The CCS Knockout MES-OV Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the MES-OV human ovarian carcinoma cell line. This product provides a loss-of-function model for studying the copper chaperone for superoxide dismutase (CCS) gene. CRISPR/Cas9-mediated gene disruption has been employed to eliminate functional CCS expression, enabling researchers to investigate the role of CCS in copper delivery and oxidative stress defense. The polyclonal nature of this knockout cell population ensures heterogeneous gene editing outcomes, offering a robust tool for functional studies without clonal artifacts.
The parental MES-OV cell line is a human ovarian adenocarcinoma cell line with mesenchymal morphology, representing a subtype that has undergone epithelial-mesenchymal transition (EMT). Originating from ovarian surface epithelium, these cells retain characteristics of hormone-responsive tissue and have acquired invasive properties, making them a relevant model for studying ovarian carcinoma progression and metastasis. The mesenchymal phenotype of MES-OV cells is associated with enhanced migratory and invasive capacities, which are critical in cancer metastasis research.
CCS is a copper chaperone that specifically delivers copper ions (Cu2+) to superoxide dismutase 1 (SOD1), a process essential for SOD1 enzymatic activation. Copper-loaded CCS interacts with nascent SOD1 to facilitate disulfide bond formation and protein maturation. Mature SOD1 catalyzes the dismutation of superoxide radicals (O2??) into hydrogen peroxide (H2O2), which is further detoxified by glutathione. CCS expression is transcriptionally regulated by Sp1 and induced under oxidative stress via Nrf2 (NFE2L2) and HIF-1?? pathways. The CCS-SOD1 axis is central to cellular reactive oxygen species (ROS) metabolism and maintenance of redox homeostasis.
In the MES-OV mesenchymal ovarian carcinoma background, CCS knockout disrupts copper delivery to SOD1, leading to accumulation of superoxide and heightened oxidative stress. Given the role of oxidative stress in cancer cell signaling, survival, and EMT, this model is particularly valuable for dissecting the redox-dependent mechanisms of ovarian cancer aggressiveness. MES-OV cells already exhibit mesenchymal and invasive traits; CCS loss may exacerbate or alter these phenotypes through ROS-mediated signaling, providing insights into how oxidative stress influences EMT and metastasis. Additionally, this model can be used to explore the interplay between copper homeostasis and cancer cell proliferation.
The CCS Knockout MES-OV Polyclonal Cells are suitable for a range of functional assays. Western blotting and immunofluorescence validate loss of CCS protein and examine SOD1 expression and localization. SOD activity assays and ROS detection with DCFH-DA quantify oxidative stress. Cell viability under H2O2 challenge evaluates resistance to oxidative insult, while copper content analysis by ICP-MS monitors cellular copper levels. Proliferation and migration assays assess cancer cell behavior. This knockout model supports investigations in oxidative stress, copper metabolism, ALS-related neurodegeneration, and cancer redox biology. For further information, please contact Ascent Research.
