The HAVCR1 Knockout HGC-27 Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal knockout cell population targeting the HAVCR1 gene in HGC-27 human gastric carcinoma epithelial cells. This loss-of-function model enables broad investigation of HAVCR1-mediated processes without clonal selection artifacts. The polyclonal format provides a robust, mixed genetic background ideal for studying population-level effects of gene disruption.
The HGC-27 cell line was derived from a metastatic lymph node of a gastric adenocarcinoma patient and serves as a representative model of aggressive, invasive gastric cancer. These cells retain epithelial characteristics and key oncogenic signaling pathways, making them widely used in studies of metastasis, drug resistance, and tumor microenvironment interactions.
HAVCR1 (TIM-1) is a phosphatidylserine receptor that, upon ligand binding, activates the PI3K/AKT cascade to promote cell survival and migration. Its interaction with TIMD4 and the kinase FYN facilitates downstream signaling, leading to AKT phosphorylation and subsequent upregulation of anti-apoptotic BCL2L1. HAVCR1 is transcriptionally regulated by NF-??B in response to cytokines such as TNF-??, IL-1??, and IFN-??, and it further contributes to invasive capacity through MMP9 expression. The HAVCR1?CPtdSer?CPI3K?CAKT?CmTOR axis thus integrates signals from the tumor microenvironment to control apoptosis and motility.
In gastric cancer, HAVCR1 is implicated in immune evasion by mediating efferocytosis and suppressing anti-tumor immunity. Disruption of HAVCR1 in HGC-27 cells is predicted to attenuate PI3K/AKT pro-survival signaling, enhance apoptosis, and reduce metastatic potential. This knockout model therefore provides a valuable system for studying phosphatidylserine-mediated tumor immune escape and for evaluating therapeutic strategies targeting the HAVCR1 pathway.
These polyclonal knockout cells are suited for a range of functional assays, including Western blotting for HAVCR1, AKT, and phospho-AKT; apoptosis detection via Annexin V; transwell migration/invasion; efferocytosis assays; and flow cytometric analysis of phosphatidylserine binding. Gene expression changes can be assessed by RT-qPCR for BCL2L1 and MMP9. The model is also applicable to cisplatin sensitivity testing and macrophage co-culture experiments to examine immune modulation. Applications extend to tumor biology, signal transduction research, and preclinical drug validation. For further details, contact Ascent Research.
