The ITGAM Knockout DLD-1 Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal population of the human DLD-1 colorectal adenocarcinoma cell line harboring targeted disruptions in the ITGAM gene. This loss-of-function model enables investigation of integrin alpha M (CD11b) functions in an epithelial cancer context. The polyclonal format provides a heterogeneous knockout pool that minimizes clonal artifacts and supports robust bulk assays.
DLD-1 is a widely used epithelial colorectal adenocarcinoma line exhibiting anchorage-dependent growth and retaining key oncogenic mutations. Its epithelial morphology and genetic background make it a suitable model for studying tumor cell adhesion, migration, and inflammatory signaling interactions.
ITGAM encodes the ??M subunit that dimerizes with CD18 to form Mac-1. The receptor is regulated by pro-inflammatory signals such as TNF-??, IL-1??, and chemokines, and binds ligands including ICAM-1, fibrinogen, and complement C3b/iC3b. Ligand engagement activates FAK, Src, and Syk kinases, triggering phosphorylation of p130Cas and paxillin, and downstream PI3K-AKT, NF-??B, and Rho GTPase (Rac1, RhoA) pathways that govern cell motility and survival. Cross-communication with TLR4 and CD14 links Mac-1 to innate immune signaling upon LPS exposure.
In the DLD-1 context, ITGAM knockout allows dissection of ??M integrin contributions to epithelial tumor biology, including adhesion-dependent proliferation, migration, and response to inflammatory cues. The model is suited for screening integrin inhibitors or evaluating how aberrant CD11b expression influences colorectal cancer progression and immune evasion.
Typical applications include flow cytometry for CD11b loss, adhesion and migration assays, complement-mediated phagocytosis, and western blot detection of phosphorylated FAK, AKT, or NF-??B. These approaches support research in cancer immunology, inflammation, and drug discovery targeting integrin pathways. For inquiries, please contact Ascent Research.
