The AGGF1 Knockout HCT 116 Polyclonal Cells product constitutes a CRISPR/Cas9-edited polyclonal knockout cell population in which the AGGF1 gene has been disrupted in HCT 116 colorectal carcinoma cells. This loss-of-function model provides researchers with a genetically defined tool to dissect AGGF1-dependent signaling and angiogenic functions in a tumorigenic background. The polyclonal format captures a range of edited alleles, enabling population-level studies of gene disruption without clonal selection.
HCT 116 is a well-characterized human colorectal carcinoma cell line harboring activating mutations in KRAS and ??-catenin, making it a widely used model for colorectal adenocarcinoma. Due to its genetic stability and robust tumor formation in xenograft models, HCT 116 serves as a versatile platform for investigating oncogenic pathways, tumor?Cstroma interactions, and therapeutic responses.
AGGF1 functions as an angiogenic factor that, upon stimulation by TWEAK, associates with the Fn14 receptor and the adaptor protein TRAF2. This interaction triggers parallel activation of the PI3K/AKT and MAPK/ERK cascades, culminating in the phosphorylation of downstream effectors such as mTOR and ERK1/2. Additionally, AGGF1 signaling engages the NF-??B pathway to transcriptionally upregulate pro-angiogenic factors including VEGFA and eNOS, thereby promoting endothelial cell proliferation and vascular development. The network is further modulated by hypoxic conditions and growth factors, positioning AGGF1 at a nexus of angiogenic and inflammatory signaling.
In the context of HCT 116 colorectal cancer cells, disruption of AGGF1 illuminates its role in tumor-driven angiogenesis and may reveal dependencies on autocrine or paracrine angiogenic loops. This model is particularly relevant for exploring the contributions of AGGF1 to vascular malformation disorders such as Klippel-Trenaunay syndrome and for evaluating anti-angiogenic therapeutic strategies. The confluence of oncogenic KRAS/??-catenin signaling with AGGF1-mediated pathways provides a unique system to study interactive mechanisms governing tumor growth and vascularization.
Research applications for these knockout cells span functional validation by Western blot and RT-qPCR to confirm AGGF1 ablation and altered downstream signaling, assessment of proliferation via MTT assays, migration and invasion studies, and NF-??B luciferase reporter assays to quantify transcriptional activity. High-content readouts such as RNA-seq analysis enable transcriptome-wide profiling of AGGF1-dependent gene expression, while apoptosis assays and subcutaneous xenograft tumor growth models permit evaluation of cell survival and tumor progression. For additional information regarding product specifications, please contact Ascent Research.
