The HAVCR1 Knockout A2780 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population in which the human HAVCR1 gene has been disrupted in the A2780 ovarian carcinoma epithelial cell line. This product provides a loss-of-function model for studying the biological roles of HAVCR1, also known as TIM-1 (T-cell immunoglobulin and mucin domain 1). As a polyclonal knockout pool, the cells contain a heterogeneous mix of gene-edited alleles, offering a practical approach for functional studies without clonal isolation. The gene disruption is achieved through CRISPR/Cas9-mediated targeting, resulting in a mixed population of cells with disrupted HAVCR1 expression. This format is well-suited for bulk assays and population-based analyses.
The A2780 host cell line is a well-characterized human ovarian carcinoma epithelial model originally derived from an untreated patient with ovarian endometrioid adenocarcinoma. These cells are widely employed in research on cisplatin sensitivity and drug resistance mechanisms, as they retain sensitivity to cisplatin, making them an appropriate background for investigating chemoresistance pathways. A2780 cells exhibit epithelial morphology and are frequently used in cancer biology studies due to their reproducible growth characteristics and established signaling networks. Their use as the parental line for this knockout model ensures a physiologically relevant context for studying ovarian cancer-associated gene functions.
HAVCR1 encodes TIM-1, a phosphatidylserine receptor that, upon ligand engagement, activates PI3K/AKT/mTOR signaling. It interacts with PI3K p85 and binds phosphatidylserine on apoptotic cells or viruses like Hepatitis A virus. Upstream, T-cell receptor stimulation and IL-4/STAT6 induce HAVCR1, while downstream effectors include NFAT and GATA3 transcription factors that promote Th2 cytokine production. In cancer cells, TIM-1 drives immune evasion and EMT, upregulating Snail and Vimentin. The related receptor TIM-4 can also modulate these pathways.
In the context of ovarian cancer, HAVCR1 expression has been implicated in tumor progression and immune evasion, making the A2780 knockout model particularly valuable. The A2780 line??s cisplatin-sensitive phenotype allows researchers to dissect the contribution of TIM-1 signaling to chemoresistance. Disruption of HAVCR1 may alter phosphatidylserine-dependent clearance of apoptotic cells and impact the tumor microenvironment. Moreover, because TIM-1 promotes EMT and activates AKT/mTOR survival pathways, this knockout system enables interrogation of how HAVCR1 contributes to metastatic behaviors and resistance to platinum-based therapies. The polyclonal format facilitates population-level observations of these phenotypic changes without the confounds of clonal variation.
This knockout cell model supports diverse experimental applications, including investigation of TIM-1 function in ovarian cancer, phosphatidylserine receptor signaling, and immune checkpoint biology. Typical assays include Western blotting, flow cytometry, apoptosis and proliferation assays, migration/invasion studies, cisplatin sensitivity testing, and RT-qPCR for EMT markers. Co-immunoprecipitation with PI3K p85 and phospho-AKT analysis can further delineate signaling changes. For further information, please contact Ascent Research.
