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Cat. No. ARG39564

DOCK2 Knockout HGC-27 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Stomach

  • Disease:

    Carcinoma

The DOCK2 Knockout HGC-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the human gastric adenocarcinoma cell line HGC-27, providing a robust model for loss-of-function studies of DOCK2. DOCK2 acts as a GEF for Rac1 and Cdc42, regulating actin polymerization and cell migration downstream of chemokine receptors such as CXCR4 and integrin LFA-1. Applications include investigating gastric cancer invasion and metastasis, studying Rac1/Cdc42 signaling, and screening for inhibitors of cancer cell motility. The polyclonal format minimizes clonal artifacts, and the model is suitable for Boyden chamber assays, Western blotting, and immunofluorescence analyses.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    HGC-27

    Sex of Donor

    Unknown

    Age

    Unknown

    Derived From Site

    Metastatic; Lymph node

    Gene Name

    DOCK2

    Gene Identifier

    NCBI Gene ID 1794

    Morphology

    Epithelial-like

    Growth Mode

    Adherent

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    RPMI 1640

    Supplement(s)

    10% Fetal Bovine Serum, 1% Penicillin-Streptomycin Solution

    Temperature

    37°C

    Atmosphere

    5% CO₂

  • Quality Control

    Sterility testing

    The bacterial, yeast, and fungi are not detected in these cells by daily monitor.

    Mycoplasma testing

    Negative for mycoplasma through PCR analysis

  • Disclaimer

    Intended Use

    This product is intended for laboratory in vitro use only. lt is not intended for diagnostic, therapeutic, or clinical applications.

    Disclaimer

    Ascent Research endeavors to provide accurate and up-to-date product information. However, no warranties or representations are made regarding its completeness or reliability. References to scientific literature and patents are for informational purposes only, and the customer assumes sole responsibility for verifying their accuracy.

    By accepting this product, the customer acknowledges and agrees to assume all risks associated with its receipt, handling, storage, disposal, and use, including compliance with all applicable safety and environmental regulations and precautions. Relevant laws, regulations, and ethical guidelines must be followed in conducting any research, modifications, or derivatives derived from this product.

    This product is provided "AS IS", and except as expressly stated herein, Ascent Research disclaims all other warranties, express or implied. Under no circumstances shall Ascent Research, its affiliates, or representatives be liable for indirect, incidental, consequential, or punitive damages arising from the use of this material. While Ascent Research employs rigorous quality control measures, we shall not be held responsible for damages resulting from misidentification or misinterpretation of the provided materials.

Description

The DOCK2 Knockout HGC-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population in the HGC-27 human gastric carcinoma line, enabling loss-of-function studies of the DOCK2 gene. This polyclonal format avoids single-cell cloning, offering a robust heterogeneous model for investigating DOCK2-dependent phenotypes in cancer and immunology research.

The parental HGC-27 cell line, derived from a human gastric adenocarcinoma, serves as a relevant epithelial model for gastric cancer pathogenesis. Exhibiting adherent growth, epithelial morphology, and invasive capacity, HGC-27 retains key tumor characteristics, making it suitable for studying gene function in metastatic signaling and tumor-immune interactions.

DOCK2 encodes a guanine nucleotide exchange factor (GEF) for the Rho GTPases Rac1 and Cdc42, forming a complex with ELMO proteins to catalyze GTP loading and trigger actin reorganization. Activation occurs downstream of chemokine receptors (CXCR4, CXCR5), T cell receptor, and integrin LFA-1 via PI3K-generated PIP3, engaging PAK kinases and the WAVE complex to promote Arp2/3?mediated actin polymerization. This cascade governs cell migration, polarization, and adhesion, and its dysregulation contributes to cancer cell invasion and immune cell trafficking. Core pathway components include DOCK2, ELMO, Rac1, Cdc42, PAK1, WAVE2, and the Arp2/3 complex.

In gastric adenocarcinoma, DOCK2-driven cytoskeletal remodeling is implicated in tumor invasion and metastasis. HGC-27 cells display robust invasive behavior, and DOCK2 knockout in this polyclonal model enables quantitative evaluation of its contribution to 3D invasion and transendothelial migration. Given that peritoneal dissemination is a frequent route of gastric cancer progression, the model provides a tractable system to investigate DOCK2-dependent signaling that drives peritoneal metastasis. Moreover, co-culture with immune cells can be used to dissect the role of DOCK2 in tumor-immune cell interactions within the gastric tumor microenvironment.

Experimental applications encompass migration and invasion assays (Boyden chamber, wound healing), Rac1/Cdc42 activation assays, and immunofluorescence for actin cytoskeleton architecture. Downstream signaling can be assessed by western blotting for phosphorylated PAK and DOCK2 expression, or by RT?qPCR verification of knockout efficiency. The population is suited for drug screening campaigns targeting GEF activity and for rescue experiments to validate specificity. For further technical details and ordering information, please contact Ascent Research.

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