The IL3 Knockout HGC-27 Polyclonal Cells product comprises a CRISPR/Cas9-edited polyclonal knockout population of HGC-27 gastric carcinoma cells with targeted disruption of the IL3 gene. This cell pool provides a heterogeneous loss-of-function model that recapitulates diverse allelic editing events, enabling robust functional studies without clonal bias. The knockout strategy abolishes IL-3 expression, allowing researchers to interrogate IL-3-dependent signaling cascades and downstream biological processes in a gastric cancer background.
HGC-27 is a human epithelial cell line originating from the lymph node metastasis of a gastric adenocarcinoma. As a well-characterized model of gastric cancer progression, HGC-27 retains key features of metastatic epithelial cells and is widely utilized for studying tumor invasion, metastasis, and the tumor microenvironment. Its derivation from a metastatic site makes it particularly suitable for investigating molecular mechanisms of lymphatic dissemination and the role of cytokine networks in disease advancement.
IL-3 is a hematopoietic growth factor that stimulates the differentiation and proliferation of multipotent hematopoietic stem cells and committed myeloid, erythroid, and lymphoid progenitors. Mechanistically, IL-3 binds to the heterodimeric receptor composed of IL3RA and CSF2RB, triggering JAK2-mediated phosphorylation of STAT5. Activated STAT5 translocates to the nucleus and upregulates target genes such as BCL2, MYC, PIM1, and CCND1, thereby promoting cell survival and proliferation. Concurrently, IL-3R engagement recruits the adaptor proteins SHC1 and GRB2, which activate the RAS?CRAF?CMEK?CERK mitogenic cascade, and PIK3R1, which stimulates PI3K?CAKT pro-survival signaling. Upstream, IL-3 expression is induced by T-cell receptor stimulation, calcium flux, NF-??B, AP-1 transcription factors, and interleukin-1, predominantly in activated T cells and immune cells.
In the context of HGC-27 gastric carcinoma cells, the IL3 knockout model provides a unique platform to dissect IL-3-mediated signaling within the tumor microenvironment. While IL-3 is classically associated with hematopoiesis, aberrant IL-3 production or signaling has been observed in solid tumors and may influence cancer cell growth, immune evasion, and metastatic niche formation. This polyclonal knockout population enables the investigation of autocrine or paracrine IL-3 effects on gastric cancer cell biology and the interaction between tumor cells and the surrounding stromal or immune components, particularly in lymph node metastasis research.
These polyclonal IL3-knockout HGC-27 cells enable detailed analysis of JAK-STAT, MAPK, and PI3K-AKT signaling, drug screening for gastric and hematologic cancers, cytokine signaling perturbation, and tumor microenvironment studies. Typical assays include Western blotting for phospho-STAT5, RT-qPCR for BCL2 and MYC, flow cytometry, proliferation and apoptosis assays, colony-forming units, and RNA-seq transcriptomic profiling. For technical inquiries, please contact Ascent Research.
