The DOCK2 Knockout KYSE-30 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population in which the DOCK2 gene has been disrupted in the KYSE-30 human esophageal squamous cell carcinoma (ESCC) background. This product provides a pooled population of edited cells, serving as a loss-of-function model for investigating DOCK2-dependent signaling and cellular phenotypes. It is intended for advanced biomedical research applications in cancer biology, immunology, and signal transduction without clonal isolation or characterization of single-cell-derived clones.
The host KYSE-30 cell line is a well-established human ESCC model derived from a poorly differentiated esophageal squamous cell carcinoma. These epithelial tumor cells retain characteristic features of ESCC and are widely used for studying oncogenic signaling, tumor microenvironment interactions, and therapeutic responses. The KYSE-30 background is particularly relevant for exploring the role of DOCK2 in esophageal cancer cell motility, invasion, and potential crosstalk with immune components in the tumor milieu.
DOCK2 encodes a guanine nucleotide exchange factor (GEF) that specifically activates Rac GTPases, functioning as a critical mediator of actin cytoskeleton reorganization. Signaling is initiated by upstream chemokine receptors such as CXCR4 and CCR7, as well as the T cell receptor (TCR) and Toll-like receptors. Upon activation, DOCK2 forms a complex with ELMO1 and CRK, facilitating GDP/GTP exchange on Rac1. Active Rac1 then engages downstream effectors including PAK1/2 and LIMK, which phosphorylate cofilin, leading to actin polymerization via the WAVE complex and Arp2/3 complex. This pathway is essential for directed cell migration, immunological synapse formation, and immune cell activation, and it may also influence tumor cell behavior.
In the KYSE-30 ESCC context, DOCK2 disruption provides a mechanism to dissect the gene??s contribution to tumor cell-intrinsic processes. DOCK2 is known to regulate lymphocyte migration and immune responses; however, its expression in cancer cells suggests potential roles in modulating cytoskeletal dynamics, invasion, and interactions with the tumor microenvironment. This polyclonal knockout population enables researchers to study DOCK2 loss in a homogeneous epithelial tumor background, distinguishing cancer-autonomous effects from its established immune functions. The model is thus suited for elucidating how DOCK2-mediated Rac signaling impacts ESCC progression and response to therapeutic agents targeting the actin cytoskeleton or Rac pathway.
Research applications include functional studies of DOCK2 in esophageal cancer by comparing knockout and wild-type KYSE-30 cells in transwell migration and invasion assays, Rac activation assays (e.g., G-LISA), and immunofluorescence for F-actin rearrangement. The cells can be employed in drug screening for Rac pathway inhibitors, assessed by cell viability and migration endpoints. Interaction dynamics between DOCK2 and ELMO1 may be explored via co-immunoprecipitation, while downstream signaling is monitored by western blotting for PAK and LIMK phosphorylation. Additional uses encompass RT-qPCR validation of DOCK2 ablation and flow cytometry for phenotypic characterization. For further technical details or custom inquiries, please contact Ascent Research.
