The AKR1C2 Knockout Hela Cell Line is a CRISPR/Cas9-edited knockout cell line derived from the HeLa human cervical adenocarcinoma epithelial line. It provides a loss-of-function model for studying AKR1C2-dependent steroid hormone metabolism and its interplay with androgen, progesterone, and prostaglandin signaling. This product is supplied as a live cell culture and is intended for advanced research applications in endocrinology, oncology, and drug metabolism.
HeLa cells originate from an HPV18-immortalized cervical adenocarcinoma featuring p53 and Rb inactivation by viral oncoproteins. As a widely used cervical cancer model, HeLa offers a robust and genetically tractable platform for examining hormone-responsive gene networks. Their rapid growth and ease of manipulation facilitate high-throughput screening of steroid-modifying enzymes and receptor-mediated transcriptional responses.
AKR1C2 encodes a NADPH-dependent aldo-keto reductase that inactivates the potent androgen 5??-dihydrotestosterone (DHT) by converting it to 5??-androstane-3??,17??-diol, thereby attenuating androgen receptor (AR) signaling. The enzyme also metabolizes progesterone and influences prostaglandin E2 levels. Transcription of AKR1C2 is regulated by AR, progesterone receptor (PGR), estrogen receptor (ESR1), and NFE2L2 (Nrf2). Within the steroidogenic network, AKR1C2 competes with paralogs AKR1C1 and AKR1C3 for steroid substrates and interacts with SRD5A1/SRD5A2 (5??-reductases) and HSD17B enzymes that control androgen and estrogen interconversions. Consequently, AKR1C2 occupies a central position in androgen, progesterone, and prostaglandin metabolism, integrating signals from multiple nuclear receptors.
Disruption of AKR1C2 in HeLa cells eliminates the primary DHT inactivation route, causing DHT accumulation and sustained activation of AR downstream targets. This shift alters the balance between AR and PGR signaling, as DHT can influence progesterone receptor activity. Although HeLa cells are not endocrine-target tissue, they express functional steroid receptors and metabolic enzymes, permitting dissection of AKR1C2-dependent hormone cross-talk in a cancer background. The knockout line is thus a valuable tool for examining how loss of steroid inactivation impacts proliferation, gene expression, and signaling in hormone-related contexts.
This model is applicable to research on steroid-driven cancers (prostate, breast, endometrial), endometriosis, and polycystic ovary syndrome. It supports drug metabolism studies exploring AKR1C2??s role in xenobiotic clearance via cytochrome P450. Typical assays include RT-qPCR of androgen- and progesterone-responsive genes, Western blot for AR/PGR, LC-MS steroid profiling, proliferation assays, and luciferase reporter tests. The AKR1C2 Knockout HeLa Cell Line thus provides a versatile platform for mechanistic and pharmacological investigations. For further details, contact Ascent Research.
