DLAT Knockout HGC-27 Polyclonal Cells provide a CRISPR/Cas9-engineered polyclonal knockout cell population targeting the DLAT gene in the HGC-27 human gastric carcinoma cell line. This loss-of-function model disrupts expression of the E2 component of the pyruvate dehydrogenase complex, enabling functional studies of DLAT-dependent metabolic processes. The polyclonal nature of the edited population reflects a heterogeneous pool of knockout alleles without clonal selection, making it suitable for initial characterization of gene disruption effects in a cellular context.
Host HGC-27 cells are an adherent human gastric carcinoma line derived from a lymph node metastasis of a poorly differentiated adenocarcinoma, widely used in gastric cancer research. Originating from a metastatic site, this line retains aggressive features of advanced gastric cancer, including altered metabolic and proliferative programs. Its characterized genomic landscape and established culture protocols make HGC-27 an ideal platform for dissecting molecular mechanisms underlying gastric tumorigenesis and metabolic reprogramming.
DLAT encodes the E2 component of the pyruvate dehydrogenase complex (PDHc), catalyzing acetyl group transfer to CoA and linking glycolysis to the citric acid cycle. The E2 subunit scaffolds the complex through interactions with pyruvate dehydrogenase (E1), dihydrolipoamide dehydrogenase (E3), and PDHX. DLAT is inhibited by pyruvate dehydrogenase kinase (PDK) phosphorylation and activated by pyruvate dehydrogenase phosphatase (PDP) dephosphorylation, responding to NADH/NAD+ and acetyl-CoA/CoA ratios and insulin signaling. Downstream, acetyl-CoA fuels the TCA cycle, citrate production, fatty acid synthesis, and cholesterol biogenesis, positioning DLAT as a central regulator of cellular metabolism.
In HGC-27 gastric carcinoma cells, DLAT knockout impairs pyruvate entry into the TCA cycle, forcing metabolic rewiring that may expose vulnerabilities in tumor bioenergetics. This model allows dissection of how loss of PDH function alters redox balance, mitochondrial respiration, and lipid biosynthesis, relevant to pyruvate dehydrogenase deficiency disorders and metabolic reprogramming in cancer. It facilitates studies on the role of DLAT in sustaining anabolic demands and survival signaling in metastatic gastric cancer.
Key applications include Seahorse metabolic flux analysis, PDH activity assays, acetyl-CoA quantification, and validation by Western blot and RT-qPCR. Functional assays for proliferation, apoptosis, and clonogenicity assess cancer cell fitness. Cells are suited for drug target validation and biomarker discovery in gastric cancer metabolism. For additional information and technical support, contact Ascent Research.
