The DYNLT3 Knockout HGC-27 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population in which the DYNLT3 gene has been disrupted. This product provides a heterogeneous pool of gene-edited HGC-27 cells, enabling functional studies of DYNLT3 loss without clonal selection. The polyclonal format preserves genetic diversity and reduces clonal artifacts, making it suitable for pooled loss-of-function analyses in gastric cancer research.
HGC-27 is an undifferentiated adherent epithelial cell line derived from a lymph node metastasis of a human gastric carcinoma. It is widely employed as a model system for gastric adenocarcinoma, including studies on tumorigenesis, invasion, and metastasis. The cells maintain key features of metastatic gastric cancer, offering a relevant background for investigating the molecular drivers of tumor progression and for evaluating therapeutic targets.
DYNLT3 encodes a subunit of the cytoplasmic dynein motor complex, which mediates minus-end-directed transport along microtubules. It is essential for retrograde trafficking of signaling endosomes, mitotic spindle assembly, cell migration, and signal transduction. DYNLT3 interacts directly with dynein intermediate chains (DYNC1I1/2), DYNLT1, and cargo adaptors such as BICD2 and HOOK3. It also binds to Fyn kinase, TrkA/B receptors, and integrins, linking dynein motor activity to downstream effectors including mitotic checkpoint proteins and Wnt pathway components. These interactions place DYNLT3 at the convergence of transport and signaling pathways critical for tumor cell behavior.
Disruption of DYNLT3 in HGC-27 cells impairs cytoplasmic dynein function, leading to defective retrograde transport of signaling endosomes and compromised mitotic spindle assembly. This knockout model is expected to exhibit altered cell proliferation, migration, and invasion, thereby providing a platform to dissect dynein-dependent mechanisms in gastric cancer metastasis. By mimicking loss-of-function conditions, it allows researchers to evaluate the contribution of DYNLT3 to integrin-mediated adhesion, Wnt signaling, and mitotic regulation in a gastric carcinoma context, and to identify vulnerabilities that could be exploited therapeutically.
This polyclonal knockout population is suitable for diverse applications, including western blotting and immunofluorescence to confirm DYNLT3 depletion and dynein localization, wound healing and Transwell invasion assays to assess migratory and invasive capacity, flow cytometry for cell cycle analysis, and live-cell imaging to track endosome transport. Co-immunoprecipitation and RNA-seq can further characterize altered protein interactions and transcriptomic responses. These cells are also valuable for drug target validation and mitotic regulation studies in gastric cancer. For additional information, please contact Ascent Research.
