The HMOX1 Knouckout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed to disrupt the HMOX1 gene in the SK-HEP-1 human liver adenocarcinoma cell line. This loss-of-function model enables investigation of heme oxygenase-1 (HO-1) functions by abolishing its enzymatic activity, providing a robust system for exploring the molecular consequences of HMOX1 deficiency in a relevant cellular context. The use of a polyclonal population allows researchers to study gene disruption effects across a heterogeneous cell pool, mitigating clonal variation artifacts.
The parental SK-HEP-1 cell line was originally derived from the ascitic fluid of a 50-year-old male patient with adenocarcinoma of the liver. These cells exhibit a unique dual phenotype, combining features of both hepatic adenocarcinoma and endothelial-like characteristics, making them a valuable model for studying liver cancer biology, angiogenesis, and endothelial cell function. The SK-HEP-1 background supports robust growth and is well-suited for genetic manipulation, facilitating a wide range of functional assays.
HMOX1 encodes heme oxygenase-1, the rate-limiting enzyme in heme catabolism that cleaves heme into biliverdin, carbon monoxide (CO), and ferrous iron (Fe2?). Biliverdin is rapidly converted to bilirubin by biliverdin reductase, both acting as potent antioxidants. CO functions as a signaling molecule with anti-inflammatory and anti-apoptotic properties, while iron induces ferritin expression, providing additional cytoprotection. HMOX1 expression is transcriptionally activated by Nrf2 and HIF1A under oxidative stress, and repressed by Bach1; it also responds to cytokines such as TNF-?? and IL-6. The knockout disrupts this entire cascade, abrogating downstream production of bilirubin and CO, thereby sensitizing cells to oxidative damage and apoptosis.
In the SK-HEP-1 background, which displays both malignant and endothelial-like traits, HMOX1 knockout provides a powerful platform to dissect the role of HO-1 in liver cancer progression, drug resistance, and endothelial inflammatory responses. The cells are expected to exhibit heightened reactive oxygen species levels and increased susceptibility to stress-induced cell death, making them ideal for evaluating the cytoprotective networks mediated by HO-1. Additionally, the model allows examination of how carbon monoxide signaling and iron homeostasis modulate tumor cell behavior and immune interactions in the hepatic microenvironment.
These polyclonal knockout cells are suitable for a broad spectrum of experimental techniques, including western blotting and RT-qPCR to confirm gene disruption, bilirubin production measurement to assess heme oxygenase activity, reactive oxygen species (ROS) assays to quantify oxidative stress, TUNEL and caspase-3 activity assays for apoptosis detection, cell viability assays under oxidative challenges, and immunocytochemistry for protein localization studies. Key research applications encompass oxidative stress response, cytoprotection mechanisms, carbon monoxide signaling, cancer biology, inflammation, and drug resistance. For additional technical information or to request a quotation, please contact Ascent Research.
