The ACOD1 Knockout MCF-7 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population with targeted disruption of ACOD1 in MCF-7 cells. This loss-of-function model enables study of aconitate decarboxylase 1 (ACOD1/IRG1) and itaconate biology in an epithelial context. As a polyclonal pool, the cells avoid clonal bias and reflect diverse editing events.
The MCF-7 cell line is a well-established human breast adenocarcinoma derived from metastatic pleural effusion. It is ER-positive, PR-positive, and HER2-negative, serving as a representative model for hormone-responsive breast cancer. MCF-7 cells maintain epithelial characteristics and retain key signaling pathways, offering a relevant system for investigating tumor cell-intrinsic inflammatory and metabolic processes.
ACOD1 encodes the enzyme that converts cis-aconitate to itaconate, a metabolite with anti-inflammatory and antioxidant functions. Upon activation by LPS, TNF-??, or IFN-?? via NF-??B and STAT1, ACOD1 expression leads to itaconate accumulation. Itaconate alkylates KEAP1, stabilizing NRF2 and promoting transcription of antioxidant genes (HMOX1, NQO1). Itaconate also inhibits SDH and NLRP3 inflammasome activation, suppressing IL-1?? and IL-6 secretion.
In MCF-7 cells, ACOD1 knockout disrupts itaconate-mediated regulation, potentially altering crosstalk between metabolic reprogramming and hormone signaling. Given the ER-positive status, loss of ACOD1 may affect how inflammatory stimuli influence steroid receptor activity and downstream gene expression. This model is thus valuable for dissecting tumor cell-autonomous roles of itaconate in shaping the inflammatory microenvironment of breast cancer.
Researchers can apply this knockout model in immunometabolism studies, anti-inflammatory drug screening, and cancer immunology. Representative assays include western blotting and RT-qPCR for target validation, ELISA for cytokine quantification, LC-MS for itaconate measurement, Seahorse flux analysis for metabolic profiling, and reporter assays for NRF2 or NF-??B activity. For further details and ordering, contact Ascent Research.
