The ACSL4 Knockout A2780 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population targeting the human ACSL4 gene. This product provides a heterogeneous knockout model for investigating ACSL4-driven lipid metabolism and ferroptosis, circumventing the clonal effects associated with single-cell-derived cell lines.
The host A2780 cell line is a human ovarian epithelial carcinoma cell line established from an untreated patient tumor. As a well-characterized ovarian cancer model, A2780 cells retain properties of malignant ovarian epithelium and are extensively utilized in mechanistic oncology and drug response studies.
ACSL4 encodes a long-chain fatty acyl-CoA synthetase that preferentially activates polyunsaturated fatty acids, facilitating their incorporation into membrane phospholipids and sensitizing cells to ferroptosis. The enzyme functions under transcriptional control by PPAR??, SREBP1, and STAT3, and is activated downstream of IL-4 signaling. Biochemically, ACSL4 interacts with GPX4 and ALOX5, and cooperates with ACSL1. Within the ferroptotic cascade, ACSL4 acts upstream of LPCAT3 and 15-LOX, promoting the accumulation of phosphatidylethanolamine hydroperoxides (PE-OOH); this process is counterbalanced by GPX4-mediated lipid peroxide reduction.
In A2780 ovarian carcinoma cells, ACSL4 knockout abrogates the metabolic incorporation of polyunsaturated fatty acids into phospholipids, thereby diminishing sensitivity to ferroptosis inducers such as erastin and RSL3. The polyclonal knockout population enables examination of ACSL4-dependent phenotypes across a diverse genetic background, mirroring the heterogeneity of clinical tumors and providing a robust platform for studying ferroptosis regulation and ovarian cancer lipid dependency.
This knockout model is applicable in ferroptosis induction experiments using erastin or RSL3, coupled with lipid peroxidation detection via C11?BODIPY staining, cell viability assays, and immunoblotting for ACSL4. It also supports RT?qPCR, RNA?seq transcriptomics, and drug sensitivity screens targeting lipid metabolic pathways. For further details, please contact Ascent Research.
