ANXA2 Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population derived from the HT29 human colorectal adenocarcinoma line. This product features targeted disruption of the ANXA2 gene via CRISPR/Cas9-mediated gene editing, resulting in a heterogeneous population of cells with loss-of-function mutations in ANXA2. The polyclonal format provides a pool of edited cells suitable for studying ANXA2-dependent phenotypes without clonal bias, offering a robust model for functional genomics and pathway analysis.
HT29 cells are an adherent epithelial cell line originally isolated from a 44-year-old female patient with primary colorectal adenocarcinoma. This cell line is widely used as a model for colorectal cancer and intestinal epithelial biology, retaining key characteristics of the transformed phenotype, including the ability to form tumors in immunocompromised mice. The HT29 background provides a well-characterized platform for investigating oncogenic signaling, cell adhesion, and response to therapeutic agents in a colorectal cancer context.
ANXA2 encodes a calcium-dependent phospholipid-binding protein that functions as a receptor for plasminogen and tissue plasminogen activator (PLAT) on the cell surface, forming a heterotetrameric complex with S100A10 (p11). This complex promotes localized plasmin generation, facilitating extracellular matrix degradation and cell migration. In cancer cells, ANXA2 is activated downstream of EGF and HGF through SRC kinase and is transcriptionally regulated by NF-kB and STAT3. It further interacts with actin to remodel the cytoskeleton and upregulates cathepsin B, MMP-9, and c-Myc, driving invasion and proliferation. ANXA2 also integrates signals from EGFR, Src, and Wnt/beta-catenin pathways, positioning it as a critical node in tumor progression.
In HT29 cells, ANXA2 contributes to the malignant phenotype by enhancing migratory and invasive capacity through plasmin-dependent matrix proteolysis and by modulating adhesion and proliferative signaling. The knockout of ANXA2 in this colorectal cancer model enables dissection of its role in fibrinolytic-driven invasion and cross-talk with oncogenic pathways. This model is particularly relevant for studying colorectal cancer metastasis, as well as the contributions of ANXA2 to chemoresistance and epithelial-mesenchymal transition.
Researchers can employ ANXA2 Knockout HT29 Polyclonal Cells in a variety of assays including Western blotting, RT-qPCR, flow cytometry, and immunofluorescence to confirm knockdown and assess downstream effects. Functional studies such as migration/invasion assays, fibrin zymography, proliferation assays, and colony formation assays are readily applicable. These cells are valuable for drug target validation, biomarker discovery, and investigating fibrinolysis in cancer biology. For further information, please contact Ascent Research.
