AR Knockout DLD-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed to disrupt the androgen receptor (AR) gene in the DLD-1 human colorectal adenocarcinoma cell line. This loss-of-function model enables investigation of AR-mediated transcriptional regulation and signaling networks in a colon carcinoma background. The polyclonal nature preserves a heterogeneous knockout profile, reflecting the inherent complexity of pooled editing events without clonal selection, thereby offering a representative system for studying gene function in a population context.
DLD-1 cells are a well-established human colorectal adenocarcinoma cell line with epithelial morphology, originally derived from a Duke??s type C colorectal carcinoma. They serve as a robust in vitro model for colon cancer biology, exhibiting characteristic mutations in genes such as APC, KRAS, and TP53. Their adherent growth and stable karyotype make them highly suitable for genetic manipulation and functional assays, providing a physiologically relevant platform to dissect molecular mechanisms underlying colorectal tumorigenesis and therapy response.
The AR gene encodes a ligand-dependent transcription factor that belongs to the nuclear receptor superfamily. Upon binding to androgens such as testosterone and dihydrotestosterone, AR dissociates from the HSP90 chaperone complex, homodimerizes, and translocates to the nucleus. There, it associates with androgen response elements (AREs) in the promoters of target genes, including PSA (KLK3), TMPRSS2, NKX3.1, FKBP5, c-MYC, and cyclin D1, to regulate processes like proliferation, differentiation, and apoptosis. AR transcriptional activity is modulated by coactivators such as SRC-1 (NCOA1), TIF2 (NCOA2), and p300/CBP, and corepressors including NCoR and SMRT. Upstream regulators beyond androgens include EGF, IGF-1, and IL-6, linking AR to MAPK, PI3K/AKT, Wnt, and TGF-?? signaling cascades.
In the context of colorectal cancer, AR expression has been detected in a subset of colon tumors, and its crosstalk with the Wnt/??-catenin pathway is particularly relevant given the frequent APC mutations in DLD-1 cells. This knockout model provides a clean genetic background to dissect AR-dependent effects on cell growth, survival, and hormonal responsiveness without interference from endogenous AR. It facilitates elucidation of how androgens may modulate colon cancer progression and how AR signaling intersects with other oncogenic pathways, offering insights into potential therapeutic vulnerabilities.
Researchers can employ AR Knockout DLD-1 Polyclonal Cells for a wide range of applications, including functional studies of AR-mediated transcriptional programs, screening of AR antagonists or selective androgen receptor modulators, and investigation of hormone-dependent colorectal cancer mechanisms. Representative assays include western blotting for AR protein levels, RT-qPCR to quantify downstream target gene expression, luciferase reporter assays driven by ARE-containing promoters, immunofluorescence to assess AR subcellular localization, and functional assays such as colony formation, MTT proliferation, and migration/invasion analyses. For further information, please contact Ascent Research.
