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Cat. No. ARG38902

DLG5 Knockout HGC-27 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Stomach

  • Disease:

    Carcinoma

The DLG5 Knockout HGC-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HGC-27 human gastric carcinoma cell line. This model disrupts DLG5, a scaffold protein essential for tight junction and adherens junction assembly, enabling loss-of-function studies in an epithelial gastric cancer context. DLG5 interacts with ZO-1, occludin, and E-cadherin to maintain barrier integrity, and its loss is implicated in inflammatory bowel disease and cancer progression. These cells are ideal for TEER, permeability, and migration assays, supporting research into epithelial polarity, Hippo signaling, and therapeutic screening.

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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

    DLG5

    Gene Identifier

    NCBI Gene ID 9231

    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 DLG5 Knockout HGC-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population that enables functional studies of the DLG5 gene in a gastric carcinoma context. These cells were generated by disrupting DLG5 in the HGC-27 human gastric cancer cell line, yielding a heterogeneous pool of gene-edited variants ideal for studying loss-of-function phenotypes without clonal selection biases.

The HGC-27 cell line originates from a signet ring cell gastric carcinoma derived from a lymph node metastasis, maintaining characteristics of epithelial cells from the gastric mucosa. This model retains key features of gastric cancer, including alterations in cell polarity, adhesion, and invasive potential, making it a suitable host for investigating genes involved in epithelial integrity and tumor suppression.

At the molecular level, DLG5 acts as a scaffold that orchestrates tight junction assembly by tethering ZO-1, occludin, and claudins to F-actin, while also stabilizing adherens junctions through interactions with E-cadherin, ??-catenin, and ??-catenin. It functions downstream of epithelial polarity cues and Wnt/PCP components, and its loss leads to defective junctional complex formation, increased paracellular permeability, and potential derepression of YAP/TAZ transcriptional activity. DLG5 also interfaces with the LKB1?CAMPK energy-sensing pathway, implicating it in cellular responses to metabolic stress.

Given the origin of HGC-27 from a metastatic gastric carcinoma, DLG5 knockout in this background allows dissection of how polarity loss contributes to invasive behavior. Studies have linked DLG5 to inflammatory bowel disease and colorectal cancer, and its disruption may promote oncogenic signaling through Hippo pathway dysregulation. The polyclonal nature enables evaluation of heterogeneous responses, recapitulating the diversity seen in tumor cell populations.

Typical applications include monitoring tight junction integrity via TEER and permeability assays, analyzing protein expression and localization by Western blotting and immunofluorescence, and assessing cell migration and invasion in 2D and 3D culture systems. Co-immunoprecipitation can validate protein interactions, while RT-qPCR and RNA-seq enable transcriptional profiling. The polyclonal population provides a robust system for drug screening campaigns aimed at restoring epithelial barrier function or inhibiting metastasis. For technical inquiries, please contact Ascent Research.

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