The IGFBP5 Knockout LoVo Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population targeting the IGFBP5 gene in the LoVo human colorectal adenocarcinoma cell line. This loss-of-function model provides a genetically disrupted pool for studying IGFBP5-dependent signaling, proliferation, apoptosis, and migration in a metastatic cancer context.
The LoVo parental line originated from a supraclavicular lymph node metastasis of colon adenocarcinoma in a 56-year-old Caucasian male. With adherent epithelial morphology and tumorigenic properties, LoVo cells are widely used to model colorectal cancer metastasis and invasion. The inclusion of IGFBP5 knockout in this background enables direct assessment of gene function in a clinically relevant metastatic system.
IGFBP5 is a member of the insulin-like growth factor binding protein family that modulates IGF bioavailability by binding IGF1 and IGF2 with high affinity. It also exerts IGF-independent functions in apoptosis, senescence, and cell migration through interactions with integrins, heparin, and SERPINE1. Upstream, TP53, TGFB1, and TNF transcriptionally regulate IGFBP5, while downstream it influences BAX/BCL2-mediated apoptosis, ITGB1 integrin signaling, and MMP2/MMP9-mediated matrix remodeling. Disruption of IGFBP5 alters signaling through the IGF1-IGF1R-IRS1-AKT1-MAPK1 axis and impinges on CTNNB1-dependent Wnt pathway activity, thereby removing a regulatory node that integrates p53, TGF-beta, and IGF signaling.
In colorectal cancer, IGFBP5 can function as a tumor suppressor or promoter depending on molecular context. The LoVo knockout system allows dissection of these opposing roles by measuring effects on cell proliferation, apoptotic response, and migratory capacity. As a metastatic epithelial line, LoVo is particularly suited for investigating IGFBP5’s impact on chemosensitivity, epithelial-mesenchymal transition, and metastatic colonization, and for revealing adaptive signaling mechanisms that circumvent IGF pathway inhibition.
Standard applications include Western blotting and RT-qPCR for expression analysis, MTT or BrdU proliferation assays, Annexin V apoptosis assays, and Transwell migration/invasion assays. Phospho-AKT and phospho-ERK pathway readouts facilitate investigation of IGF signaling crosstalk. The model supports drug sensitivity screening against IGF1R inhibitors and functional genomic studies of IGFBP5 in colorectal cancer progression. For additional technical details, please contact Ascent Research.
