The CD274 Knockout TE1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated from the human TE-1 esophageal squamous cell carcinoma line. This product comprises a heterogeneous pool of cells with targeted disruption of CD274, offering a versatile loss-of-function model to study PD-L1 biology in a cancer-relevant context while avoiding clonal selection artifacts.
The TE-1 cell line is a well-differentiated human esophageal squamous cell carcinoma (ESCC) model, originally established from a primary tumor. TE-1 cells display epithelial morphology and are widely utilized in esophageal cancer research to investigate tumorigenesis, drug resistance mechanisms, and signaling networks. As an ESCC-derived line, it provides a clinically relevant platform for examining immune checkpoint pathways and their crosstalk with oncogenic processes.
CD274 encodes programmed death-ligand 1 (PD-L1), a transmembrane immune checkpoint molecule that interacts with PD-1 (PDCD1) on activated T cells. This engagement recruits the tyrosine phosphatase SHP2 to dephosphorylate proximal TCR signaling components, including ZAP70 and LCK, thereby dampening PI3K/AKT activation and attenuating T cell proliferation, cytokine production, and cytotoxicity. In tumor cells, PD-L1 can also bind CD80 and propagate intrinsic signals through AKT/mTOR and MAPK/ERK pathways, promoting survival and proliferation. CD274 expression is induced by interferon-gamma (IFNG) via STAT1 and IRF1 transcription factors, and is further modulated by NFKB1, EGF, and TNF, linking inflammatory stimuli to both immune evasion and tumor cell-autonomous growth.
In esophageal squamous cell carcinoma, PD-L1 overexpression is frequently observed and linked to immune escape, aggressive behavior, and resistance to therapy. The TE-1 CD274 knockout model allows precise dissection of PD-L1??s dual roles??as an immune checkpoint ligand that shapes T cell responses within the tumor microenvironment, and as a mediator of tumor-intrinsic signals that sustain proliferation and survival. By comparing parental and CD274-disrupted TE-1 cells, investigators can delineate PD-L1-dependent regulation of AKT/mTOR and MAPK/ERK cascades, evaluate alterations in cytokine profiles, and measure differential sensitivity to immune cell-mediated killing. This system is especially valuable for exploring mechanisms of primary and acquired resistance to PD-1/PD-L1 blockade in ESCC.
Representative applications include T cell co-culture experiments to assess T cell proliferation and effector cytokine release (e.g., IFN-??, IL-2) by flow cytometry or ELISA, as well as PD-1 binding assays to validate ligand-receptor interactions. Tumor-intrinsic effects can be interrogated using apoptosis assays, migration and invasion assays, and signaling analysis via western blotting and phospho-specific antibodies. RT-qPCR and flow cytometry enable quantification of CD274 knockout efficiency and surface PD-L1 levels. This product is suited for immunotherapy target validation, study of immune checkpoint biology, investigation of drug resistance mechanisms, and biomarker discovery in esophageal cancer and beyond. For further information, please contact Ascent Research.
