The CD274 Knockout HGC-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from HGC-27 human gastric adenocarcinoma cells, with targeted disruption of the CD274 gene. This polyclonal model yields a heterogeneous pool of cells bearing loss-of-function mutations, effectively eliminating PD-L1 expression while preserving biological variability. Rigorous quality control ensures consistent viability, sterility, and gene disruption, providing a reproducible platform for PD-L1 functional studies without the biases of monoclonal selection.
The HGC-27 cell line originates from a lymph node metastasis of a human gastric adenocarcinoma. It serves as a metastatic gastric cancer model characterized by invasive behavior and oncogenic pathway activation, widely applied in tumor biology research. Its metastatic derivation makes HGC-27 particularly suited for investigating immune checkpoint mechanisms, as PD-L1-mediated immune evasion is critical in metastatic niches.
CD274 encodes PD-L1, an immune checkpoint ligand that binds the PD-1 receptor on T cells, inhibiting T-cell proliferation, cytokine production, and cytotoxicity. In HGC-27 cells, PD-L1 expression is induced by interferon-?? (IFNG) via the IFNGR-JAK-STAT axis, primarily through STAT1 and STAT3, and by oncogenic factors including MYC, HIF1A, and NF-kB. PD-L1 engagement of PD-1 recruits SHP-2 phosphatase, which dephosphorylates key signaling molecules, thereby suppressing TCR-driven PI3K-AKT-mTOR and RAS-MAPK cascades and promoting T-cell exhaustion. PD-L1 surface stability is modulated by interactions with CD80, CMTM6, and CMTM4. Thus, CD274 integrates inflammatory and oncogenic signals to mediate immune evasion.
In HGC-27 gastric cancer cells, CD274 knockout removes a central mediator of immune suppression, enabling dissection of PD-L1-dependent tumor-immune interactions. HGC-27 cells upregulate PD-L1 under inflammatory or oncogenic stress, contributing to T-cell inhibition. This polyclonal knockout model allows researchers to assess how loss of PD-L1 alters signaling through pathways such as JAK-STAT, PI3K-AKT, and MAPK, and to evaluate enhanced T-cell-mediated killing. The model is valuable for studying PD-L1??s role in metastatic gastric cancer and for developing combination therapies targeting immune checkpoints.
This product is suited for functional assays including co-culture with T cells to measure restored cytotoxicity and cytokine release via ELISA, as well as migration and invasion studies. Standard characterization employs western blotting, RT-qPCR, and flow cytometry to confirm PD-L1 loss. The polyclonal format supports drug screening for PD-L1 inhibitors and investigation of resistance mechanisms, avoiding clonal artifacts. For additional details or custom requests, please contact Ascent Research.
