ArticleOncogene2024
COL5A1 promotes triple-negative breast cancer progression by activating tumor cell-macrophage crosstalk.
Article in Oncogene, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 26 papers.
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
26 citing papers in PubMed, 21 citations in OpenAlex.
- Ubiquitin signaling in tumor-associated macrophage reprogramming: mechanisms and therapeutic opportunities in cancers.Biomarker research · 2026Review
- Plasma Proteomic Signatures Predict Incident Amyotrophic Lateral Sclerosis: A Prospective Study Stratified by C9orf72 Expansion.Journal of cachexia, sarcopenia and muscle · 2026Article
- GAS5 Downregulation Promotes the Progression of Triple-Negative Breast Cancer by Regulating Tumor Cells-MDSCs Crosstalk.Cancers · 2026Article
- Decoding the Collagenome in Breast Cancer: Mechanotransduction, Microenvironment, and Translational Opportunities.International journal of molecular sciences · 2026Review
- Impact of the loss of tenascin X on tissue architecture and wound healing of the murine corneal stroma.The ocular surface · 2026Article
- StringTie3 improves total RNA-seq assembly by resolving nascent and mature transcripts.Nature methods · 2026Article
- Integrated environmental and genomic analysis reveals the drivers and genetic mechanisms of agro-climatic adaptation in geese.BMC genomics · 2026Article
- Network toxicology and bioinformatics reveal potential molecular links between cadmium exposure and pancreatic cancer.BMC pharmacology & toxicology · 2026Article
- Doxorubicin-Induced Cardiotoxicity in Breast Cancer: Mechanistic Pathways, Pharmacogenomic Modifiers, and Translational Strategies.Cardiovascular toxicology · 2026Review
- Loss of biomechanical features reveals smooth muscle disruption and disease progression in prostate cancer.Cancer cell international · 2026Article
- Macrophage-cancer cell crosstalk in breast cancer chemotherapy resistance.Medical oncology (Northwood, London, England) · 2025Review
- Collagen dynamics in the breast cancer tumor microenvironment and therapeutic perspectives.Discover oncology · 2025Review
- The Duality of Collagens in Metastases of Solid Tumors.International journal of molecular sciences · 2025Review
- Cerebrospinal Fluid-Derived Small Extracellular Vesicles May Better Reflect Medulloblastoma Proteomes than Those from Blood Plasma.International journal of molecular sciences · 2025Article
- Single-cell transcriptomic analysis reveals metastatic and immunosuppressive characteristics in meningioma brain-tumor interface.Journal of translational medicine · 2025Article
- Macrophage regulation of tumor cell dormancy and the dormant niche: an overview in solid tumors.Cancer metastasis reviews · 2025Review
- Targeting COL5A1 enhances anoikis thus attenuating malignancy of glioblastoma via inhibiting the Wnt/β-catenin signaling pathway.Journal of neuro-oncology · 2025Article
- Upregulation of long non-coding RNA SNHG11 promotes apoptosis and its molecular mechanisms in human osteosarcoma U2OS cells.Scientific reports · 2025Article
- The ADAMTS2 metalloproteinase inhibits tumor growth by regulating the innate immune system.Cancer cell international · 2025Article
- Interleukin-1β mediates a tumor-supporting environment prompted by IGF1 in triple-negative breast cancer (TNBC).Journal of translational medicine · 2025Article
Corrections and comments
- Erratum issued
Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Triple-negative breast cancer (TNBC) is an exceptionally aggressive subtype of breast cancer. Despite the recognized interplay between tumors and tumor-associated macrophages in fostering drug resistance and disease progression, the precise mechanisms leading these interactions remain elusive. Our study revealed that the upregulation of collagen type V alpha 1 (COL5A1) in TNBC tissues, particularly in chemoresistant samples, was closely linked to an unfavorable prognosis. Functional assays unequivocally demonstrated that COL5A1 played a pivotal role in fueling cancer growth, metastasis, and resistance to doxorubicin, both in vitro and in vivo. Furthermore, we found that the cytokine IL-6, produced by COL5A1-overexpressing TNBC cells actively promoted M2 macrophage polarization. In turn, TGFβ from M2 macrophages drived TNBC doxorubicin resistance through the TGFβ/Smad3/COL5A1 signaling pathway, establishing a feedback loop between TNBC cells and macrophages. Mechanistically, COL5A1 interacted with TGM2, inhibiting its K48-linked ubiquitination-mediated degradation, thereby enhancing chemoresistance and increasing IL-6 secretion. In summary, our findings underscored the significant contribution of COL5A1 upregulation to TNBC progression and chemoresistance, highlighting its potential as a diagnostic and therapeutic biomarker for TNBC.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.