The CCS Knockout SK-HEP-1 Polyclonal Cells product supplies a CRISPR/Cas9-edited polyclonal knockout cell population in which the human CCS gene has been disrupted within the SK-HEP-1 hepatocellular carcinoma cell line. This loss-of-function model allows researchers to study the copper chaperone for superoxide dismutase (CCS) directly. By abolishing functional CCS protein, the model supports investigations of copper trafficking and oxidative stress defense mechanisms without the limitations of transient knockdown.
The parental SK-HEP-1 cell line was originally isolated from the ascites of a liver adenocarcinoma patient and exhibits epithelial morphology with tumorigenic properties. As a well-characterized human hepatocellular carcinoma model, SK-HEP-1 is frequently employed in liver cancer research to examine tumor cell signaling, drug metabolism, and the cellular response to oxidative insults, providing a robust background for genetic perturbations.
CCS functions as a dedicated copper chaperone that delivers copper ions directly to superoxide dismutase 1 (SOD1), a step essential for the maturation and enzymatic activation of this antioxidant enzyme. Once copper is inserted, SOD1 catalyzes the dismutation of superoxide radicals into hydrogen peroxide, thereby safeguarding cells from oxidative stress. CCS expression is transcriptionally regulated by the SP1 transcription factor and is modulated by intracellular copper levels and oxidative stress. Upon copper loading, CCS physically interacts with SOD1 and facilitates metal incorporation. In the knockout setting, disruption of CCS leads to failed SOD1 activation, superoxide accumulation, and elevated oxidative stress, highlighting its critical role in cellular redox control.
In the context of hepatocellular carcinoma, redox homeostasis strongly influences tumor progression, apoptotic evasion, and drug resistance. The CCS Knockout SK-HEP-1 Polyclonal Cells provide a valuable tool to dissect the contribution of copper-dependent SOD1 activity to the redox balance of liver cancer cells. Using this model, investigators can explore how loss of CCS alters susceptibility to oxidative stress-inducing agents, examine crosstalk between copper homeostasis and ROS signaling, and identify potential compensatory antioxidant pathways, with implications for redox-targeted therapeutic strategies in liver cancer.
This polyclonal knockout population is suitable for a diverse array of applications, including oxidative stress response profiling, copper metabolism investigations, and neurodegenerative disease modeling such as amyotrophic lateral sclerosis (ALS). Supported assays encompass western blotting for CCS and SOD1 protein analysis, SOD activity assays, ROS detection using DCFDA, cell viability tests under oxidative challenge, and intracellular copper quantification. This product is ideally suited for researchers investigating antioxidant defense mechanisms and metal homeostasis in cancer and neurodegeneration. For additional information, please contact Ascent Research.
