The ACSL1 Knockout A-549 Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal knockout cell population with targeted disruption of the ACSL1 gene in the A-549 human lung adenocarcinoma cell line. The heterogeneous knockout profile, characteristic of pooled gene editing, provides a physiologically relevant loss-of-function model free from clonal selection biases, enabling robust functional studies of ACSL1-dependent pathways in a cancer cell context.
The host A-549 cell line is a widely used model of human alveolar type II epithelial cells derived from lung adenocarcinoma. These adherent cells are employed extensively in cancer research for investigating tumor cell biology, drug responses, and metabolic pathways. Their reliance on both glycolysis and oxidative phosphorylation makes them suitable for studying lipid metabolism in malignant phenotypes.
ACSL1 encodes a long-chain acyl-CoA synthetase that catalyzes the ATP-dependent activation of long-chain fatty acids to acyl-CoA esters, a key step in lipid metabolism. ACSL1 is transcriptionally regulated by SREBP1, PPAR??, and LXR and functions downstream of insulin and glucagon signaling. It channels activated fatty acids primarily into mitochondrial ??-oxidation via interaction with CPT1A and FATP1 at the mitochondrial membrane. Downstream, ACSL1 activity modulates the acyl-CoA pool, ceramide synthesis, lipid droplet formation, and ATP production. Its knockout disrupts these processes, causing accumulation of free fatty acids, impaired ATP generation, and compensatory changes in PPAR??-mediated gene expression.
In A-549 cells, which are lung adenocarcinoma?Cderived, ACSL1 knockout is significant because these cells rely on reprogrammed lipid metabolism for proliferation and survival. Loss of ACSL1 impairs mitochondrial fatty acid oxidation and may force metabolic adaptation via enhanced glycolysis. This model can reveal how altered lipid handling affects tumor aggressiveness, drug sensitivity, and resistance to nutrient stress. Moreover, as ACSL1 connects fatty acid metabolism to PPAR and insulin signaling, the knockout cells serve as a platform to investigate hormonal and oncogenic crosstalk in an epithelial context.
This product supports diverse applications, including Seahorse metabolic flux analysis, fatty acid oxidation assays, lipidomics, and Oil Red O staining. These can be combined with ATP assays, western blotting, and RT-qPCR to dissect ACSL1 loss consequences. Key research areas include fatty acid metabolism in lung adenocarcinoma, lipid droplet?Cmediated drug resistance, and PPAR??-driven transcription. The model also facilitates studies on metabolic syndrome?Crelated pathways and small-molecule screening. For inquiries, contact Ascent Research.
