HAVCR1 Knockout KYSE-150 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the KYSE-150 human esophageal squamous cell carcinoma line, featuring targeted disruption of the HAVCR1 gene. This product provides a versatile loss-of-function model for investigating TIM-1 biology in an epithelial tumor context. The polyclonal format reflects a heterogeneous pool of edited cells, generated without single-cell cloning, and is suitable for population-level functional assays where genetic diversity can recapitulate more physiologically relevant responses than monoclonal lines. The gene disruption is achieved through CRISPR/Cas9-mediated genomic editing, resulting in a knockout model that enables dissection of HAVCR1-dependent signaling and cellular processes.
KYSE-150 is a well-characterized human esophageal squamous cell carcinoma (ESCC) cell line originally established from a poorly differentiated tumor resected from a Japanese female patient. These adherent epithelial cells exhibit hallmark features of ESCC, including TP53 mutations and chromosomal instability, and are widely employed in esophageal cancer research for studies of oncogenic signaling, drug resistance, and metastatic behavior. The cell line??s stable growth characteristics and the availability of extensive molecular profiling data make it an ideal host for gene-editing experiments. By engineering HAVCR1 knockout in KYSE-150, researchers gain a tool to explore gene function in a cancer-relevant background that retains many native oncogenic pathways.
HAVCR1 encodes T-cell immunoglobulin and mucin domain 1 (TIM-1), a type I transmembrane glycoprotein that functions as a receptor for phosphatidylserine (PtdSer) on apoptotic cells and for the hepatitis A virus capsid. Ligand engagement triggers TIM-1 phosphorylation and subsequent recruitment of the Src-family kinase LCK and the Syk-family kinase ZAP70, initiating intracellular cascades that include PI3K/AKT and NF-??B signaling. These pathways converge on downstream targets such as AKT1 and NF-??B p65, regulating gene expression programs that promote T-cell activation, cytokine production, and cell survival. In non-immune cells, TIM-1 can modulate phagocytosis and apoptosis. Upstream, TIM-1 expression is regulated by cytokines like IL-4 and TGF-??, and its activity is influenced by interactions with co-receptors such as TIM-4 and adaptor proteins including PIK3R1 and ITK. This network positions TIM-1 at the intersection of immune regulation, viral entry, and clearance of apoptotic debris.
Although HAVCR1 is predominantly studied in immune cells, its expression in esophageal epithelium and ESCC tumors suggests non-immune functions that may influence tumor biology. In KYSE-150 cells, HAVCR1 knockout likely disrupts PtdSer-mediated signaling, potentially attenuating PI3K/AKT-driven survival and NF-??B-dependent inflammatory gene expression. This can alter tumor cell responses to apoptotic stimuli, phagocytic clearance, or interactions with the tumor microenvironment. By eliminating TIM-1 from the epithelial compartment, the model allows researchers to disentangle tumor-intrinsic HAVCR1 effects from its immunomodulatory roles, providing a clean system to investigate how TIM-1 signaling affects ESCC cell proliferation, migration, and resistance to therapy.
This product is suitable for a broad range of research applications, including the dissection of TIM-1-mediated signaling in esophageal cancer, identification of phosphorylation-dependent interactors via co-immunoprecipitation, and functional validation using phagocytosis assays or reporter gene assays. It can be employed in co-culture systems to evaluate tumor?Cimmune cell crosstalk, in high-throughput screens for modulators of TIM-1 pathways, and in studies of hepatitis A virus entry and replication. Representative assays such as flow cytometry, Western blotting, RT-qPCR, migration and invasion assays, and cytokine ELISA are fully compatible with these polyclonal knockout cells. For additional details or technical support, please contact Ascent Research.
