The FGFR2 Knockout KYSE-510 Cell Line is a CRISPR/Cas9-edited knockout cell line engineered for loss-of-function analysis of the fibroblast growth factor receptor 2 (FGFR2) gene. This product provides a targeted disruption of FGFR2 in a human esophageal squamous cell carcinoma background, enabling researchers to dissect its functional roles in oncogenic signaling, proliferation, and epithelial-mesenchymal transition. The knockout model serves as a robust tool for studying FGFR2-dependent pathways and validating therapeutic targets.
The host cell line, KYSE-510, is a well-characterized human esophageal squamous cell carcinoma (ESCC) line derived from an epithelial tumor. It retains key characteristics of esophageal cancer, making it an ideal model for investigating molecular mechanisms driving ESCC pathogenesis. KYSE-510 cells exhibit typical epithelial morphology and are commonly used in cancer biology research, particularly in studies of cell signaling, drug response, and metastasis. The availability of the FGFR2 knockout in this background offers a disease-relevant context for functional studies.
FGFR2 encodes a receptor tyrosine kinase that mediates cellular responses to fibroblast growth factors (FGFs), including FGF1, FGF2, FGF7, and FGF10. Upon ligand binding and receptor dimerization, FGFR2 activates multiple downstream signaling cascades through phosphorylation of adaptor proteins such as FRS2 and GRB2. This triggers the RAS?CRAF?CMEK?CERK pathway and the PI3K?CAKT?CmTOR axis, while also engaging PLC?? and STAT signaling. These pathways converge on transcriptional regulators like cyclin D1, MYC, SNAI1, and TWIST1, driving proliferation, survival, and epithelial-mesenchymal transition (EMT). FGFR2 activity is modulated by interacting factors including heparin/heparan sulfate, and it can form heterodimers with FGFR1.
In esophageal squamous cell carcinoma, FGFR2 signaling contributes to tumorigenicity and aggressive cellular behaviors. Knockout of FGFR2 in KYSE-510 cells is anticipated to attenuate MAPK/ERK and PI3K/AKT pathway activation, thereby reducing cell proliferation, migration, and EMT potential. This model is particularly valuable for elucidating FGFR2??s role in ESCC and for exploring its functional significance in other FGFR2-associated malignancies such as gastric, breast, and lung cancers. The loss-of-function context enables dissection of FGFR2-specific signaling versus compensatory mechanisms.
Researchers can employ this knockout line in a variety of experimental setups, including western blotting to assess downstream phospho-protein levels (e.g., phospho-ERK, phospho-AKT), RT-qPCR for transcriptional changes, and functional assays such as MTT/CCK-8 proliferation assays or Transwell migration/invasion studies. The line also facilitates drug sensitivity profiling with FGFR inhibitors like AZD4547 and erdafitinib, and can be integrated into RNA-seq or flow cytometry workflows to probe global transcriptomic and cell cycle alterations. For further information or customized inquiries, please contact Ascent Research.
