The ACOD1 Knockout CAL-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the CAL-27 human tongue squamous cell carcinoma cell line, engineered for loss-of-function studies of ACOD1. ACOD1 encodes aconitate decarboxylase 1 (IRG1), which catalyzes the conversion of cis-aconitate to the immunomodulatory metabolite itaconate. As a polyclonal product, this heterogeneous cell pool enables population-level investigation of ACOD1 function, avoiding clonal selection artifacts.
The CAL-27 parental cell line is an epithelial model established from a 56-year-old male with tongue squamous cell carcinoma. It is extensively utilized in head and neck cancer research due to its retention of key characteristics of oral squamous cell carcinoma, including aberrant signaling pathways and metabolic reprogramming. CAL-27 cells are adherent and display aggressive growth properties, making them ideal for investigating tumor cell biology, invasion, and the interplay with the immune microenvironment.
ACOD1 (IRG1) is a mitochondrial enzyme transcriptionally upregulated by pro-inflammatory signals such as LPS, IFN-??, TNF-??, and type I interferons via the transcription factors NF-??B, IRF1, and STAT1. The active homodimer catalyzes the decarboxylation of cis-aconitate to itaconate, which exerts anti-inflammatory effects through multiple mechanisms: alkylation of KEAP1 stabilizes NRF2, inducing antioxidant genes (e.g., HMOX1, NQO1); inhibition of succinate dehydrogenase (SDH) modulates mitochondrial respiration; and direct blockade of NLRP3 inflammasome assembly suppresses IL-1?? maturation. Thus, ACOD1 serves as a critical negative regulator linking metabolic reprogramming to innate immune control.
In CAL-27 oral cancer cells, knockout of ACOD1 is expected to ablate itaconate synthesis, thereby dysregulating NRF2/KEAP1 signaling, SDH activity, and NLRP3 inflammasome activation. This disruption may alter tumorigenic properties such as proliferation, migration, and immune evasion, offering a powerful tool to dissect the role of immunometabolism in oral squamous cell carcinoma progression. The model is particularly suited for studying the functional consequences of lost itaconate-dependent feedback in a cancer context.
This knockout cell product supports diverse research applications, including investigation of itaconate-mediated anti-inflammatory pathways, metabolic profiling by LC-MS?Cbased itaconate measurement, and evaluation of ACOD1 as a therapeutic target. Researchers can employ functional assays (cell proliferation, migration, cytokine ELISA), molecular analyses (western blotting for NRF2, SDH, and downstream targets; RT-qPCR; NF-??B reporter assays), and global transcriptomic profiling (RNA-seq). The polyclonal nature is advantageous for drug screening and population-level pathway studies. For further details, please contact Ascent Research.
