The EGFL7 Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HT29 human colorectal adenocarcinoma cell line, designed for targeted disruption of the EGFL7 gene. This loss-of-function model enables investigation of EGFL7-dependent mechanisms in angiogenesis, tumor progression, and integrin-mediated signaling. The polyclonal population preserves the genetic heterogeneity of the editing event, making it suitable for studying population-level responses to EGFL7 ablation without clonal selection bias.
HT29 cells are a well-established human colorectal adenocarcinoma cell line harboring the BRAF V600E mutation, which drives constitutive MAPK pathway activation. These cells exhibit a differentiated epithelial morphology and retain the capacity for enterocytic differentiation, making them a versatile model for colorectal cancer biology. The BRAF V600E background is clinically relevant for studying targeted therapies and resistance mechanisms in colorectal tumors. The HT29 line is widely used in investigations of tumor cell adhesion, migration, invasion, and drug sensitivity, thus providing a robust context for functional analysis of angiogenic factors such as EGFL7.
EGFL7 is a secreted angiogenic factor that regulates endothelial cell adhesion, migration, and tube formation. Mechanistically, EGFL7 binds to integrin ??v??3 and ??5??1, activating downstream FAK and Akt signaling to modulate cytoskeletal dynamics and cell motility. It also intersects with Notch signaling by interacting with Notch1 and its ligand DLL4, influencing the transcription of HES1 and HEY1 target genes. Upstream, EGFL7 expression is induced by VEGF through VEGFR2/PI3K/Akt signaling and by the hypoxia-induced transcription factor HIF1A, as well as the ERG transcription factor. Through these interactions, EGFL7 promotes vascular tube formation during development and contributes to pathological angiogenesis in tumors.
Disruption of EGFL7 in HT29 cells provides a physiologically relevant model to dissect its autocrine and paracrine functions in colorectal cancer. Since HT29 cells express integrins and components of the Notch pathway, the knockout allows interrogation of EGFL7??s role in modulating tumor cell adhesion, migration, and crosstalk with endothelial cells within the tumor microenvironment. The BRAF V600E mutation further contextualizes the study of EGFL7 in the setting of oncogenic MAPK signaling, potentially revealing cooperative pathways driving angiogenesis and metastasis. This model is instrumental for elucidating how tumor-derived EGFL7 influences vascular recruitment and tumor growth in colorectal adenocarcinoma.
This polyclonal knockout cell product is suited for a wide range of functional assays, including tube formation, migration, and invasion studies to assess angiogenic capacity; western blotting and RT-qPCR for confirmatory expression analysis; RNA-seq for transcriptomic profiling; co-immunoprecipitation to probe EGFL7 interactors like integrin ??v??3 and Notch1; and immunofluorescence to visualize subcellular localization changes. Additionally, the cells can be employed in proliferation assays and drug sensitivity testing to evaluate anti-angiogenic compounds targeting the EGFL7 pathway. Researchers can utilize this model to investigate integrin-mediated signaling, Notch pathway modulation, and tumor microenvironment interactions in colorectal cancer. For further information, please contact Ascent Research.
