AR Knockout AGS Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting the human AR gene in AGS human gastric adenocarcinoma cells. This product provides a heterogeneous pool of cells with AR gene disruption, enabling loss-of-function studies of androgen receptor signaling in a gastric epithelial context. The polyclonal format represents a population-level model of AR ablation without clonal selection, suitable for investigating the consequences of AR inactivation on gastric cancer cell behavior.
The AGS host cell line is derived from a moderately differentiated human gastric adenocarcinoma, serving as a gastric mucosal epithelial model with a cancerous phenotype. AGS cells exhibit aberrant proliferation and migration, making them relevant for studying gastric carcinogenesis and drug responses. This gastric origin provides a platform for examining AR, a gene with emerging roles in gastric cancer biology beyond its classical functions in androgen-responsive tissues.
AR encodes a steroid hormone-activated transcription factor that mediates androgen signaling upon binding testosterone or dihydrotestosterone. Ligand-bound AR translocates to the nucleus, interacts with coactivators NCOA1, NCOA2, NCOA4, and FOXA1, and is stabilized by HSP90. It transcriptionally regulates targets including KLK3, TMPRSS2, NKX3-1, FKBP5, IGF1R, and VEGFA, influencing proliferation and survival. AR activity is modulated by upstream kinases SRC, AKT, and MAPK1 and intersects with MAPK/ERK, PI3K/AKT, and Wnt/??-catenin pathways.
In AGS gastric adenocarcinoma cells, AR knockout abolishes androgen-dependent transcriptional activation, potentially reducing proliferation and migration and altering cell cycle and apoptosis regulators. This model allows dissection of AR??s contribution to gastric cancer phenotypes, independent of prostate tissue. It is valuable for exploring AR crosstalk with oncogenic pathways like PI3K/AKT and Wnt/??-catenin in gastric tumorigenesis and for evaluating therapeutic responses in a gastric mucosal environment.
Research applications include functional studies of AR in gastric cancer, androgen pathway analysis, drug sensitivity screening, proliferation (MTS/MTT), apoptosis (annexin V), and migration/invasion (Transwell) assays. Validation employs western blotting, RT-qPCR for AR and target genes, and androgen response reporter assays. Transcriptomic analysis via RNA-seq identifies AR-dependent gene networks. For further technical details, please contact Ascent Research.
