The IL3 Knockout 143B Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal knockout population of the human 143B osteosarcoma cell line with targeted disruption of the IL3 gene. This heterogeneous pool facilitates loss-of-function studies of interleukin-3 in a bone tumor context without clonal limitations. The polyclonal format preserves genetic diversity while effectively eliminating functional IL-3 expression, enabling robust characterization of IL-3-dependent signaling networks in downstream assays.
The 143B cell line is a well-established human osteosarcoma model derived from a bone tumor. These adherent cells are widely used to study bone cancer biology, metastasis, and therapeutic responses, providing a relevant environment for investigating cytokine-mediated interactions within the bone tumor microenvironment.
Interleukin-3 (IL-3), encoded by IL3, is a hematopoietic growth factor that binds to the heterodimeric receptor IL3RA/CSF2RB. This interaction activates JAK2, which phosphorylates STAT5, and triggers PI3K/AKT and MAPK/ERK cascades via adaptors SHC and GRB2. Under physiological conditions, IL-3 stimulates proliferation and differentiation of hematopoietic progenitors and promotes survival by upregulating BCL2 and MYC. Upstream, T-cell receptor stimulation and cytokines such as IL-1 and TNF induce IL3 expression through NFAT and AP-1. Disruption of IL3 abolishes these signaling axes, cutting off JAK/STAT, PI3K/AKT, and MEK/ERK activation.
In the 143B osteosarcoma background, IL-3 knockout offers a tool to dissect non-canonical roles of this cytokine in bone malignancies. Although 143B cells are not typically IL-3-dependent, autocrine or paracrine IL-3 signaling may influence tumor cell behavior and stromal cross-talk. Eliminating IL-3 expression potentially alters JAK2/STAT5 and AKT/ERK signaling, impacting proliferation, apoptosis, or secretion of factors that modify the microenvironment. This model enables investigation of how loss of IL-3-driven pathways affects osteosarcoma progression and interactions with infiltrating immune or hematopoietic cells.
Applications include dissecting IL-3-dependent JAK/STAT and MAPK signaling in osteosarcoma, exploring cytokine-mediated tumor-immune crosstalk, and cancer immunotherapy research. Representative assays such as Western blotting, RT-qPCR, and ELISA quantify pathway changes, while co-culture colony-forming assays assess hematopoietic support. RNA-seq and phospho-kinase arrays provide high-resolution pathway mapping. The cells are also useful for drug discovery targeting the IL-3/IL-3 receptor axis. For technical inquiries, please contact Ascent Research.
