The AKR1C3 Knockout HeLa Polyclonal Cells product comprises a CRISPR/Cas9?edited polyclonal population of HeLa cells harboring targeted disruption of the AKR1C3 gene, which encodes aldo?keto reductase family 1 member C3. This heterogeneous pool of knockout cells provides a robust loss?of?function model for investigating the multifaceted roles of AKR1C3 in steroid hormone and prostaglandin metabolism. The polyclonal format ensures representation of multiple editing events, offering a system?level view of gene disruption without clonal bias.
HeLa cells are an immortalized epithelial cell line originally derived from a human cervical adenocarcinoma in 1951 and are positive for human papillomavirus type 18 (HPV18). As a widely employed model in cancer biology, HeLa cells offer a well?characterized genetic background and reproducible growth properties, making them suitable for interrogating oncogenic signaling, metabolic reprogramming, and drug response mechanisms. Their robust culture characteristics facilitate high?throughput screening and detailed biochemical analyses.
AKR1C3 functions as an NADPH?dependent oxidoreductase that catalyzes the reduction of ketosteroids, such as androstenedione to testosterone and estrone to estradiol, thereby promoting androgen and estrogen receptor signaling. The enzyme is transcriptionally regulated by NRF2, AhR, and steroidogenic factor?1 (SF?1), and is responsive to inflammatory cues including IL?6 and TNF???. AKR1C3 also converts prostaglandin H2 to prostaglandin F2??, linking it to the COX?2/PTGES pathway and PPAR?? signaling. Representative pathway components include HSD17B3, CYP17A1, and AR upstream, and PGF2?? and 9?cis?retinoic acid downstream. Consequently, AKR1C3 sits at the intersection of steroidogenesis and prostaglandin metabolism, influencing both hormone?dependent and inflammatory processes.
In the HeLa cellular context, ablation of AKR1C3 disrupts intratumoral androgen and estrogen synthesis and impairs prostaglandin metabolism, thereby attenuating hormone?driven proliferative signals. Although HeLa cells are not classical models of hormone?responsive cancers, they enable dissection of AKR1C3?dependent metabolic pathways that are critical in prostate, breast, and endometrial malignancies. This knockout model is particularly valuable for studying the enzyme??s role in modulating steroid hormone bioavailability and for identifying compensatory metabolic adaptations.
Researchers can employ these polyclonal knockout cells to investigate cancer metabolism, steroidogenesis, endocrine therapy resistance, and drug?discovery targets. Representative assays include western blotting and RT?qPCR for target validation, enzyme?activity measurements using androstenedione reduction, steroid hormone quantification by LC?MS/MS, prostaglandin profiling, proliferation assays (MTT/BrdU), androgen receptor reporter gene assays, and transcriptome?wide RNA?seq. The AKR1C3 Knockout HeLa Polyclonal Cells provide a versatile platform for mechanistic and pharmacological studies. For further details, please contact Ascent Research.
