Human Colon Cancer-Associated Fibroblasts

Human Colon Cancer-Associated Fibroblasts

Cat.No.: CSC-C4710Z

Species: Human

Source: Colon; Intestine

Cell Type: Fibroblast

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Cat.No.
CSC-C4710Z
Description
The primary human colon cancer-associated fibroblasts isolate was prepared from human tissue. Tissue was dissected and treated with collagenase and chelation. A colon cancer associated fibroblast population (CAF) was isolated using FSP-1 selection and the resulting cells were propagated in customized colon fibroblast medium.
Species
Human
Source
Colon; Intestine
Cell Type
Fibroblast
Disease
Colon Cancer; Cancer
Quality Control
Human Colon Cancer-Associated Fibroblasts are negative for bacteria, yeast, fungi, and mycoplasma.
Storage and Shipping
Creative Bioarray ships frozen cells on dry ice. On receipt, immediately transfer frozen cells to liquid nitrogen (-180 °C) until ready for experimental use.
Never can cryopreserved cells be kept at -20 °C
Citation Guidance
If you use this products in your scientific publication, it should be cited in the publication as: Creative Bioarray cat no. If your paper has been published, please click here to submit the PubMed ID of your paper to get a coupon.

Cancer-associated fibroblasts (CAFs) constitute the predominant mesenchymal cell population within the colorectal cancer (CRC) tumor microenvironment (TME), comprising a substantial proportion of the stromal compartment. The principal advantage of human colon CAFs lies in their remarkable functional heterogeneity and their central role in orchestrating tumor progression. Single-cell transcriptomic analyses have identified multiple CAF subtypes, including inflammatory CAFs (iCAFs), myofibroblastic CAFs (myCAFs), matrix CAFs (mCAFs), and antigen-presenting CAFs (apCAFs), each exhibiting distinct functional roles. These subpopulations coordinate diverse pro-tumorigenic activities: remodeling the extracellular matrix (ECM), secreting growth factors and cytokines such as TGF-β, IL-6, and VEGF, promoting angiogenesis, and modulating immune evasion.

Human colon CAFs are invaluable as an in vitro model system. They are extensively utilized in co-culture systems with CRC cell lines and patient-derived organoids (PDOs) to recapitulate tumor-stroma interactions, study CAF-mediated chemoresistance, and evaluate therapeutic interventions. Furthermore, CAF-related gene signatures have demonstrated prognostic value, with specific subtypes such as LOXL2⁺ CAFs and P4HA1⁺ CAFs associated with poor outcomes and therapeutic resistance. The intimate crosstalk between CAFs and cancer cells makes them compelling targets for novel CRC therapies. Collectively, human colon CAFs represent an indispensable tool for dissecting CRC pathogenesis and advancing precision oncology.

Fusobacterium Nucleatum Interacts with Cancer-Associated Fibroblasts to Promote Colorectal Cancer

Gut microbial species contribute to colorectal cancer (CRC) by interacting with tumor or immune cells, however if CRC-associated bacteria engage with stromal components of the tumor microenvironment remains unclear. Here, Karta, Jessica, et al. report interaction between the CRC-associated bacterium Fusobacterium nucleatum and cancer-associated fibroblasts (CAFs), and show that F. nucleatum is present in the stromal compartment in murine CRC models in vivo and can attach to and invade CAFs. F. nucleatum-exposed CAFs exhibit a pronounced inflammatory-CAF (iCAF) phenotype, marked by elevated expression of established iCAF markers, secretion of pro-inflammatory cytokines such as CXCL1, IL-6 and IL-8, generation of reactive oxygen species (ROS), and an increased metabolic activity. In co-culture experiments, the interaction of cancer cells with F. nucleatum-stimulated CAFs enhances invasion, a finding further validated in vivo. Altogether, these results point to a role for the tumor microbiome in CRC progression by remodeling the tumor microenvironment through its influence on cancer-associated fibroblasts, suggesting novel therapeutic strategies for targeting CRC.

F. nucleatum-exposed CAFs exhibit enhanced production of inflammatory cytokines and increased metabolic activity.
Fig. 1. F. nucleatum exposure induces CAFs to secret pro-inflammatory cytokines and increases their metabolic activity (Karta, Jessica, et al., 2025).
F. nucleatum promotes CAF-induced migration and invasion of tumor cells.
Fig. 2. F. nucleatum-exposed CAFs increase the migration and invasion of CRC tumor cells in vitro and in vivo (Karta, Jessica, et al., 2025).

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