The DLAT Knockout A2780 Polyclonal Cells product is a CRISPR/Cas9-edited polyclonal knockout cell population derived from the A2780 human ovarian carcinoma cell line, featuring disruption of the endogenous dihydrolipoamide S-acetyltransferase (DLAT) gene. This polyclonal pool provides a heterogeneous knockout model enabling evaluation of DLAT-dependent phenotypes without clonal selection. The gene-edited population is suitable for functional studies of the pyruvate dehydrogenase complex in cancer cell metabolism.
The A2780 cell line was established from an untreated patient with ovarian carcinoma and displays epithelial morphology. As a widely used model in ovarian cancer research, A2780 cells facilitate investigations into tumor biology, metabolic reprogramming, and mechanisms of drug resistance. Their genetic background and growth characteristics make them particularly valuable for metabolic flux analyses and cell signaling studies.
DLAT encodes the E2 subunit of the pyruvate dehydrogenase complex (PDC), a mitochondrial multienzyme assembly that catalyzes the oxidative decarboxylation of pyruvate to acetyl-CoA. This reaction represents a key regulatory step linking glycolysis to the tricarboxylic acid (TCA) cycle. DLAT is allosterically regulated by upstream signals including insulin and AMPK, and transcriptionally modulated by PGC-1?? and FOXO1. It functionally interacts with PDC components (PDHA1, PDHB, PDHX) and is dynamically controlled by PDK1-4 kinases and PDP1-2 phosphatases, which coordinate cellular energy status with metabolic flux.
Inactivation of DLAT in A2780 ovarian cancer cells disrupts PDC integrity, leading to impaired mitochondrial acetyl-CoA synthesis and diminished TCA cycle activity. This metabolic perturbation can reduce oxidative phosphorylation, alter ATP generation, and shift cellular reliance toward glycolysis. The resulting metabolic reprogramming may impact cell proliferation, survival, and apoptotic sensitivities, providing a physiologically relevant system to dissect DLAT??s role in ovarian cancer metabolism and its contribution to drug resistance phenotypes.
This knockout model is ideally suited for applications in cancer metabolism research, including investigation of metabolic reprogramming, mitochondrial function, and therapeutic resistance in ovarian cancer. Researchers can employ a range of experimental approaches, such as Seahorse metabolic flux analysis, RNA-seq, metabolomics, Western blotting, RT-qPCR, MTT assays, apoptosis assays, and flow cytometry, to characterize the functional consequences of DLAT disruption. For additional information about this product, please contact Ascent Research.
