This CRISPR/Cas9-edited polyclonal knockout cell population targets the EFCAB14 gene in the human gastric adenocarcinoma cell line HGC-27, offering a physiologically relevant loss-of-function model for investigating calcium-mediated signaling in gastric cancer. The polyclonal composition maintains genetic heterogeneity while ensuring robust gene disruption, thereby avoiding clonal artifacts and reflecting population-level cellular responses that are more representative of tumor heterogeneity.
The HGC-27 cell line was originally established from a metastatic lymph node of a gastric cancer patient and exhibits epithelial morphology characteristic of adenocarcinoma. As a widely employed model in gastric cancer research, HGC-27 cells retain key oncogenic signaling networks and are particularly suited for studies on tumor cell proliferation, invasion, and metastatic progression. Their derivation from a secondary site enhances their utility for dissecting molecular mechanisms that drive late-stage disease and resistance to therapy.
EFCAB14 encodes an EF-hand calcium-binding protein predicted to participate in calcium-mediated signal transduction. It likely senses intracellular calcium fluctuations triggered by upstream regulators such as calcium-mobilizing hormones and growth factors. Upon calcium binding, EFCAB14 may modulate downstream calcium-dependent signaling cascades involving calmodulin, CaMKII, and calcineurin. These effectors control critical cellular processes including proliferation, migration, and apoptosis. Voltage-gated calcium channels also shape the calcium signals that may influence EFCAB14 activity, integrating it into broader calcium homeostasis networks.
In the context of HGC-27 gastric cancer cells, disruption of EFCAB14 can perturb calcium-dependent pathways that are often dysregulated during oncogenesis. This polyclonal knockout model enables researchers to dissect the specific contribution of EFCAB14 to malignant phenotypes such as aberrant growth signaling and enhanced metastatic capacity. By uncovering the protein’s role in calcium-dependent regulation, this system helps identify potential vulnerabilities in calcium signaling nodes that could be targeted therapeutically in gastric adenocarcinoma.
This product is suitable for a wide array of functional assays, including western blotting and RT-qPCR for knockout validation, and Fura-2-based ratiometric calcium flux measurements to assess alterations in calcium dynamics. Cell proliferation can be evaluated using MTT or BrdU incorporation, while transwell assays enable quantitation of migration and invasion. Apoptosis can be monitored via Annexin V/PI staining, and immunofluorescence provides spatial information on protein localization changes. Furthermore, RNA-sequencing can uncover transcriptomic adaptations to EFCAB14 loss. Together, these approaches facilitate detailed phenotypic characterization and screening of calcium pathway modulators as potential therapeutic leads for gastric cancer. For additional technical details or product inquiries, please contact Ascent Research.
