The IDO1 Knockout KYSE-150 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human esophageal squamous cell carcinoma line KYSE-150. This product features disruption of the IDO1 gene, which encodes the immunosuppressive tryptophan-catabolizing enzyme indoleamine 2,3-dioxygenase 1. The polyclonal format provides a heterogeneous pool of edited cells, offering a robust model for studying IDO1 loss without clonal selection artifacts. CRISPR/Cas9-mediated gene disruption introduces loss-of-function mutations across the target locus, enabling functional interrogation of IDO1 in cancer and immune contexts.
KYSE-150 is a well-characterized human esophageal squamous cell carcinoma (ESCC) cell line originally established from a primary tumor of a moderately differentiated squamous cell carcinoma. This cell line retains key features of ESCC, including epithelial morphology and genetic alterations common in upper aerodigestive tract malignancies. KYSE-150 serves as a valuable model for investigating esophageal cancer biology, drug responses, and tumor-immune interactions. Its origins in a moderately differentiated tumor provide a context for studying both tumor-intrinsic pathways and their impact on the microenvironment.
IDO1 catalyzes the rate-limiting step of tryptophan degradation along the kynurenine pathway. Its expression is induced by IFNG, TNF-alpha, IL6, IL1B, and TLR ligands. IDO1 depletes tryptophan and generates kynurenine, an AHR agonist. AHR activation induces FOXP3, suppresses MTOR, promoting regulatory T cell differentiation and inhibiting effector T cells. IDO1 interacts with BIN1 and SOCS3 and requires heme.
In the KYSE-150 esophageal carcinoma background, IDO1 disruption provides a powerful tool to dissect the contribution of tryptophan catabolism to tumor immune evasion. ESCC tumors often exploit IDO1-mediated immunosuppression to escape host immunity, creating a microenvironment rich in kynurenine that fosters regulatory T cell infiltration and T cell exhaustion. The polyclonal knockout population enables bulk studies of IDO1-dependent effects on cancer cell proliferation, invasion, and interactions with immune cells in co-culture systems. This model is particularly relevant for preclinical validation of IDO1 inhibitors and for exploring combination therapies that target the IDO1/AHR/FOXP3 axis alongside standard chemotherapeutics or immune checkpoint blockers.
Research applications include cancer immunology studies, tumor microenvironment modeling, and drug target validation for IDO1 inhibitors. Assays range from Western blotting and LC-MS quantification of tryptophan/kynurenine to T cell proliferation, flow cytometry, RNA-seq, and functional assays such as migration and drug sensitivity screening. This polyclonal knockout model is suited for screening immunomodulatory compounds and dissecting the IDO1 signaling network. For additional technical details or to request a quotation, please contact Ascent Research.
