The AGGF1 Knockout 143B Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human 143B osteosarcoma cell line. This product provides a heterogeneous pool of cells harboring targeted disruption of the AGGF1 gene, offering a robust loss-of-function model for investigating angiogenic signaling. The polyclonal format eliminates clonal selection bias and is ideally suited for bulk population studies where functional redundancy and cellular heterogeneity are relevant. The knockout cells enable the dissection of AGGF1-mediated molecular mechanisms without the confounding effects of single-cell-derived artifacts.
The 143B host cell line is a highly metastatic subclone of the TE85 human osteosarcoma line, characterized by a TP53-deficient background that facilitates aggressive tumor behavior. These cells are widely employed as a model for metastatic osteosarcoma and tumor angiogenesis due to their robust in vivo tumorigenicity and angiogenic potential. The TP53 deficiency additionally impairs genomic stability, making the 143B line a relevant platform for studying cancer-associated vascularization and therapeutic resistance in a clinically pertinent genetic context.
AGGF1 encodes a multifunctional angiogenic factor that functions as a transcriptional coactivator for serum response factor (SRF). It is activated by upstream signals including VEGF and FGF2, and it interacts directly with SRF and SMAD4 to drive expression of target genes involved in endothelial cell proliferation, migration, and tube formation. AGGF1-mediated signaling enhances the VEGF pathway, leading to phosphorylation of AKT and ERK, and downstream activation of eNOS. These molecular events orchestrate vascular development and pathological angiogenesis, positioning AGGF1 as a critical node in the RAS/MAPK and angiogenesis cascades.
In the TP53-deficient 143B background, disruption of AGGF1 provides a powerful tool to dissect its contribution to tumor-driven angiogenesis independently of p53 status. This model enables researchers to study how loss of AGGF1 affects SRF-dependent transcriptional programs, AKT/ERK phosphorylation dynamics, and subsequent angiogenic outputs in a highly metastatic osteosarcoma environment. It is particularly relevant for exploring the molecular underpinnings of vascular malformations and Klippel-Trenaunay syndrome, where AGGF1 plays a central role.
The AGGF1 Knockout 143B Polyclonal Cells are suitable for a range of downstream applications, including western blotting for AGGF1 protein levels, RT-qPCR analysis of angiogenic markers, and endothelial tube formation assays to assess functional angiogenesis. The cells can be used for phospho-AKT and phospho-ERK analysis to probe signaling pathway activity, cell migration assays to evaluate metastatic potential, and RNA-seq for transcriptome-wide profiling. Immunofluorescence staining for vascular markers further supports phenotypic characterization. For further inquiries, please contact Ascent Research.
