article
- scSDNE: A semi-supervised method for inferring cell-cell interactions based on graph embedding.PLoS computational biology · 2025Article
- Integrated multi-omics analysis reveals the functional and prognostic significance of lactylation-related gene PRDX1 in breast cancer.Frontiers in molecular biosciences · 2025Article
- Tumor cell-derived hyaluronan fragments induce endocytosis of S1PR1 to promote lymphangiogenesis through LYVE-1-Src pathway.Journal of Cancer · 2025Article
- MDM2 inhibitors in cancer immunotherapy: Current status and perspective.Genes & diseases · 2024Review
- The inhibition of pancreatic cancer progression by K-Ras-overexpressing mesenchymal stem cell-derived secretomes.Scientific reports · 2023Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Collective detachment of cancer cells at the invading front could generate efficient metastatic spread. However, how cancer cell clusters shed from the leading front remains unknown. We previously reported that the dynamic expression of CD44 in breast cancers (BrCas) at collectively invading edges was associated with tumor-associated macrophages (TAMs). In this study, we first observed that the highly expressed CD44 (CD44
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Registered trials
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