The IGFBP5 Knockout HGC-27 Polyclonal Cells are a CRISPR/Cas9-mediated gene-disrupted polyclonal cell population in the HGC-27 human gastric carcinoma cell line. This loss-of-function model targets the IGFBP5 gene, enabling functional studies of IGFBP5 in a metastatic cancer context. Supplied as a heterogeneous knockout pool, the cells avoid clonal artifacts and are ready for downstream molecular and cellular assays.
HGC-27 is a gastric epithelial carcinoma cell line established from the lymph node metastasis of a 60-year-old female patient. It serves as a relevant model for studying gastric cancer progression, metastasis, and therapeutic resistance due to its metastatic origin and conserved signaling networks including IGF-1R, PI3K/AKT, and MAPK/ERK pathways.
IGFBP5 binds insulin-like growth factors (IGF-I/II), modulating their interaction with IGF-1R and thereby regulating PI3K/AKT and MAPK/ERK signaling cascades involved in proliferation, survival, and differentiation. Independently, IGFBP5 engages integrin ??v??3 to activate FAK and Src kinases, promoting cell adhesion and migration. Upstream regulators such as TGF-??, p53, and Wnt3a control IGFBP5 expression, while downstream effectors include AKT1, MAPK1/3 (ERK1/2), MMP-9, and CCND1. The protein also interacts with ALS, CTGF, and vitronectin, situating it at a critical interface between growth factor signaling and the extracellular matrix.
In HGC-27 cells, IGFBP5 knockout disrupts integration of IGF and integrin signaling, potentially reducing proliferation, survival, and metastatic traits. This model aids in dissecting contributions to pathways such as PI3K/AKT/mTOR, MAPK/ERK, p53/BAX/BCL2, and Wnt/??-catenin/TCF/LEF, and is valuable for investigating drug resistance and apoptotic evasion in gastric cancer. Furthermore, the model enables investigation of IGFBP5’s role in tumor-microenvironment crosstalk and integrin-mediated signal transduction.
The polyclonal knockout population is suitable for a range of functional assays, including proliferation (CCK-8, MTT), apoptosis (Annexin V/PI), migration and invasion (transwell, wound healing), colony formation, and xenograft tumor growth. These cells support detailed signaling analyses via western blotting, RT-qPCR, and immunofluorescence to probe downstream targets such as AKT1 and MMP-9, as well as drug sensitivity screening targeting IGF-1R, PI3K, or MAPK pathways. For technical support or inquiries, please contact Ascent Research.
