The HAVCR1 Knockout NCI-H1703 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of human lung squamous carcinoma cells carrying targeted disruption of the HAVCR1 (TIM-1) gene. This heterogeneous pool of NCI-H1703 derivatives harbors diverse loss-of-function mutations, enabling pooled functional studies without clonal selection bias. The product is designed for investigating TIM-1-mediated phosphatidylserine recognition, viral entry, immune costimulation, and biomarker shedding within a non-small cell lung cancer (NSCLC) model.
The parental NCI-H1703 line was established from pleural effusion of a 54-year-old male smoker and is widely used to model lung squamous cell carcinoma. These epithelial cells exhibit aberrant growth signaling and inflammatory pathway activation characteristic of advanced NSCLC, providing a clinically relevant platform for studying tumor progression, metastasis, and therapeutic resistance. The host background is particularly suitable for dissecting how tumor-intrinsic HAVCR1 influences apoptotic cell clearance and immune evasion.
HAVCR1 encodes TIM-1, a transmembrane receptor for phosphatidylserine on apoptotic cells and for TIM-4 on immune cells. Ligand binding triggers PI3K/AKT and ERK/MAPK signaling via interactions with PIK3R1 and GRB2. Regulated shedding of TIM-1 produces soluble KIM-1, a kidney injury biomarker. In T cells, TIM-1 costimulation recruits LCK, activating NF-??B and STAT3, which promotes IL-4 production and regulates Bcl-2 family members. Thus, HAVCR1 links extracellular phosphatidylserine sensing to pathways controlling phagocytosis, cell survival, and cytokine output.
Knockout of HAVCR1 in the NCI-H1703 squamous carcinoma background permits investigation of tumor-cell-autonomous functions of TIM-1 in efferocytosis, signal transduction, and microenvironmental interactions. Impaired phosphatidylserine-dependent clearance may alter inflammatory responses and immune surveillance. Additionally, as a Hepatitis A virus receptor, TIM-1 removal provides a tool for studying viral entry mechanisms in a lung cancer model relevant to oncolytic virotherapy. The polyclonal format avoids clonal artifacts, yielding a more robust population for functional assays.
Applications include Western blotting and flow cytometry for confirming TIM-1 protein loss, phagocytosis assays for apoptotic cell uptake, viral entry studies, and RT-qPCR for transcriptional analyses. The knockout cells are suitable for KIM-1 ELISA, apoptosis assays, and cytokine profiling to map downstream inflammatory events. They also enable immune checkpoint and costimulation studies, and validation of drug delivery strategies targeting TIM-1. This product supports research in oncology, immunology, virology, and biomarker science. For further details, contact Ascent Research.
