The AR Knockout CAL-27 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population targeting the androgen receptor (AR) gene in the human CAL-27 oral squamous cell carcinoma line. This product provides a heterogeneous pool of cells with AR gene disruption, offering a versatile loss-of-function model that avoids clonal selection biases. The polyclonal format enables researchers to assess AR-dependent phenotypes within a population context, facilitating robust and reproducible functional studies.
CAL-27 is an epithelial cell line derived from a human tongue squamous cell carcinoma, widely employed as a model for oral cancer. It retains key characteristics of head and neck squamous cell carcinoma (HNSCC), including aggressive growth and invasive potential. The CAL-27 background is particularly relevant for investigating molecular mechanisms underlying oral carcinogenesis and for preclinical evaluation of therapeutic strategies targeting this tumor type.
The AR encodes a ligand-activated nuclear receptor transcription factor that mediates androgen signaling. Upon binding ligands such as dihydrotestosterone (DHT) or testosterone, AR undergoes conformational change, dissociates from chaperones including HSP90 and FKBP52, dimerizes, and translocates to the nucleus with the assistance of importins. There, it associates with pioneer factor FOXA1 and coactivators such as SRC-1 (NCOA1) and p300 (EP300) to regulate transcription of target genes like KLK3, TMPRSS2, NKX3.1, CCND1, and CDKN1A. AR activity is modulated by upstream regulators including epidermal growth factor (EGF) and insulin-like growth factor 1 (IGF-1) and interfaces with pathways such as PI3K/AKT, MAPK/ERK, and Wnt/??-catenin.
In the context of HNSCC, AR signaling has been implicated in tumor cell proliferation, survival, and metastatic dissemination. The CAL-27 model with disrupted AR allows dissection of androgen-driven pathways in oral cancer biology. This knockout system is valuable for distinguishing AR-dependent from AR-independent malignant phenotypes and for exploring crosstalk with pathways commonly activated in HNSCC. It also serves as a platform for evaluating anti-androgen compounds or novel inhibitors targeting AR signaling in squamous carcinomas.
Typical research applications include investigating AR-mediated regulation of oral cancer cell growth and migration, validating downstream effectors identified in transcriptomic studies, and performing drug sensitivity screens for AR antagonists. Compatible assays encompass Western blotting for AR and target proteins, RT-qPCR analysis, proliferation assays such as MTT or BrdU, transwell migration and invasion assays, and luciferase reporter assays to measure AR transcriptional activity following stimulation with DHT. For inquiries or technical support, please contact Ascent Research.
