ArticleCommunications biology2021
Runt related transcription factor-1 plays a central role in vessel co-option of colorectal cancer liver metastases.
Article in Communications biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 54 citations in OpenAlex.
- Review
- Deciphering Colorectal Liver Metastasis Perfusion Heterogeneity: Identification of Distinct Vascular Phenotypes through High-Lateral-Resolution Photoacoustic Microscopy.Radiology. Imaging cancer · 2026Article
- RUNX1-regulated ITGB1-enriched extracellular vesicles drive pancreatic cancer liver metastasis via fibrotic pre-metastatic niche formation.Journal of translational medicine · 2026Article
- Effect of intratumoral alpha radiation on tumor growth delay and tumor microenvironment in an orthotopic colorectal liver metastasis murine model.Scientific reports · 2026Article
- High levels of serum cholesterol increase the risk of developing vessel co-opting tumors in colorectal cancer liver metastases.The FEBS journal · 2026Article
- RUNX1 is expressed in a subpopulation of dermal fibroblasts and is associated with disease severity of systemic sclerosis.Annals of the rheumatic diseases · 2026Article
- Prediction of colorectal cancer liver metastasis through an MRI radiomic model.Scientific reports · 2026Article
- Navigating the Tumor Microenvironment in Colorectal Liver Metastasis: Barriers to Therapy and Emerging Opportunities.Oncology research · 2026Review
- RUNX1/SLAMF3 Axis Drives Immunosuppression to Contribute to Colorectal Cancer Liver Metastasis by Blocking Phagocytosis and Depleting C1QCAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Multi-omics in colorectal cancer liver metastasis: applications and research advances.Cancer biology & medicine · 2025Review
- Article
- Runt-related transcription factors: from pathogenesis to therapeutic targets in multiple-organ fibrosis.Frontiers in cell and developmental biology · 2025Review
- Molecular characterization of the histopathological growth patterns of colorectal cancer liver metastases by RNA sequencing of targeted samples at the tumor-liver interface.Clinical & experimental metastasis · 2024Article
- High CIB1 expression in colorectal cancer liver metastases correlates with worse survival and the replacement histopathological growth pattern.Molecular therapy. Oncology · 2024Article
- The multifaceted role of PCSK9 in cancer pathogenesis, tumor immunity, and immunotherapy.Medical oncology (Northwood, London, England) · 2024Review
- TGF-β Modulated Pathways in Colorectal Cancer: New Potential Therapeutic Opportunities.International journal of molecular sciences · 2024Review
- Milestones in tumor vascularization and its therapeutic targeting.Nature cancer · 2024Review
- RUNX1-induced upregulation of PTGS2 enhances cell growth, migration and invasion in colorectal cancer cells.Scientific reports · 2024Article
- RUNX transcription factors: biological functions and implications in cancer.Clinical and experimental medicine · 2024Review
- PTEN-restoration abrogates brain colonisation and perivascular niche invasion by melanoma cells.British journal of cancer · 2024Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Colorectal cancer liver metastasis (CRCLM) has two major histopathological growth patterns: angiogenic desmoplastic and non-angiogenic replacement. The replacement lesions obtain their blood supply through vessel co-option, wherein the cancer cells hijack pre-existing blood vessels of the surrounding liver tissue. Consequentially, anti-angiogenic therapies are less efficacious in CRCLM patients with replacement lesions. However, the mechanisms which drive vessel co-option in the replacement lesions are unknown. Here, we show that Runt Related Transcription Factor-1 (RUNX1) overexpression in the cancer cells of the replacement lesions drives cancer cell motility via ARP2/3 to achieve vessel co-option. Furthermore, overexpression of RUNX1 in the cancer cells is mediated by Transforming Growth Factor Beta-1 (TGFβ1) and thrombospondin 1 (TSP1). Importantly, RUNX1 knockdown impaired the metastatic capability of colorectal cancer cells in vivo and induced the development of angiogenic lesions in liver. Our results confirm that RUNX1 may be a potential target to overcome vessel co-option in CRCLM.
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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.