The IGF2BP3 Knockout UM-UC-3 Polyclonal Cells product is a CRISPR/Cas9-edited polyclonal knockout cell population derived from the UM-UC-3 human cell line. This tool enables loss-of-function studies of the IGF2BP3 gene, which encodes an RNA-binding protein implicated in post-transcriptional regulation. By disrupting the IGF2BP3 locus via CRISPR/Cas9, the resulting polyclonal mixture eliminates functional protein expression and allows researchers to interrogate gene function in a relevant cellular context. The polyclonal format provides a robust population that can be used directly in functional assays, minimizing clonal variability.
UM-UC-3 is a well-characterized transitional cell carcinoma (TCC) cell line originally established from a male patient with bladder cancer. It serves as a representative model of high-grade urothelial carcinoma, widely employed in studies of bladder cancer biology, drug response, and metastasis. The line exhibits hallmark features of epithelial-to-mesenchymal transition (EMT) and invasive behavior, making it particularly suitable for investigating the molecular drivers of tumor progression.
IGF2BP3 functions as a key regulator of mRNA fate by binding to and stabilizing target transcripts, enhancing their translation. It is transcriptionally activated by MYC and ??-catenin/TCF signaling, and its expression is further induced by hypoxia-inducible factors. Among its validated mRNA targets are CD44, MYC, IGF2, HMGA2, and SNAI1, which encode proteins that promote proliferation, survival, and EMT. IGF2BP3 physically interacts with translation initiation factors such as EIF4E and PABPC1, as well as the RNA-binding protein YBX1, to form mRNP complexes; it is also subject to regulation by microRNAs. Through these interactions, IGF2BP3 orchestrates post-transcriptional networks that drive oncogenic phenotypes.
In the UM-UC-3 bladder cancer model, knockout of IGF2BP3 is expected to destabilize key oncogenic mRNAs, leading to reduced cell proliferation, attenuated migratory and invasive capacities, and diminished EMT traits. This system provides a clinically relevant platform for dissecting the contribution of IGF2BP3 to urothelial carcinoma aggressiveness and therapy resistance. Because UM-UC-3 retains the genetic background of a human tumor, the polyclonal knockout population reflects heterogeneity that more closely mimics patient-derived scenarios.
Researchers can deploy this model in a wide range of experimental workflows, including Western blotting to confirm IGF2BP3 ablation, RT-qPCR and RNA-seq to quantify transcriptome-wide changes in mRNA stability, and RNA immunoprecipitation (RIP) to map RNA-protein interactions. Functional assays such as cell proliferation, migration, and invasion assays allow direct assessment of phenotypic consequences. Additionally, the knockout population can serve as a comparator for drug sensitivity screening against standard-of-care chemotherapeutics or targeted agents, facilitating preclinical validation of IGF2BP3 as a therapeutic node. For further information, technical support, or custom configuration requests, please contact Ascent Research.
