This product is a CRISPR/Cas9-edited polyclonal knockout cell population derived from TE1 human esophageal squamous cell carcinoma cells, with targeted disruption of the DOCK2 gene. The polyclonal nature provides a heterogeneous loss-of-function model that recapitulates genetic variability, enabling robust functional studies without clonal bias. DOCK2 encodes a critical Rac-specific guanine nucleotide exchange factor (GEF) essential for actin cytoskeleton reorganization, cell migration, and immune cell activation. This knockout resource is particularly suited for investigating DOCK2-mediated signaling in a non-hematopoietic epithelial context.
The host cell line, TE1, is a well-characterized human esophageal squamous cell carcinoma line derived from a well-differentiated tumor of a 58-year-old Japanese male. It is widely used in cancer research for its adherent epithelial morphology and relevance to esophageal carcinogenesis. TE1 cells express squamous differentiation markers and have been extensively employed to study migration, invasion, and therapy responses. Introducing DOCK2 knockout into this background provides a unique platform to dissect tumor-intrinsic functions of DOCK2.
DOCK2 functions as a Rac-specific GEF, catalyzing the exchange of GDP for GTP on Rac1 and Rac2. Its activation is primarily induced by PI3K-generated PIP3 and ELMO1 binding, typically downstream of chemokine receptors (CCR7, CXCR4). Active Rac-GTP then engages downstream effectors including PAK1, the WAVE regulatory complex, and Arp2/3 to drive actin polymerization. Additionally, Rac-mediated activation of JNK and p38 MAPK connects DOCK2 to broader transcriptional control and stress responses. Thus, the DOCK2/ELMO1/Rac module is central to coordinating receptor-triggered cytoskeletal rearrangement and cell motility.
While DOCK2 is predominantly known for hematopoietic roles, its expression and functions in epithelial cancers like ESCC are increasingly recognized. Ablating DOCK2 in TE1 cells allows dissection of its contribution to cancer cell migration, invasion, and cytoskeletal dynamics independent of immune cells. This model may reveal DOCK2-dependent networks driving tumor progression and offer therapeutic insights. The polyclonal population better reflects tumor heterogeneity than clonal lines.
The DOCK2 Knockout TE1 Polyclonal Cells are suited for Transwell migration/invasion assays, actin immunofluorescence, immune cell co-culture, phospho-signaling analysis (PAK, JNK), RNA-seq, and drug screening targeting DOCK2 pathways. For further information, contact Ascent Research.
