HAVCR1 Knockout AGS Polyclonal Cells are a CRISPR/Cas9-mediated gene-disrupted polyclonal cell population derived from the AGS human gastric adenocarcinoma cell line, in which the HAVCR1 (Hepatitis A Virus Cellular Receptor 1) gene encoding the T-cell immunoglobulin and mucin domain?containing protein 1 (TIM?1) is targeted for functional knockout. This polyclonal knockout model provides a heterogeneous pool of edited alleles to facilitate the study of HAVCR1 loss-of-function in a gastric cancer context.
The AGS cell line, originally isolated from a poorly differentiated gastric adenocarcinoma, serves as an epithelial model widely employed to investigate signal transduction, apoptosis, and drug responses in gastric malignancy. These adherent cells retain key characteristics of gastric epithelium and are reactivated with oncogenic pathways commonly dysregulated in gastric tumors, making them a suitable host for exploring the tumor?promoting functions of HAVCR1.
HAVCR1 functions as a high?affinity receptor for phosphatidylserine, mediating the recognition and engulfment of apoptotic cells and triggering intracellular signaling cascades. Upon engagement, HAVCR1 interacts with PI3K p85 and integrin ??v??3, leading to activation of downstream effectors including AKT, ERK, and NF???B. Upstream, HAVCR1 expression is induced by cytokines such as IL?4 and IL?13 through STAT6, as well as by hypoxia and Helicobacter pylori infection. Downstream, it promotes cell survival via Bcl?2, proliferation through cyclin D1, and invasion by matrix metalloproteinases, while also cross?talking with the TIM?4?mediated phagocytosis pathway. Representative pathway components include phosphatidylserine, PI3K, AKT, mTOR, NF???B, and ERK.
In the context of gastric adenocarcinoma, HAVCR1 overexpression is associated with enhanced tumor growth and metastatic dissemination, mediated largely through sustained activation of the PI3K/AKT and MAPK/ERK pathways. By disrupting HAVCR1 in AGS cells, this polyclonal knockout model enables dissection of TIM?1?dependent signaling in an epithelial tumor background, facilitating analyses of cell survival, apoptosis regulation, autophagy, and immune modulatory functions that are critical to gastric cancer progression.
Typical research applications include investigation of phosphatidylserine?driven signaling and its impact on gastric cancer biology, screening of small?molecule inhibitors targeting TIM?1, elucidation of immune evasion mechanisms within the tumor microenvironment, and studies on the role of HAVCR1 in autophagy and apoptotic clearance. Researchers can validate the knockout and assess downstream effects using techniques such as western blotting for phosphorylated AKT and ERK, flow cytometry?based apoptosis assays, cell viability and migration/invasion assays, co?immunoprecipitation of TIM?1 binding partners, qPCR for target genes, and immunofluorescence microscopy. For additional product details or technical support, please contact Ascent Research.
