The BTK Knockout AGS Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting the BTK gene in the AGS gastric adenocarcinoma cell line. The CRISPR/Cas9-mediated gene disruption generates a heterogeneous pool of cells with loss-of-function mutations, avoiding clonal selection bias. This polyclonal format provides a robust model for studying BTK-dependent signaling in gastric epithelial cells.
AGS cells are a human gastric adenocarcinoma epithelial line widely used as a model for gastric cancer. They exhibit key features of gastric tumors, including dysregulated proliferation and survival pathways. The epithelial origin of AGS makes them particularly relevant for investigating oncogenic mechanisms in gastric epithelium, and the BTK knockout in this background offers a specific tool to interrogate BTK’s contributions to these processes.
BTK is a Tec-family non-receptor tyrosine kinase essential for BCR signaling, where it is activated by LYN/SYK downstream of the BCR complex (CD79A/CD79B). Phosphorylated BTK then activates BLNK and PLC??2, triggering Ca2+ flux and downstream activation of NF-??B, NFAT, and MAPK/ERK pathways, which promote expression of survival genes like BCL-XL, CCND1, and MYC. In gastric cancer, BTK may be engaged by alternative receptors such as TLR4, IL-6R, and integrins, signaling via MyD88 and the IKK complex to sustain oncogenic NF-??B and MAPK activity. Thus, BTK integrates multiple inputs to drive proliferation and apoptosis resistance.
In AGS gastric cancer cells, BTK signaling has been associated with enhanced cell survival and proliferation. The polyclonal BTK knockout allows dissection of BCR-like signaling in a solid tumor context, revealing non-canonical BTK functions independent of adaptive immunity. Loss of BTK in this model may perturb downstream effectors like NF-??B and ERK, providing insight into therapeutic vulnerabilities. This system is ideal for evaluating BTK’s role in gastric adenocarcinoma and its interplay with other oncogenic drivers.
Researchers can utilize this product for functional studies of BTK in gastric cancer, including drug sensitivity screening with inhibitors such as ibrutinib, analysis of apoptosis and proliferation pathways, and biomarker validation. Representative assays include western blotting for phospho-BTK and phospho-ERK, RT-qPCR for NF-??B targets, flow cytometry for Annexin V staining, MTT proliferation assays, and phospho-signaling profiling. The polyclonal population is robust for population-based readouts and reduces clonal artifacts. For additional information, please contact Ascent Research.
