The IGFBP5 Knockout UM-UC-3 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population of the UM-UC-3 human bladder carcinoma cell line, with targeted disruption of the IGFBP5 gene encoding insulin-like growth factor-binding protein 5. This pool of diverse IGFBP5-modified cells provides a loss-of-function model for studying average gene-knockout effects without clonal artifacts. IGFBP5 knockout disrupts modulation of insulin-like growth factor (IGF) signaling, enabling investigation of tumorigenic processes driven by IGF-dependent and IGF-independent functions in bladder cancer.
UM-UC-3 is a well-established human transitional cell carcinoma line from a male patient with high-grade bladder cancer. It serves as a robust model, featuring wild-type p53, PTEN loss, and active PI3K/AKT and MAPK/ERK pathways, making it suitable for dissecting oncogenic signaling and drug responses. Dysregulation of IGF signaling is common in bladder carcinoma progression, positioning UM-UC-3 as a relevant context for interrogating IGFBP5 function.
IGFBP5 binds IGF1 and IGF2 with high affinity, modulating their bioavailability and receptor activation. It also exerts IGF-independent effects via interactions with extracellular matrix proteins such as vitronectin and osteopontin. Disruption of IGFBP5 in the UM-UC-3 knockout pool may alter downstream targets including IGF1R, AKT, ERK, the BCL2/BAX ratio, MMP9, and E-cadherin. Upstream regulators TP53 and TGFB1 link IGFBP5 to stress and TGF-?? signaling. Loss of IGFBP5 might relieve inhibition of IGF1R-mediated PI3K/AKT and MAPK/ERK pathways or disrupt tumor-suppressive functions, affecting proliferation, apoptosis, and migration.
In UM-UC-3, IGFBP5 knockout is significant for examining how IGF axis disruption contributes to malignancy. IGFBP5 can be a context-dependent tumor suppressor or promoter; its loss may enhance AKT and ERK signaling, promote EMT via E-cadherin and MMP9 modulation, and influence chemosensitivity. The polyclonal knockout population enables assessment of IGFBP5 deficiency??s integrated biological effects, supporting robust comparisons with wild-type controls in functional assays.
This product suits bladder cancer biology, IGF signaling studies, migration/invasion (Boyden chamber), proliferation (MTT), apoptosis (Annexin V/PI), and drug resistance profiling. Assays include Western blotting for phospho-AKT and phospho-ERK, RT-qPCR for IGFBP5, co-IP for IGF1?CIGFBP5 interactions, and RNA-seq. These tools facilitate mechanistic dissection of IGFBP5 function and therapeutic vulnerability identification in urothelial carcinoma. For technical inquiries, please contact Ascent Research.
