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Tissue factor and cancer stem cells: is there a linkage?
Arterioscler Thromb Vasc Biol. 2009 Dec; 29(12):2005-14.AT

Abstract

A common feature in the progression of multiple human malignancies is the protracted deregulation of the coagulation system, often referred to as cancer coagulopathy. Indeed, cancer cells and their vascular stroma often exhibit procoagulant properties, of which deregulation of tissue factor (TF) expression is a notable, although not the sole example. These changes can be traced to oncogenic influences affecting epidermal growth factor receptor (EGFR), EGFRvIII, K-ras, p53, PTEN, and probably many other proto-oncogenes and tumor suppressors in tumor parenchyma. Cancer stem cells (CSCs)/tumor initiating cells (TICs) are thought to represent the primary target and the main cellular effector through which oncogenic mutations exert their tumor-inducing effects. In so doing, CSCs/TICs depend on interactions with the tumor vasculature, which forms supportive niches for their clonal growth. We postulate that TF contributes to these interactions (directly or indirectly) through procoagulant and signaling effects, the latter executed in concert with juxtaposed protease activated receptors (mainly PAR-1 and PAR-2). TF/PAR system acts as a "blood sensing" mechanism, whereby cancer cells, including CSCs/TICs, may respond to plasma proteases (Factors VIIa, Xa, and IIa) and their related microenvironmental changes (fibrin deposition, activation of platelets). A growing body of still largely circumstantial evidence suggests that these events may contribute to the CSC/TIC niche, which could influence tumor initiation, metastasis, recurrence, and therapeutic intractability. Indeed, certain types of cancer cells harboring markers of CSCs (CD133) exhibit elevated TF expression and depend on this receptor to efficiently initiate tumor growth. We propose that both tumor cell-associated and host-related TF could influence the properties of CSCs, and that agents targeting the TF/PAR system may represent a hitherto unappreciated therapeutic opportunity to control cancer progression by influencing the CSC/TIC compartment.

Authors+Show Affiliations

Montreal Children's Hospital, McGill University, QC, Canada.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

19628788

Citation

Milsom, Chloe, et al. "Tissue Factor and Cancer Stem Cells: Is There a Linkage?" Arteriosclerosis, Thrombosis, and Vascular Biology, vol. 29, no. 12, 2009, pp. 2005-14.
Milsom C, Magnus N, Meehan B, et al. Tissue factor and cancer stem cells: is there a linkage? Arterioscler Thromb Vasc Biol. 2009;29(12):2005-14.
Milsom, C., Magnus, N., Meehan, B., Al-Nedawi, K., Garnier, D., & Rak, J. (2009). Tissue factor and cancer stem cells: is there a linkage? Arteriosclerosis, Thrombosis, and Vascular Biology, 29(12), 2005-14. https://doi.org/10.1161/ATVBAHA.108.177444
Milsom C, et al. Tissue Factor and Cancer Stem Cells: Is There a Linkage. Arterioscler Thromb Vasc Biol. 2009;29(12):2005-14. PubMed PMID: 19628788.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Tissue factor and cancer stem cells: is there a linkage? AU - Milsom,Chloe, AU - Magnus,Nathalie, AU - Meehan,Brian, AU - Al-Nedawi,Khalid, AU - Garnier,Delphine, AU - Rak,Janusz, Y1 - 2009/07/23/ PY - 2009/7/25/entrez PY - 2009/7/25/pubmed PY - 2009/12/16/medline SP - 2005 EP - 14 JF - Arteriosclerosis, thrombosis, and vascular biology JO - Arterioscler Thromb Vasc Biol VL - 29 IS - 12 N2 - A common feature in the progression of multiple human malignancies is the protracted deregulation of the coagulation system, often referred to as cancer coagulopathy. Indeed, cancer cells and their vascular stroma often exhibit procoagulant properties, of which deregulation of tissue factor (TF) expression is a notable, although not the sole example. These changes can be traced to oncogenic influences affecting epidermal growth factor receptor (EGFR), EGFRvIII, K-ras, p53, PTEN, and probably many other proto-oncogenes and tumor suppressors in tumor parenchyma. Cancer stem cells (CSCs)/tumor initiating cells (TICs) are thought to represent the primary target and the main cellular effector through which oncogenic mutations exert their tumor-inducing effects. In so doing, CSCs/TICs depend on interactions with the tumor vasculature, which forms supportive niches for their clonal growth. We postulate that TF contributes to these interactions (directly or indirectly) through procoagulant and signaling effects, the latter executed in concert with juxtaposed protease activated receptors (mainly PAR-1 and PAR-2). TF/PAR system acts as a "blood sensing" mechanism, whereby cancer cells, including CSCs/TICs, may respond to plasma proteases (Factors VIIa, Xa, and IIa) and their related microenvironmental changes (fibrin deposition, activation of platelets). A growing body of still largely circumstantial evidence suggests that these events may contribute to the CSC/TIC niche, which could influence tumor initiation, metastasis, recurrence, and therapeutic intractability. Indeed, certain types of cancer cells harboring markers of CSCs (CD133) exhibit elevated TF expression and depend on this receptor to efficiently initiate tumor growth. We propose that both tumor cell-associated and host-related TF could influence the properties of CSCs, and that agents targeting the TF/PAR system may represent a hitherto unappreciated therapeutic opportunity to control cancer progression by influencing the CSC/TIC compartment. SN - 1524-4636 UR - https://www.unboundmedicine.com/medline/citation/19628788/Tissue_factor_and_cancer_stem_cells:_is_there_a_linkage L2 - https://www.ahajournals.org/doi/10.1161/ATVBAHA.108.177444?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -