The PVR Knockout NCI-H292 Cell Line is a CRISPR/Cas9-edited knockout cell line featuring targeted disruption of the PVR gene in the NCI-H292 host cell background. This loss-of-function model eliminates surface expression of the CD155 protein, providing a defined system to dissect PVR-mediated adhesion, immune signaling, and viral entry mechanisms without altering the fundamental epithelial characteristics of the parental line.
NCI-H292 is a human mucoepidermoid lung carcinoma epithelial cell line originally derived from a lymph node metastasis. It exhibits an adherent morphology and robust expression of mucins and cytokeratins, making it a widely validated model for respiratory disease research. The cells retain key signaling networks found in pulmonary epithelia, serving as a reproducible platform for studying lung cancer biology, host?Cpathogen interactions, and immune checkpoint regulation.
PVR (CD155) is a transmembrane adhesion molecule of the nectin/nectin-like family that mediates cell?Ccell adhesion and functions as a ligand for the immune receptors TIGIT, CD226 (DNAM-1), and CD96. PVR expression is transcriptionally regulated by NF-??B and p53, and can be induced by TNF-?? and ATM/ATR-dependent stress signaling. PVR engagement of TIGIT delivers inhibitory signals in T and natural killer (NK) cells, whereas binding to CD226 promotes NK cell activation and cytotoxicity; CD96 further modulates NK cell adhesion. In addition, PVR serves as the primary entry receptor for poliovirus, interacting directly with the viral capsid. Downstream of PVR, the SHIP-1 phosphatase contributes to TIGIT-driven inhibitory signaling, while poliovirus replication is dependent on PVR-mediated entry.
In the NCI-H292 background, PVR knockout disrupts both physiological adhesion and pathological interactions. The loss of CD155 abrogates poliovirus entry, making this cell line a powerful tool for viral infection studies in a lung epithelial context. Simultaneously, elimination of the TIGIT ligand removes an inhibitory ??don??t kill me?? signal, which can shift immune responses in co-culture assays with T cells or NK cells. Since NCI-H292 cells express p53 and NF-??B, this model also enables the interrogation of DNA damage-responsive or inflammatory upregulation of PVR and its consequences for immune evasion.
This knockout cell line is suited for a broad range of experimental applications, including poliovirus entry and replication assays, TIGIT/CD155 immune checkpoint blockade studies, and co-culture cytotoxicity assays with NK cells or tumor-infiltrating lymphocytes to evaluate CD226- and CD96-mediated activation. Additional typical uses encompass flow cytometry and immunofluorescence for CD155 surface expression validation, Western blotting, RT-qPCR, TIGIT binding assays, and cell adhesion assays. Researchers leveraging this tool can dissect the dual roles of PVR in viral pathogenesis and cancer immune escape within a clinically relevant lung cancer model. For further information, please contact Ascent Research.
