The ACSL4 Knockout LoVo Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the LoVo human colorectal adenocarcinoma cell line (Homo sapiens). This product provides a heterogeneous pool of edited cells carrying target-gene disruption at the ACSL4 locus, enabling loss-of-function studies without clonal selection. The polyclonal format preserves genetic diversity and mitigates clonal artifacts, making it suitable for pooled functional assays and high-throughput screening. Each lot is confirmed for reduced ACSL4 expression and is ready for downstream experimental manipulations.
The host LoVo cell line was established from a metastatic tumor nodule in the left supraclavicular lymph node of a 56-year-old male with colon adenocarcinoma. These cells retain features of metastatic colorectal cancer, including deregulated lipid metabolism and altered ferroptosis susceptibility. LoVo cells are widely used as a model system to study colon cancer progression, metastatic dissemination, and therapeutic response, particularly in the context of oxidative stress and lipid-dependent cell death pathways.
ACSL4 (Acyl-CoA Synthetase Long Chain Family Member 4) encodes an enzyme that activates long-chain polyunsaturated fatty acids (PUFAs) such as arachidonic acid by ligating them to coenzyme A. The resulting acyl-CoA esters are subsequently incorporated into membrane phospholipids by LPCAT3, enriching phosphatidylethanolamine species with PUFAs (AA-PE). These PUFA-containing phospholipids are susceptible to iron-dependent peroxidation, a process that accumulates lipid peroxides and triggers ferroptosis, an oxidative form of regulated cell death. ACSL4 is transcriptionally regulated by SP1, PPAR??, SREBP1, HIF-1??, and p53, and it functionally interacts with LPCAT3, GPX4, and the system Xc? cystine/glutamate antiporter. Its activity is opposed by GPX4, which reduces lipid hydroperoxides, and by system Xc?, which maintains intracellular glutathione levels. Disruption of ACSL4 abrogates the incorporation of PUFAs into phospholipids, thereby blunting lipid peroxidation and conferring resistance to ferroptotic stimuli.
In the LoVo cell context, ACSL4 knockout provides a critical model for dissecting ferroptosis sensitivity in colorectal adenocarcinoma. LoVo cells express a functional ferroptosis machinery, and ACSL4 loss-of-function allows researchers to interrogate how lipid metabolic reprogramming influences tumor cell fate under oxidative stress. This model is particularly relevant for studying resistance to ferroptosis-inducing agents such as erastin and RSL3, and for exploring the interplay between p53 status, SP1-driven transcription, and lipid peroxidation signaling. The polyclonal knockout cells enable population-level analysis of ferroptosis commitment and metabolic adaptation without the confounding effects of clonal heterogeneity.
This product is suited for a range of experimental applications, including investigation of ferroptosis sensitivity, lipid metabolism reprogramming, and drug resistance in colorectal cancer. Representative assays include lipid peroxidation detection using C11-BODIPY or malondialdehyde measurement, ferroptosis induction with erastin or RSL3 followed by cell viability assessment, phospholipid profiling via mass spectrometry, fluorescence microscopy for lipid ROS, flow cytometric analysis of cell death, colony formation assays, and tumor xenograft models. The ACSL4 Knockout LoVo Polyclonal Cells can also be employed in siRNA or inhibitor rescue experiments to validate specificity. For further technical specifications and lot-to-lot performance data, please contact Ascent Research.
