The ADAM9 Knockout HCT 116 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HCT 116 human colorectal carcinoma cell line, providing a heterogeneous loss-of-function model for the ADAM9 gene. This product is supplied as a pooled population of edited cells, enabling robust and cost-effective gene disruption studies without clonal isolation, and is suitable for applications where a genetically diverse cell pool better recapitulates tumor heterogeneity.
The parental HCT 116 cell line, isolated from a male colorectal carcinoma patient, is a neoplastic colon epithelial model with a near-diploid genome, microsatellite stability, and deficient MLH1 mismatch repair. These features make it a foundational system for colorectal cancer research, widely utilized for investigating oncogenic signaling, drug sensitivity, and mechanisms of tumor progression in a well-defined genetic background.
ADAM9 is a transmembrane metalloprotease and disintegrin that mediates ectodomain shedding of membrane-bound substrates, notably HB-EGF and ephrin-A2, which activate EGFR/RAS/ERK1/2-AKT and EphA4 signaling, respectively. It interacts with integrins ??v??3 and ??6??1, Src kinase, and tetraspanin CD9 to regulate integrin-mediated adhesion. ADAM9 expression is upregulated by EGF, TNF-??, HIF-1??, TGF-??, and PKC, and it processes additional substrates including CD44, ICAM-1, collagen IV, and fibronectin, positioning it as a hub for extracellular signal integration that drives cell migration and matrix remodeling.
In HCT 116 colorectal cancer cells, ADAM9 knockout impairs cell migration, invasion, and proliferation, attributable to diminished shedding of oncogenic growth factors and disrupted integrin-mediated adhesion. This polyclonal knockout model thus captures the multifaceted role of ADAM9 in promoting the metastatic phenotype, offering a powerful tool to dissect the interplay between proteolytic shedding, adhesion dynamics, and downstream signaling in colon cancer.
This polyclonal knockout is suited for Boyden chamber migration/invasion assays, MTS proliferation measurements, ELISA for soluble HB-EGF, and phospho-EGFR/ERK western blotting. Integrin expression can be profiled by flow cytometry, and ADAM9 interactors analyzed by co-immunoprecipitation. Transcriptomic changes are assessable via RNA-seq and RT-qPCR. These applications enable detailed studies of colorectal cancer metastasis and ADAM9-driven signaling. For further assistance, contact Ascent Research.
