The H6PD Knockout TE1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population produced from the human esophageal squamous cell carcinoma line TE1, in which the H6PD gene has been disrupted. This product offers a mixed pool of edited cells that collectively eliminate H6PD function, avoiding clonal artifacts and preserving the inherent diversity of the parent line. No exogenous transgenes are expressed, ensuring that phenotypic outcomes are directly attributable to loss of the target gene.
The parental TE1 cell line was derived from a human esophageal squamous cell carcinoma and is extensively used as a preclinical model of esophageal cancer. TE1 cells recapitulate hallmark cancer phenotypes, including aberrant proliferation, migration, and altered metabolism, offering a physiologically relevant backdrop to study gene function in tumorigenesis and disease progression.
The H6PD gene encodes hexose-6-phosphate dehydrogenase, which generates NADPH within the endoplasmic reticulum. This NADPH fuels HSD11B1-mediated conversion of cortisone to cortisol, making H6PD essential for local glucocorticoid activation. H6PD expression is induced by stress-responsive transcription factors such as NFE2L2, ATF6, and XBP1, and it interacts with the glucose-6-phosphate transporter SLC37A4. Downstream, H6PD-dependent cortisol production activates the glucocorticoid receptor NR3C1 and modulates redox-sensitive factors like NF-??B and AP-1. Thus, H6PD integrates ER redox balance with hormonal signaling.
In esophageal squamous cell carcinoma, H6PD-mediated NADPH production and cortisol activation may influence tumor redox homeostasis and stress adaptation. The TE1 knockout model allows dissection of how ER-localized NADPH generation supports cancer cell proliferation and survival under oxidative stress. It also enables investigation of local glucocorticoid action on tumor progression and therapy response. Beyond cancer, this model is relevant to metabolic disorders such as cortisone reductase deficiency and polycystic ovary syndrome, where impaired H6PD function disrupts glucocorticoid metabolism.
The H6PD Knockout TE1 Polyclonal Cells are suitable for cortisol ELISA, NADPH/NADP+ measurement, co-immunoprecipitation, and assays of cell viability, colony formation, migration, and drug sensitivity. These tools facilitate studies on glucocorticoid metabolism in esophageal cancer, ER redox balance, and metabolic vulnerabilities. For further information, contact Ascent Research.
