IDH2 Knockout TE1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the TE1 human esophageal squamous cell carcinoma (ESCC) line. This loss-of-function model, achieved through targeted IDH2 gene disruption, provides a heterogeneous cell pool for studying metabolic and redox processes in cancer. The polyclonal format reflects a diverse spectrum of genetic alterations, avoiding clonal artifact and enhancing physiological relevance.
The TE1 cell line originates from a primary esophageal tumor of a 58-year-old Japanese male with well-differentiated squamous cell carcinoma. As an epithelial ESCC model, TE1 cells retain oncogenic traits and are extensively used in esophageal cancer research, drug sensitivity assays, and metabolic studies. This background is ideal for examining IDH2 function, given the reliance of esophageal cancers on redox balance and metabolic plasticity.
IDH2 encodes mitochondrial NADP+-dependent isocitrate dehydrogenase, which converts isocitrate to ??-ketoglutarate (??-KG) while producing NADPH. This reaction sustains redox homeostasis, drives NADPH-dependent biosynthesis, and regenerates reduced glutathione (GSH). IDH2 operates within the TCA cycle and glutamine metabolism, responding to upstream regulators such as PGC-1??, FOXO3a, SIRT3, and HIF-1??. It partners with IDH1 and requires isocitrate, NADP+, and Mg2+. Knockout of IDH2 eliminates mitochondrial ??-KG production and NADPH generation, compromising antioxidant defenses and elevating reactive oxygen species (ROS).
In TE1 ESCC cells, IDH2 knockout mirrors the loss of normal NADPH production, offering a unique tool to dissect redox adaptation and metabolic vulnerabilities specific to esophageal cancer. This model is distinct from IDH2-mutant contexts, enabling researchers to probe synthetic lethality with oxidative stress inducers and to study compensatory glutamine metabolism. The resulting ROS accumulation underscores the importance of IDH2 for ESCC survival and therapy resistance.
These polyclonal cells support applications in redox signaling, metabolic reprogramming, and drug sensitivity screening under oxidative stress. Common assays include Western blotting, RT-qPCR, NADP+/NADPH ratio determination, ROS detection, and cell viability tests. Metabolomics for ??-KG and 2-HG, along with Seahorse flux analysis, can map metabolic changes. Functional complementation with IDH2 variants further validates pathway dependencies. For technical inquiries, contact Ascent Research.
