The AMIGO2 Knockout PaTu 8988s Polyclonal Cells are a CRISPR/Cas9-edited polyclonal human cell population designed to disrupt the AMIGO2 gene, creating a robust loss-of-function model for functional analysis of this adhesion molecule in pancreatic ductal adenocarcinoma. The heterogeneous polyclonal pool enables investigation of AMIGO2-dependent phenotypes without clonal selection bias, offering a genetically tractable system for signaling, adhesion, and motility studies in a well-characterized metastatic PDAC background.
The parental PaTu 8988s cell line originates from a liver metastasis of human PDAC and harbors KRAS G12V and TP53 R175H mutations while retaining wild-type SMAD4, recapitulating key driver events in aggressive metastatic disease. These genetic alterations constitutively activate the MAPK/ERK and PI3K/Akt cascades, providing an oncogenically primed context in which AMIGO2 function can be dissected.
AMIGO2 is a transmembrane adhesion receptor that promotes proliferation, migration, and invasion through homophilic interactions and coupling to PI3K/Akt and MAPK/ERK pathways. Its expression increases phosphorylation of Akt (Ser473) and ERK1/2 (Thr202/Tyr204), upregulates cyclin D1, and drives epithelial?Cmesenchymal transition (EMT) by inducing Snail and vimentin while suppressing E-cadherin. Transcription is activated by SP1 and TGF-??1 and modulated by DNA methylation; the protein interacts with PDZD2 and AMIGO1/3. Disruption of AMIGO2 therefore uncouples these oncogenic signals, providing a platform to dissect adhesion-dependent and adhesion-independent signaling.
In the PaTu 8988s background, AMIGO2 knockout is expected to attenuate the aggressive phenotype driven by mutant KRAS and TP53 loss, impairing adhesion, EMT, and invasive capacity. The polyclonal population preserves cellular heterogeneity, closely mimicking therapeutic targeting scenarios, and enables researchers to evaluate contributions to chemoresistance, metastatic colonization, and EMT dynamics. This model is particularly valuable for linking AMIGO2-mediated adhesion to cytoskeletal remodeling and survival in a physiologically relevant PDAC context.
Typical applications include Western blotting and RT-qPCR to confirm AMIGO2 ablation and quantify phospho-Akt, phospho-ERK, cyclin D1, Snail, vimentin, and E-cadherin; colony formation, wound healing, and Matrigel invasion assays; cell adhesion and immunofluorescence studies; drug sensitivity screening; and CRISPR-based target validation. For detailed lot-specific characterization data or ordering information, please contact Ascent Research.
