The ACOD1 Knockout TE1 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population engineered for loss-of-function studies of the ACOD1 gene. This product provides a heterogeneous pool of TE1 cells carrying targeted disruptions in ACOD1, enabling investigation of gene function without clonal selection artifacts. The polyclonal format preserves the genetic diversity inherent to CRISPR/Cas9-mediated gene disruption, making it suitable for population-level analyses of ACOD1-dependent phenotypes.
The host cell line, TE1, is a well-characterized human esophageal squamous cell carcinoma (ESCC) line originally derived from a Chinese male patient. TE1 cells exhibit epithelial morphology and harbor oncogenic alterations typical of ESCC, serving as a clinically relevant model for studying cancer biology, drug response, and tumor immunology. Their cancerous epithelial background makes them particularly valuable for examining how metabolic enzymes like ACOD1 influence malignant phenotypes.
ACOD1 (aconitate decarboxylase 1) mediates the decarboxylation of cis-aconitate to produce itaconate, a metabolite with potent immunomodulatory properties. Itaconate acts as a key node linking metabolism and inflammation by inhibiting succinate dehydrogenase (SDH), leading to succinate accumulation and activation of anti-inflammatory pathways. Mechanistically, itaconate stabilizes NRF2 and induces ATF3, while also dampening NLRP3 inflammasome activation, ultimately driving antimicrobial and anti-oxidative responses. ACOD1 expression is transcriptionally upregulated by immune stimuli including LPS, TNF, and IFN-gamma via NF-kB and STAT1 signaling, positioning ACOD1 at the center of immunometabolic crosstalk.
In the context of esophageal squamous cell carcinoma, ACOD1-mediated itaconate production may modulate the tumor immune microenvironment. By altering itaconate levels, the knockout model allows dissection of how ACOD1 influences cancer cell-intrinsic metabolic reprogramming and interactions with surrounding immune cells. Itaconate??s known effects on macrophage polarization and T-cell function suggest that ACOD1 disruption could reshape antitumor immunity, making these polyclonal knockout cells a powerful tool for exploring immunometabolism in ESCC.
These cells are ideal for a range of research applications including cancer immunology, metabolic flux analysis, and inflammatory disease modeling. Experimentally, they can be utilized for Western blotting to confirm ACOD1 loss, itaconate quantification assays, RT-qPCR profiling of downstream targets such as NRF2 and ATF3, flow cytometry-based immune cell profiling, and metabolic flux analysis. For additional technical details and custom inquiries, please contact Ascent Research.
