The DOCK2 Knockout MCF-7 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the MCF-7 human breast adenocarcinoma cell line, featuring targeted disruption of the DOCK2 gene. This polyclonal cell pool provides a robust loss-of-function model to interrogate DOCK2-dependent processes without clonal biases, making it ideal for population-level analyses of signaling and migration.
The MCF-7 host cell line is a widely utilized luminal A breast cancer model, characterized by estrogen receptor (ER) positivity, progesterone receptor (PR) expression, and lack of HER2 amplification. These epithelial cells retain hormone-responsive growth and invasive potential, serving as a relevant system for studying endocrine-driven tumorigenesis, cell motility, and metastatic progression.
DOCK2 functions as a dedicated guanine nucleotide exchange factor (GEF) for the small GTPase Rac, facilitating GDP/GTP exchange to activate Rac signaling cascades. Upstream activation is mediated by chemokine receptors (e.g., CXCR4, CCR7), T-cell and B-cell receptors, and growth factor receptors, leading to recruitment of ELMO1 and CRK adaptor proteins. Active DOCK2?CELMO complexes promote Rac-GTP loading, which stimulates downstream effectors including PAK1, the WAVE regulatory complex, and the Arp2/3 complex. This signaling axis drives actin polymerization, lamellipodia formation, and cellular migration. While essential for immune cell trafficking and activation, DOCK2 also contributes to cancer cell invasion and metastasis.
In the context of MCF-7 cells, DOCK2 disruption offers a unique tool to dissect Rac-dependent migration independent of hematopoietic lineage factors. Although DOCK2 is best known for its immune roles, its expression in breast cancer cells has been linked to enhanced motility and metastatic behavior. The knockout model enables investigation of how loss of DOCK2-mediated Rac activation affects MCF-7 cell spreading, migration, and invasion, potentially revealing crosstalk between hormone receptor signaling and cytoskeletal dynamics.
Applications for this knockout polyclonal population include cell migration and invasion assays (wound-healing or Boyden chamber), immunofluorescence imaging of actin cytoskeleton reorganization, and biochemical assessment of Rac1 activation via PAK1 pull-down or western blotting. The cells are amenable to co-immunoprecipitation studies of DOCK2?CELMO interactions and flow cytometric evaluation of receptor expression and signaling. These tools support investigations into GTPase signaling networks, cancer cell motility, and evaluation of small-molecule inhibitors targeting the DOCK2?CRac axis. For further information on applications or custom services, please contact Ascent Research.
