The IL3 Knockout KYSE-150 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal human esophageal squamous cell carcinoma (ESCC) population designed for loss-of-function analysis of interleukin-3 (IL-3). This product is generated by CRISPR/Cas9-mediated disruption of the IL3 gene in the KYSE-150 background, yielding a heterogeneous pool of edited cells that collectively eliminate IL-3 expression. The polyclonal format avoids clonal artifacts, enabling robust population-level investigation of IL-3-dependent processes.
KYSE-150 is an established ESCC cell line derived from a poorly differentiated carcinoma, displaying epithelial morphology and tumorigenicity in nude mice. It retains key oncogenic features and expresses the IL-3 receptor subunits CD123 and CD131, rendering it responsive to IL-3 stimulation. This knockout model provides a clean genetic background to dissect the contribution of autocrine or paracrine IL-3 signaling to ESCC pathogenesis.
IL-3 is a pleiotropic cytokine that binds the IL-3 receptor complex (IL3RA/CD123 and CSF2RB/CD131), inducing receptor dimerization and activation of JAK2. This triggers phosphorylation of STAT5A and STAT5B, which dimerize and translocate to the nucleus to regulate genes such as CCND1, BCL2, MYC, PIM1, and SOCS3. Concurrently, IL-3 activates PI3K-AKT and RAS-MAPK pathways via adaptors GRB2 and SOS1, leading to AKT1, mTOR, and MAPK1 engagement. Key upstream transcription factors controlling IL3 expression include TCF/LEF, NFAT, AP-1, NF-??B, and GATA2. In cancer, sustained IL-3 signaling can enhance cell cycle progression, survival, and chemoresistance.
In the context of esophageal squamous cell carcinoma, IL-3 may be produced by tumor cells or stromal components, establishing an autocrine loop that promotes oncogenicity. The KYSE-150 IL3 knockout model disrupts this loop, enabling researchers to assign precise roles to IL-3 in ESCC proliferation, apoptosis evasion, migration, and colony formation. Because IL-3R is expressed in some solid tumors, this model also facilitates evaluation of IL-3R-directed therapies and investigation of compensatory signaling mechanisms after IL-3 deprivation.
This polyclonal knockout cell population is suited for a spectrum of functional and molecular assays. Phospho-STAT5 Western blotting and RT-qPCR for IL3, CCND1, BCL2, and SOCS3 verify pathway inactivation. Proliferation (MTS, BrdU), apoptosis (Annexin V), Transwell migration, and colony formation assays quantify phenotypic changes. RNA-seq transcriptomics and drug sensitivity profiling reveal broader network adaptations and therapeutic responses. For further details, please contact Ascent Research.
