The HSDL1 Knockout SK-HEP-1 Polyclonal Cells consist of an SK-HEP-1 cell population edited via CRISPR/Cas9 to disrupt the HSDL1 gene, generating a loss-of-function model for hydroxysteroid dehydrogenase-like 1. The polyclonal format encompasses multiple knockout variants, offering a representative pool that minimizes clonal selection artifacts. Each lot is verified for target gene disruption and is suitable for downstream molecular biology and biochemistry applications.
The SK-HEP-1 host cell line derives from a human hepatic adenocarcinoma and serves as a well-characterized model for liver cancer research. This adherent, epithelial-like cell line exhibits metabolic and tumorigenic properties relevant to hepatocellular carcinoma, including dysregulated lipid metabolism and altered steroid hormone processing. SK-HEP-1 cells express markers consistent with a liver origin and are widely used in functional genomics and drug metabolism studies.
HSDL1 encodes a putative hydroxysteroid dehydrogenase that likely catalyzes the oxidation-reduction of steroid substrates using NAD+ or NADP+ as cofactors. The protein participates in steroid hormone metabolism, biotransformation phase I, and fatty acid metabolism pathways. Upstream regulators include PPARA, HNF4A, and CEBPA, while downstream effects influence lipid metabolite levels, steroid hormone concentrations, and fatty acid oxidation products. HSDL1 operates within a network that includes CYP17A1, HSD17B2, and AKR1C3, linking it to broader metabolic and signaling processes.
In SK-HEP-1 liver cancer cells, HSDL1 knockout is predicted to impair steroid catabolism and lipid homeostasis, processes frequently dysregulated in hepatic malignancies. Disruption of this enzyme may alter energy metabolism, redox balance, or steroid receptor signaling, potentially affecting cell proliferation and drug responsiveness. This model is especially pertinent for exploring the intersection of metabolic syndrome and liver cancer, as both conditions involve aberrant fatty acid oxidation and steroid hormone pathways.
These polyclonal knockout cells are suitable for diverse experimental applications, including steroid profiling by LC-MS, lipidomics, RT-qPCR, RNA-seq, and Western blotting for target validation and downstream effector analysis. Functional assays such as cell proliferation and drug metabolism studies can be conducted to assess the impact of HSDL1 loss on liver cancer cell behavior. The model supports investigations into metabolic syndrome-associated hepatocarcinogenesis. For further information or lot-specific data, please contact Ascent Research.
