The HAVCR1 Knockout LoVo Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the LoVo human colorectal adenocarcinoma line, designed for loss-of-function studies of the HAVCR1 (TIM-1) gene. As a polyclonal knockout model, it maintains the genetic heterogeneity typical of CRISPR-mediated gene disruption, making it ideal for population-level functional analyses without clonal artifacts. This product provides a convenient system to abrogate HAVCR1-mediated signaling and investigate its roles in phosphatidylserine recognition, immune modulation, and viral entry.
The LoVo host cell line was isolated from a metastatic lymph node of a male colon adenocarcinoma patient and harbors the oncogenic KRAS G13D mutation. It exhibits hallmark features of metastatic colorectal cancer, including high proliferation, migration, and invasion potential. LoVo cells are widely used to model colorectal cancer metastasis, drug resistance, and tumor-immune interactions, with the KRAS mutation driving constitutive PI3K/AKT pathway activation, which provides a relevant background for dissecting HAVCR1-related signaling in an aggressive cancer setting.
HAVCR1, a phosphatidylserine receptor, initiates signaling upon binding its ligands phosphatidylserine or Hepatitis A virus. Ligand engagement recruits the adaptor GRB2 and activates PI3K, leading to AKT phosphorylation and NF-??B nuclear translocation, while interactions with ITK and integrins link HAVCR1 to T-cell receptor cascades. HAVCR1 expression is upregulated by IL-4 and IL-13 via STAT6, and its activation promotes production of IL-4, IL-13, and Amphiregulin, reinforcing Type 2 immunity. Downstream mTOR activation influences cell growth. CRISPR-mediated HAVCR1 disruption eliminates these signaling events and abrogates phagocytic uptake, providing a clean loss-of-function model.
In the LoVo context, HAVCR1 may contribute to immune evasion and metastatic behavior. Studies suggest TIM-1 can act as an immune checkpoint on T cells and facilitate efferocytosis by tumor cells, shaping the microenvironment. With the KRAS G13D mutation constitutively activating AKT, knocking out HAVCR1 disrupts additional PI3K/AKT input and NF-??B-mediated transcriptional programs, potentially impairing survival, migration, and invasion. This model thus enables systematic dissection of HAVCR1??s role in colorectal cancer progression and its crosstalk with KRAS-driven pathways.
Typical research applications include transwell migration and invasion assays, phagocytosis assays using fluorescent apoptotic cells, and phospho-AKT ELISA or Western blotting to measure PI3K pathway activity. Flow cytometry and RT-qPCR confirm HAVCR1 knockout efficiency. Co-culture experiments with T cells facilitate investigation of immune checkpoint function, T-cell proliferation, and cytokine production. This model also supports drug resistance studies and viral entry research. For further technical assistance or custom solutions, please contact Ascent Research.
