The HSD17B11 Knockout HeLa Polyclonal Cells product provides a pooled population of CRISPR/Cas9-edited HeLa cells carrying targeted disruption of the HSD17B11 gene. This polyclonal knockout pool offers a genetically heterogeneous loss-of-function model for studying the role of 17??-hydroxysteroid dehydrogenase type 11 in multiple cellular contexts. The product is supplied as a frozen vial of polyclonal knockout cells, suitable for immediate expansion and downstream functional analysis.
HeLa cells are an immortalized human epithelial cell line derived from cervical adenocarcinoma and are positive for human papillomavirus type 18 (HPV18). Widely used as a model for cancer biology, these cells exhibit robust growth characteristics and retain key signaling pathways relevant to hormone-dependent cancer research. The HeLa line serves as a practical host for studying estrogen metabolism and retinoid signaling due to its endogenous expression of nuclear receptors and metabolic enzymes, though it does not fully recapitulate normal epithelial physiology.
HSD17B11 encodes a short-chain dehydrogenase/reductase that interconverts 17??-hydroxysteroids and retinoids, converting estradiol to estrone and retinaldehyde to retinol using NAD+ or NADP+ as cofactors. It operates upstream of estrogen receptor alpha (ESR1) and retinoic acid receptor alpha (RAR??), modulating ligand availability and downstream transcriptional programs. Expression of HSD17B11 may be regulated by ESR1, androgen receptor, PPAR??, and RAR??, while its activity influences the production of estrone, androstenedione, and all-trans-retinoic acid, thereby coordinating estrogen, androgen, and retinoic acid signaling. Key pathway partners include HSD17B1, HSD17B2, CYP19A1, HSD3B1, RDH10, ALDH1A1, and RXR??.
In HeLa cells, HSD17B11 knockout disrupts local steroid and retinoid metabolism, providing a defined model to dissect hormone-dependent proliferation and differentiation programs. The loss of HSD17B11 function is expected to shift the estradiol-to-estrone equilibrium, reducing ESR1 activation and downstream estrogen-responsive gene expression. Additionally, impaired retinaldehyde-to-retinol conversion may attenuate retinoic acid receptor signaling, affecting cellular growth control and apoptotic pathways. HeLa cells, as HPV18-transformed epithelial cells, offer a relevant background for investigating how HSD17B11-mediated metabolism intersects with viral oncoprotein-driven carcinogenesis. This knockout model thus enables researchers to explore the crosstalk between steroid hormone metabolism, retinoid signaling, and cervical cancer cell biology.
The HSD17B11 Knockout HeLa Polyclonal Cells are suited for a wide range of experimental applications, including functional studies of hormone-dependent cancer biology, retinoid signaling in cervical cells, drug target validation, and metabolic pathway dissection. Representative assays include Western blotting, RT-qPCR, LC-MS steroid profiling, retinoid quantification, estrogen receptor reporter assays, cell proliferation (MTT), apoptosis assays, and migration assays. The polyclonal knockout population is also an ideal tool for CRISPR screening and comparative analyses of steroid and retinoid metabolism. Researchers can use this resource to validate HSD17B11 as a therapeutic target in hormone-sensitive cancers. For technical inquiries and support, please contact Ascent Research.
