The CBL Knockout HGC-27 Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal knockout cell population targeting the CBL gene in the human gastric adenocarcinoma cell line HGC-27. This product provides a heterogeneous pool of gene-disrupted cells, generated through CRISPR/Cas9-mediated gene disruption, offering a loss-of-function model for studying CBL-dependent pathways without clonal selection. The polyclonal format preserves genetic variation, useful for functional genomics and drug response assays.
HGC-27 is a human gastric cancer cell line derived from a metastatic lymph node of a patient with gastric adenocarcinoma. It displays epithelial morphology and is widely used in gastric cancer studies, including tumor invasion, metastasis, and signaling. The cell line contains alterations typical of advanced gastric carcinoma, serving as a robust in vitro model for investigating oncogenic mechanisms and therapeutic vulnerabilities.
CBL encodes an E3 ubiquitin-protein ligase that negatively regulates receptor tyrosine kinase (RTK) signaling. It mediates ubiquitination and degradation of activated RTKs such as EGFR and MET. Following ligand stimulation, SRC family kinases phosphorylate CBL, which then interacts with adaptors GRB2 and SHC to target receptors for degradation, attenuating downstream PI3K/AKT and MAPK/ERK pathways. CBL also participates in T cell receptor signaling and binds the PI3K regulatory subunit. Loss of CBL disrupts receptor downregulation, leading to sustained signaling.
In gastric cancer, CBL dysfunction is linked to aberrant RTK signaling, driving proliferation, survival, and invasion. The CBL knockout in HGC-27 provides a model to study how unchecked EGFR/MET signaling promotes gastric adenocarcinoma progression. This model may exhibit hyperactivation of AKT and ERK, mimicking oncogenic signaling seen in tumors with CBL loss, useful for dissecting molecular mechanisms and testing targeted therapies against the RTK?CPI3K?CMAPK axis.
Applications include investigating RTK trafficking and ubiquitin-dependent receptor downregulation, functional genomics screens, and drug sensitivity testing against kinase inhibitors. Representative assays: Western blotting for total/phospho-EGFR, AKT, ERK; co-immunoprecipitation for receptor ubiquitination; RT-qPCR for CBL; proliferation, migration, invasion assays; and flow cytometry for surface receptor expression. The polyclonal format aids in studying phenotypic heterogeneity in drug response. For further information, contact Ascent Research.
