The DOCK2 Knockout 786-O Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed for targeted disruption of the DOCK2 gene in the human 786-O renal cell carcinoma line. This product provides a heterogeneous pool of edited cells, generated via sequence-specific Cas9-mediated cleavage, resulting in a mixed population with DOCK2 gene disruption. It serves as a versatile loss-of-function model for investigating DOCK2-dependent processes without the need for clonal isolation. The polyclonal format retains the complexity of the host cell background, enabling robust functional genomics and pharmacological studies.
Derived from a primary clear cell renal cell carcinoma of a 58-year-old male, the 786-O cell line is an established epithelial model originating from the proximal tubule. It exhibits adherent growth and maintains key characteristics of renal cell carcinoma, including expression of tumor-associated markers. The 786-O line is widely used in cancer biology for studying proliferation, migration, and drug response, making it an ideal host for DOCK2 knockout to dissect signaling pathways relevant to renal tumor progression and metastasis.
DOCK2 encodes a guanine nucleotide exchange factor (GEF) that specifically activates Rac GTPases by catalyzing the exchange of GDP for GTP. This activation is critical for downstream cytoskeletal reorganization. DOCK2 functions downstream of chemokine receptors such as CXCR4, T cell receptors, and cytokines, and it interacts with ELMO1, ELMO2, VAV1, and CRK to promote activation of Rac1 and Rac2. Subsequently, active Rac triggers the PAK1 kinase, leading to WAVE2-mediated activation of the Arp2/3 complex, which drives branched actin polymerization. This DOCK2?CELMO?CRac?CPAK?CWAVE?CArp2/3 axis controls lamellipodia formation and directional cell motility.
In the 786-O renal carcinoma context, DOCK2-mediated Rac signaling is likely to influence tumor cell migration and invasion, processes essential for metastasis. The knockout of DOCK2 in this epithelial model allows researchers to directly assess its contribution to cancer cell motility and to probe interactions between tumor cells and immune components, given DOCK2’s known role in leukocyte activation. This polyclonal knockout population thus offers a physiologically relevant platform for exploring how DOCK2 loss impacts renal cancer pathophysiology and for evaluating DOCK2 as a potential therapeutic target in metastatic clear cell carcinoma.
This product is well-suited for detailed mechanistic studies, including wound healing and transwell migration assays to measure metastatic potential, Rac-GTP pull-downs to assess Rac activation, western blotting to confirm DOCK2 protein ablation, and immunofluorescence for F-actin to visualize cytoskeletal dynamics. It also enables screening for small-molecule inhibitors of Rac signaling and investigation of DOCK2-dependent tumor-immune cell cross-talk. For further details, please contact Ascent Research.
