The DOCK2 Knockout T-47D Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population derived from the T-47D human breast cancer cell line. This product provides a loss-of-function model in which the DOCK2 gene has been disrupted across a heterogeneous population of cells, enabling researchers to investigate the functional consequences of DOCK2 deficiency without clonal isolation. The polyclonal format preserves cellular diversity while eliminating wild-type gene expression, making it well-suited for pooled functional assays and phenotypic screening in a carcinoma-relevant background.
T-47D cells are an adherent epithelial cell line isolated from the pleural effusion of a ductal breast carcinoma. They display an estrogen receptor (ER)-positive, progesterone receptor (PR)-positive, and HER2-negative expression profile, categorizing them as a luminal A breast cancer model. These hormonally responsive cells are widely employed to study ER signaling, endocrine therapy resistance, and hormone-dependent tumor progression. Their derivation from a metastatic site further underscores the relevance of T-47D cells for dissecting molecular determinants of cancer cell dissemination.
DOCK2 encodes a Rac-specific guanine nucleotide exchange factor (GEF) that transduces signals from chemokine receptors??including CXCR4 and CCR7??and phosphoinositide 3-kinase (PI3K) to the actin cytoskeleton. Upon activation, DOCK2 forms a complex with the adapter proteins ELMO1 or ELMO2, facilitating nucleotide exchange on Rac1 and promoting its GTP-loaded state. Downstream, active Rac1 recruits effectors such as PAK1 and the WAVE regulatory complex, which in turn stimulates Arp2/3-mediated actin polymerization. This cascade drives lamellipodium formation, membrane protrusion, and cell migration. Additionally, DOCK2-interacting partners like Vav1 and talin reinforce adhesion dynamics and cytoskeletal linkage, placing DOCK2 at the nexus of motility and immune cell activation pathways.
In the T-47D context, DOCK2 knockout allows dissection of Rac-dependent migration and invasion programs that may fuel breast cancer metastasis. Because T-47D cells retain estrogen responsiveness, the model is especially pertinent for examining how hormonal cues intersect with cytoskeletal regulation. Disruption of DOCK2 is predicted to impair chemokine-directed migration and actin reorganization, thereby diminishing the invasive capacity of these carcinoma cells. This knockout product therefore offers a powerful tool to deconvolute the DOCK2-Rac1-PAK1-LIMK-cofilin signaling axis in a therapeutically relevant luminal A breast cancer background.
Researchers can leverage these polyclonal knockout cells in an array of functional and biochemical assays. Transwell migration and wound-healing assays quantify cell motility defects; Matrigel invasion assays assess metastatic potential; actin cytoskeleton visualization via phalloidin immunofluorescence reveals reorganization deficits; and G-LISA specifically measures Rac1 GTP loading. Flow cytometric detection of adhesion markers and RNA-seq transcriptomic analysis provide complementary readouts of pathway perturbation. This model also supports drug target validation and studies of immune cell function if co-cultured with relevant lymphocytes. For further information, please contact Ascent Research.
