The AR Knockout A2780 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the A2780 human ovarian carcinoma epithelial cell line. Through CRISPR/Cas9-mediated gene disruption targeting the androgen receptor (AR) gene, this product generates a heterogeneous pool of cells carrying diverse loss-of-function mutations across the AR locus. The polyclonal format preserves the natural genetic heterogeneity of the edited population, enabling robust gene-function studies without the limitations of single-clone variability. This model is ideally suited for investigating androgen receptor-dependent processes in ovarian cancer biology, providing a versatile tool for loss-of-function analyses.
The A2780 cell line was established from an untreated patient with ovarian endometrioid adenocarcinoma and is widely used as a model for epithelial ovarian cancer. These adherent epithelial cells retain key features of ovarian tumorigenesis, including deregulated proliferation, migration, and hormone responsiveness. They are well-characterized for studies of chemotherapy resistance, particularly to cisplatin and paclitaxel, and are commonly employed in xenograft models. Their epithelial origin and tumorigenic properties make them an appropriate host for examining AR’s role in ovarian cancer.
The androgen receptor (AR) is a ligand-activated nuclear receptor transcription factor that binds androgens like testosterone or DHT, then translocates to the nucleus and interacts with androgen response elements (AREs) to regulate gene expression. AR activity is modulated by coregulators including NCOA1, NCOA3, NCOR1, NCOR2, and factors such as FOXA1, GATA2, and HSP90. AR transcriptionally regulates targets like KLK3, TMPRSS2, NKX3-1, FKBP5, CCND1, and Bcl-2 family members, impacting cell growth and survival. Upstream, AR integrates signals from LH, EGF, IGF-1, IL-6, AKT, and MAPK, linking androgen signaling to MAPK/ERK, PI3K/AKT, and Wnt/??-catenin pathways.
In ovarian cancer, AR expression is frequently detected, yet its precise contribution remains unclear. These knockout cells remove androgen-dependent transcriptional regulation, allowing dissection of AR-mediated effects on proliferation, apoptosis, migration, and hormone sensitivity. Disrupting AR signaling enables the study of crosstalk with other oncogenic pathways and the identification of compensatory mechanisms. They are particularly useful for investigating resistance to hormone-based treatments and for evaluating AR as a therapeutic target in ovarian cancer, where hormonal influences are increasingly recognized.
Researchers can utilize this model for functional genomics, drug screening, and mechanistic studies using assays such as western blotting and RT-qPCR to confirm knockout and assess targets; MTT and Transwell assays for proliferation and migration; luciferase reporters for AR activity; and RNA-seq for transcriptome analysis. Co-immunoprecipitation and ChIP-qPCR probe protein interactions and chromatin binding, while flow cytometry and annexin V assays analyze cell cycle and apoptosis. For technical inquiries, please contact Ascent Research.
