The HRAS Knockout AGS Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal knockout cell population of the human gastric adenocarcinoma AGS cell line, designed to disrupt the HRAS gene. This gene-edited pool provides a loss-of-function model to study HRAS-dependent signaling in a gastric cancer background. The polyclonal format offers a heterogeneous knockout population suitable for bulk analysis of pathway perturbations.
The host AGS cell line was derived from a human gastric adenocarcinoma and serves as a widely used model for gastric cancer biology and Helicobacter pylori infection research. AGS cells retain epithelial characteristics and harbor genetic alterations relevant to gastric carcinogenesis, making them an appropriate platform for investigating oncogenic signaling networks and evaluating therapeutic vulnerabilities.
HRAS encodes a small GTPase that cycles between active GTP-bound and inactive GDP-bound states, functioning as a molecular switch in signal transduction. Upon activation by upstream receptor tyrosine kinases (RTKs) such as EGFR and FGFR, HRAS is recruited to the plasma membrane via the GRB2/SOS1 adaptor complex and promotes downstream signaling through RAF1/MEK1/2/ERK1/2 and PI3K/AKT cascades. HRAS directly interacts with effectors including PI3K and RALGDS, thereby regulating cellular proliferation, differentiation, and survival. These pathways converge on transcriptional programs that govern cell cycle progression and apoptosis resistance.
In the AGS gastric cancer model, HRAS disruption attenuates oncogenic signaling and may impair tumorigenic properties such as uncontrolled growth, migration, and invasion. Because HRAS is a central node in the RTK-GRB2-SOS-HRAS-RAF-MEK-ERK axis, knockout cells enable dissection of pathway dependencies and identification of compensatory mechanisms. This model is particularly relevant for studying RAS-driven malignancies and for validating inhibitors targeting RAS effectors or upstream activators.
Researchers can employ these HRAS knockout AGS polyclonal cells in functional genomics screens, drug target validation, and signaling pathway dissection. Typical assays include Western blotting for HRAS and phospho-ERK to confirm knockout efficiency and pathway disruption, RT-qPCR for HRAS transcript analysis, and phenotypic assays such as proliferation, migration, invasion, and colony formation studies. Flow cytometry-based apoptosis assays further enable exploration of survival signaling. For additional information or personalized support, please contact Ascent Research.
