The CD274 Knockout A2780 Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal knockout cell population targeting the CD274 gene locus within the human ovarian carcinoma A2780 cell line. This pool of edited cells provides a heterogeneous loss-of-function model for investigating the PD-L1 immune checkpoint in cancer biology. The product enables researchers to study CD274 disruption across a diverse cell population, reflecting biologically relevant variation without clonal selection. Functional interrogation of this checkpoint modulator is supported by the polyclonal format, which avoids artifacts of single-cell expansion while preserving robust target gene ablation across the culture.
The A2780 cell line was established from an untreated patient with ovarian carcinoma and serves as a widely used epithelial ovarian cancer model. These adherent cells retain histological and genomic features characteristic of high-grade serous ovarian cancer, making them suitable for tumor immunology and drug response assays. The parental A2780 background exhibits detectable PD-L1 expression, which is known to influence interactions with T cells in co-culture systems, establishing a physiologically relevant context for analyzing immune evasion mechanisms.
CD274 encodes programmed death-ligand 1 (PD-L1), a transmembrane immune checkpoint protein that binds the PD-1 receptor on T cells, leading to SHP-2 recruitment and subsequent dephosphorylation of proximal TCR signaling components such as ZAP-70. This signaling axis inhibits T cell proliferation, cytokine production, and cytolytic activity. PD-L1 expression is transcriptionally regulated by multiple upstream factors, including IFN-?? acting through JAK1/JAK2?CSTAT1/STAT3, NF-??B, HIF-1??, and MYC. In addition to PD-1, PD-L1 also interacts with CD80, further modulating immune responses. Downstream, PD-L1 engagement dampens TCR- and CD28-mediated signaling cascades, contributing to T cell exhaustion and tumor immune escape.
Within the A2780 ovarian carcinoma context, CD274 disruption allows dissection of PD-L1-dependent immune evasion pathways and characterization of tumor cell-intrinsic signaling alterations. The loss of PD-L1 in this epithelial cancer model facilitates analysis of how ovarian tumor cells modulate the tumor microenvironment and respond to immune checkpoint blockade. This knockout model is particularly relevant for exploring interferon-driven PD-L1 upregulation and its consequences on T cell function, as well as for evaluating synergistic effects with chemotherapeutic agents commonly used in ovarian cancer treatment.
Typical research applications include flow cytometry-based assessment of PD-L1 surface expression, western blot and RT-qPCR quantification of CD274 mRNA and protein levels, co-culture T cell activation assays to measure cytokine release and cytotoxicity, and anti-PD-L1 drug sensitivity testing. This product also supports migration/invasion assays, apoptosis profiling, and transcriptomic analyses via RNA-seq to uncover PD-L1-regulated gene networks. These cells are instrumental for immune checkpoint regulation studies, cancer immune evasion mechanism elucidation, combination immunotherapy evaluation, and functional modeling of ovarian cancer. For further information and technical support, contact Ascent Research.
