The DOCK2 Knockout LoVo Polyclonal Cells are a genetically engineered population of human LoVo colon adenocarcinoma cells, generated through CRISPR/Cas9-mediated disruption of the DOCK2 gene. This polyclonal knockout model provides a loss-of-function system to investigate DOCK2-dependent processes in cancer cell biology, maintaining a degree of genetic diversity inherent to the edited pool. The targeted gene disruption results in robust ablation of DOCK2 protein expression, making these cells suitable for functional assays in oncology and immunology research.
LoVo cells are derived from a metastatic site of human colorectal adenocarcinoma and serve as a widely used epithelial model for studying tumor progression and metastasis. These adherent cells exhibit aggressive invasive properties and express relevant chemokine receptors and adhesion molecules, rendering them particularly useful for dissecting mechanisms of cell migration and invasion in a colorectal cancer context.
DOCK2 encodes a Rac-specific guanine nucleotide exchange factor (GEF) that transduces signals from chemoattractant receptors (e.g., CXCR4, CCR7), TCR, integrins, and growth factor receptors to the actin cytoskeleton. Upon interaction with ELMO1, DOCK2 catalyzes GTP loading on Rac1 and Rac2, which then activate downstream effectors including PAK, LIMK, cofilin, and the Arp2/3 complex, culminating in actin polymerization and regulation of cell migration, adhesion, and immune synapse formation.
In the context of LoVo colorectal adenocarcinoma, DOCK2-driven Rac signaling is thought to promote invasive and migratory behaviors. The DOCK2 Knockout LoVo Polyclonal Cells thus enable dissection of DOCK2’s role in metastasis-associated processes such as transendothelial migration, matrix degradation, and chemotaxis. This model also supports investigation of potential immunomodulatory functions of DOCK2 within tumor cells, linking cytoskeletal dynamics to cancer?Cimmune interactions.
These polyclonal knockout cells are suitable for a range of assays, including migration/invasion tests, F-actin staining, Rac activation assays, co-immunoprecipitation of DOCK2 complexes, and immunoblotting for downstream targets like phospho-cofilin or PAK1. They can be employed to screen inhibitors of the DOCK2?CRac signaling axis or to model DOCK2 deficiency in colorectal cancer research. For additional information, contact Ascent Research.
