The AGGF1 Knockout TE1 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the TE1 human esophageal squamous cell carcinoma cell line, characterized by targeted disruption of the AGGF1 gene. This loss-of-function model is generated through CRISPR/Cas9-mediated gene editing, yielding a heterogeneous pool of cells with AGGF1 inactivation, suitable for studying the functional consequences of AGGF1 depletion in a cancer cell context. The polyclonal format avoids clonal selection bias, providing a population-level representation of gene knockout effects that is valuable for functional genomics and signaling studies.
TE1 is a well-characterized human esophageal squamous cell carcinoma (ESCC) cell line with wild-type TP53 status, extensively used in cancer biology research to investigate oncogenic signaling, tumor progression, and therapeutic responses. Derived from a primary ESCC tumor, TE1 retains key features of squamous cell carcinoma and serves as a relevant in vitro model for esophageal cancer, particularly for studying angiogenesis and tumor-stroma interactions.
AGGF1 encodes an angiogenic factor that promotes endothelial cell proliferation, migration, and tube formation, primarily through activation of the PI3K/AKT and ERK signaling pathways. AGGF1 expression is induced by hypoxia via HIF-1?? and acts downstream of VEGF, engaging VEGFR2 to trigger PI3K/AKT/mTOR and ERK1/2 cascades, ultimately enhancing angiogenic processes such as endothelial cell function and expression of markers like CD31 and eNOS. This signaling network integrates multiple upstream and downstream factors, placing AGGF1 as a critical node in angiogenesis regulation.
In the context of TE1 esophageal cancer cells, AGGF1 knockout disrupts a key pro-angiogenic mechanism that may contribute to tumor vascularization and vascular mimicry. By eliminating AGGF1 expression, this model allows researchers to dissect the tumor cell-intrinsic angiogenic signaling that supports neovascularization and tumor growth. It also provides a platform to explore the relationship between AGGF1-driven signaling and the pathogenesis of vascular malformation syndromes such as Klippel-Trenaunay syndrome.
This product is applicable to a range of experimental approaches, including western blotting and RT-qPCR for validation of gene disruption, tube formation assays with endothelial co-culture to assess angiogenic capacity, migration assays to evaluate cell motility, and phospho-AKT/ERK detection for signaling pathway analysis. Additional applications include immunofluorescence for endothelial markers, RNA-sequencing for transcriptome-wide effects, and drug response studies with anti-angiogenic agents. Researchers can use these polyclonal knockout cells to investigate AGGF1-dependent angiogenesis in esophageal squamous cell carcinoma and related disease models. For further information, please contact Ascent Research.
