The HAVCR1 Knockout NCI-H1299 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human non-small cell lung cancer (NSCLC) cell line NCI-H1299. This product features targeted gene disruption of HAVCR1, the gene encoding T cell immunoglobulin and mucin domain-containing protein 1 (TIM-1), achieved through CRISPR/Cas9-mediated genome editing. The resulting polyclonal pool contains a heterogeneous mixture of edited alleles, providing a versatile loss-of-function model for studying TIM-1 biology without the need for clonal isolation. This format enables researchers to rapidly assess HAVCR1-dependent phenotypes in a lung adenocarcinoma background.
NCI-H1299 is a widely utilized human NSCLC cell line originally established from a lymph node metastasis of a lung adenocarcinoma. These cells are characterized by a p53-null status and wild-type KRAS, making them a valuable model for studying NSCLC biology, including tumor progression, metastatic behavior, and therapeutic responses. As an adherent epithelial line, NCI-H1299 exhibits robust growth in vitro and has been extensively employed to investigate signaling pathways and drug sensitivities relevant to lung adenocarcinoma.
HAVCR1 (TIM-1) functions as a type I transmembrane receptor that recognizes phosphatidylserine on apoptotic cells and serves as a cellular entry factor for several viruses, including hepatitis A virus and Ebola virus. Upon ligand engagement, TIM-1 associates with Src family kinases such as FYN and LCK and the p85 regulatory subunit of PI3K (PIK3R1), leading to activation of the PI3K/AKT signaling cascade. This pathway subsequently stimulates downstream transcription factors including NF-??B and AP-1, which promote the expression of cytokines like IL-4 and IL-13. Additionally, TIM-1 signaling is regulated by T cell receptor activation, pro-inflammatory cytokines (TNF-??, IL-1??), and oxidative stress, and it plays a role in immune tolerance, T-cell survival, and apoptotic cell clearance.
In the context of NCI-H1299 lung cancer cells, HAVCR1 disruption may significantly impact pathways governing tumor immune evasion and apoptosis. TIM-1-mediated recognition of phosphatidylserine on dying cells can suppress inflammatory responses and facilitate immune tolerance, processes that are often co-opted by tumors. Knockout of HAVCR1 in this p53-deficient and KRAS wild-type background provides a system to dissect the contributions of TIM-1 to phagocytic signaling, cell survival, and the modulation of the tumor microenvironment. This model is particularly suited to exploring how TIM-1 influences NSCLC aggressiveness and response to therapeutic interventions.
The HAVCR1 Knockout NCI-H1299 Polyclonal Cells are designed for a broad range of research applications, including investigation of HAVCR1 in NSCLC tumorigenesis and metastasis, dissection of TIM-1-mediated signal transduction in cancer cells, and evaluation of HAVCR1 as a potential therapeutic target. Researchers can employ this model in assays such as Western blotting, RT-qPCR, immunofluorescence, flow cytometry, apoptosis and proliferation assays, migration and invasion studies, cytokine ELISA, phospho-protein analysis, and RNA-seq. Furthermore, it is suitable for drug sensitivity screening and viral entry studies, facilitating the identification of compounds that modulate TIM-1 signaling. For further information or to discuss custom modifications, please contact Ascent Research.
