The IL3 Knockout HCT 116 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population with targeted disruption of the IL3 gene in the HCT 116 colorectal carcinoma cell line. This product provides a heterogeneous knockout pool that eliminates functional IL-3 expression, offering a versatile loss-of-function model for studying IL-3 biology in an epithelial context. The polyclonal format captures diverse editing outcomes while preventing clonal artifacts, making it ideal for population-based phenotypic analyses.
HCT 116 is a human colorectal carcinoma cell line established from an adult male, characterized by mutations in KRAS, PIK3CA, and CTNNB1, high microsatellite instability (MSI-H), and MLH1 deficiency. These genetic features render it a valuable model for signal transduction and tumor biology research. Its epithelial origin provides a unique platform to investigate the non-hematopoietic roles of cytokines such as IL-3.
IL-3 is a cytokine that primarily regulates hematopoiesis by binding to the IL3RA/CSF2RB receptor complex, which activates JAK2 and downstream STAT5A/B. This signaling cascade promotes transcription of survival and proliferation genes including BCL-XL, MYC, CCND1, and PIM1, while also engaging the PI3K/AKT and Ras/MAPK pathways through adaptors like GRB2. IL-3 expression is controlled by upstream regulators such as T-cell receptor signaling, NFAT, NF-kB, and AP-1. Disruption of IL-3 in this knockout model abrogates these molecular events, enabling detailed pathway dissection.
In HCT 116 cells, IL-3 knockout allows exploration of IL-3 functions beyond hematopoiesis. While IL-3 is implicated in acute myeloid leukemia, myelodysplastic syndromes, allergic asthma, and mastocytosis, its potential autocrine or paracrine contributions to solid tumor microenvironments are emerging. Eliminating IL-3 in a colorectal carcinoma background with defined oncogenic mutations enables assessment of its impact on epithelial cell behavior and tumor-immune interactions.
Applications include studying IL-3 in epithelial cell biology, evaluating IL-3 as a target in the tumor microenvironment, analyzing non-canonical IL-3 signaling, and serving as a negative control for IL-3-dependent assays. Representative techniques include western blotting for phospho-STAT5, RT-qPCR for IL3 mRNA, proliferation (MTS/WST-1) and apoptosis (Annexin V/PI) assays, cytokine secretion profiling, colony formation, and flow cytometry for IL3RA. For further details or custom requests, please contact Ascent Research.
