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Cat. No. ARG39611

DOCK7 Knockout HGC-27 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Stomach

  • Disease:

    Carcinoma

The DOCK7 Knockout HGC-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human metastatic gastric adenocarcinoma cell line HGC-27, featuring targeted disruption of the DOCK7 gene. DOCK7 is a Rac1/Cdc42 guanine nucleotide exchange factor that regulates actin cytoskeletal remodeling, lamellipodia formation, and cell migration via ELMO-DOCK complex formation and downstream PAK-WAVE-Arp2/3 signaling. This knockout model enables investigation of DOCK7-dependent migration and invasion mechanisms in gastric cancer, as well as dissection of Rac1 and Cdc42 pathways. Typical applications include wound healing assays, transwell invasion assays, and drug screening for metastasis inhibitors, with direct relevance to tumor biology and neurodevelopmental disorder research.

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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

    DOCK7

    Gene Identifier

    NCBI Gene ID 85440

    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 DOCK7 Knockout HGC-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HGC-27 gastric carcinoma epithelial cell line, with targeted disruption of the DOCK7 gene. The polyclonal format provides a heterogeneous pool of edited cells, enabling loss-of-function studies while avoiding clonal artifacts associated with single-cell-derived lines.

The parental HGC-27 cell line was established from a metastatic lymph node of an undifferentiated gastric carcinoma patient. As an epithelial model of metastatic gastric adenocarcinoma, HGC-27 cells recapitulate aggressive cancer features, including robust migration and invasion, and are widely used to study tumor progression and epithelial-mesenchymal transition.

DOCK7 encodes a guanine nucleotide exchange factor that activates Rac1 and Cdc42 by GDP/GTP exchange. It interacts with ELMO1 and ELMO2 to form an ELMO-DOCK complex, recruited to the membrane by upstream growth factor receptors and integrin signals via PI3K and PIP3. Activated Rac1 and Cdc42 stimulate PAK, the WAVE complex, and Arp2/3, driving actin polymerization, lamellipodia formation, and cell migration; LIMK and cofilin further remodel the actin cytoskeleton. DOCK7 also governs neurite outgrowth and axon guidance, and mutations cause early infantile epileptic encephalopathy.

In the HGC-27 gastric cancer context, DOCK7-dependent Rac1/Cdc42 signaling is expected to be critical for the migratory and invasive properties underlying metastasis. Disrupting DOCK7 allows dissection of its contribution to gastric adenocarcinoma cell motility and Rac1/Cdc42-dependent processes in vitro. This polyclonal knockout population serves as a physiologically relevant tool to study how DOCK7 loss impacts actin dynamics, lamellipodial protrusion, and chemotaxis in metastatic gastric epithelial cells, and to investigate crosstalk with other oncogenic pathways.

Applications include Rac1 and Cdc42 activation assays, wound healing, transwell migration/invasion assays, immunofluorescence for F-actin, and western blot for phospho-PAK. Co-immunoprecipitation can assess ELMO-DOCK complex integrity. The model is valuable for drug screening against metastasis and can be adapted for neurodevelopmental disorder research. For further details, please contact Ascent Research.

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