The AR Knockout Ca Ski Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated from the Ca Ski human cervical carcinoma cell line. This gene disruption model targets the human androgen receptor (AR) gene, providing a loss-of-function system to study AR-dependent signaling in a cervical cancer background. The polyclonal format reflects the heterogeneous nature of CRISPR-mediated modifications without clonal isolation, making it suitable for pooled functional assays, drug response studies, and experiments requiring a diverse genetic background.
Ca Ski is an established human epithelial cell line derived from an epidermoid carcinoma of the cervix. This cell line is extensively characterized as HPV16-positive and harbors wild-type p53, rendering it a valuable model for studying cervical carcinogenesis and HPV-driven oncogenic mechanisms. Ca Ski cells maintain key features of cervical tumor biology, including epithelial morphology and growth properties relevant to in vitro and in vivo cancer research, and are widely used to investigate molecular pathways in gynecological oncology.
The AR gene encodes a ligand-dependent transcription factor that mediates the biological effects of androgens such as testosterone and dihydrotestosterone (DHT). Upon androgen binding, the receptor undergoes a conformational change, dissociates from heat shock protein 90 (HSP90), and translocates to the nucleus. There, it dimerizes and binds to androgen response elements (AREs) in the promoters of target genes, including PSA (KLK3), TMPRSS2, and FKBP5, thereby regulating their transcription. AR activity is modulated by upstream regulators such as epidermal growth factor (EGF), insulin-like growth factor 1 (IGF-1), and kinases including AKT and MAPK, which converge on pathways like PI3K/AKT/mTOR and MAPK/ERK. Co-regulatory factors such as steroid receptor coactivator-1 (SRC-1), CBP/p300, NCoR, and SMRT fine-tune transcriptional output. Additionally, AR interacts with FOXO1 and ??-catenin, integrating signals to control proliferation and survival partly through induction of cyclin D1 and Bcl-2 family members.
In the context of cervical carcinoma, the role of androgen receptor signaling is increasingly recognized but not fully elucidated. Ca Ski cells, being HPV16-positive, provide a relevant system to interrogate potential crosstalk between AR signaling and HPV oncoprotein function. The AR knockout in this model enables researchers to dissect androgen-mediated transcriptional programs and their contribution to cervical cancer cell growth, migration, and apoptosis. This is particularly important given that AR pathways may influence the response to hormonal therapies and tumor progression in gynecological malignancies.
These polyclonal knockout cells are well-suited for a range of experimental applications, including quantification of AR target gene expression by RT-qPCR, analysis of AR protein levels by western blotting, and functional measurement of AR transcriptional activity using ARE-driven luciferase reporter assays. Immunofluorescence can be employed to assess AR nuclear translocation upon androgen stimulation. Cellular assays such as MTS/MTT proliferation, caspase activation apoptosis, and transwell migration/invasion allow characterization of the knockout phenotype. The model facilitates anti-androgen drug screening and mechanistic studies of androgen signaling in cervical cancer. For further information, please contact Ascent Research.
