The HAVCR1 Knockout MCF-7 Polyclonal Cells are a CRISPR/Cas9-edited heterogeneous cell population derived from the MCF-7 human breast adenocarcinoma epithelial cell line, engineered to carry a targeted disruption of the HAVCR1 (hepatitis A virus cellular receptor 1) gene. This polyclonal knockout model enables loss-of-function investigation of TIM-1 (T cell immunoglobulin and mucin domain 1) within an estrogen and progesterone receptor-positive cellular background, providing a versatile tool for functional genomics, signal transduction, and oncology research.
The host MCF-7 cell line is a widely used model of estrogen receptor-positive breast cancer, originally isolated from a metastatic pleural effusion. These adherent epithelial cells retain characteristics of luminal breast cancer, including hormone receptor expression and sensitivity to endocrine therapies. Their well-characterized signaling networks make them suitable for dissecting gene function in hormone-responsive breast cancer biology.
HAVCR1 encodes a type I transmembrane glycoprotein that acts as a co-stimulatory molecule on T cells and as a receptor for hepatitis A virus. Its engagement by phosphatidylserine, also recognized by the related TIM-4, triggers PI3K recruitment and AKT phosphorylation, leading to downstream NFAT activation and IL-4 production. This signaling axis is regulated by cytokines IL-4 and IL-13, T cell receptor stimulation, and TGF-??, positioning TIM-1 at the intersection of immune modulation, apoptotic cell clearance, and viral entry pathways.
In the MCF-7 epithelial context, HAVCR1 disruption offers a unique platform to interrogate TIM-1 functions independent of its immune cell roles. While TIM-1 is primarily studied in T cells and kidney injury, its expression in epithelial tumors suggests potential contributions to proliferation, apoptosis resistance, or migration. This knockout model enables direct assessment of TIM-1-dependent PI3K/AKT signaling, phagocytic activity, and viral susceptibility in breast cancer cells, aiding target validation and mechanistic studies.
Typical applications include monitoring protein expression by western blotting and transcript levels by RT-qPCR to confirm knockout efficiency, assessing cell viability with MTT assays, quantifying apoptosis via annexin V flow cytometry, evaluating migration and invasion using transwell assays, and measuring PI3K/AKT pathway activation with phospho-AKT ELISA. Viral entry assays using hepatitis A virus pseudotypes can further probe TIM-1-mediated host?Cpathogen interactions. For additional technical details or ordering information, please contact Ascent Research.
