The ACOD1 Knockout KYSE-150 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population engineered to disrupt the ACOD1 gene in the human KYSE-150 esophageal squamous cell carcinoma (ESCC) cell line. This polyclonal pool provides a genetically heterogeneous loss-of-function model for studying the role of the immunometabolic enzyme ACOD1 in cancer and inflammatory contexts.
The KYSE-150 cell line was established from a well-differentiated human esophageal squamous cell carcinoma and is widely employed as a model for ESCC research. These adherent epithelial cells retain critical signaling and metabolic features of esophageal malignancy, making them particularly suitable for dissecting tumor cell-intrinsic pathways in immunometabolism and cancer progression.
ACOD1 functions as a decarboxylase that converts the TCA cycle intermediate cis-aconitate into the immunomodulatory metabolite itaconate. In response to pro-inflammatory stimuli such as LPS, TNF, and IFN-??, ACOD1 expression is transcriptionally upregulated via NF-??B, STAT1, and IRF1 signaling. The resulting itaconate covalently alkylates cysteine residues on KEAP1, freeing Nrf2 to induce antioxidant gene expression, while simultaneously inhibiting succinate dehydrogenase (SDH) to reroute the TCA cycle and attenuating NLRP3 inflammasome assembly. Additional downstream targets include GAPDH inhibition and ATF3 induction, collectively suppressing inflammatory responses.
In the KYSE-150 ESCC model, ACOD1 knockout serves as a powerful tool to investigate how itaconate influences tumor cell metabolism, redox balance, and inflammatory crosstalk within the esophageal tumor microenvironment. This polyclonal cell population enables studies on the potential role of ACOD1 in modulating cancer cell susceptibility to immune attack, therapy resistance, and the metabolic adaptations that support malignant growth. The ESCC background adds relevance to research on upper aerodigestive tract cancers where inflammation-driven pathogenesis is prominent.
These knockout cells are ideally suited for a range of experimental applications, including immunometabolism studies, inflammation modulation, and host defense mechanism research. Researchers can employ western blotting and RT-qPCR to confirm ACOD1 disruption and downstream target expression, while LC?CMS-based quantification of intracellular itaconate levels directly assesses enzyme activity. Functional assays such as Nrf2 nuclear translocation immunofluorescence, metabolic flux analysis, and NLRP3 inflammasome activation measurements further enable detailed pathway interrogation. The polyclonal knockout format provides a robust population-average phenotype without clonal selection artifacts. For additional information and ordering, please contact Ascent Research.
