The HCFC1R1 Knockout UM-UC-3 Polyclonal Cells comprise a CRISPR/Cas9-mediated polyclonal knockout population derived from UM-UC-3 human bladder cancer cells, in which the HCFC1R1 gene has been disrupted. This product delivers a heterogeneous pool of loss-of-function alleles, preserving population diversity without clonal selection. It serves as a reproducible model for investigating HCFC1R1-dependent oncogenic signaling in bladder cancer, free from single-cell clonal bias. The polyclonal format is advantageous for pooled functional genomics and pharmacological assays where uniform genetic representation is critical.
The UM-UC-3 parental cell line is a widely utilized model of human transitional cell carcinoma, originally derived from a high-grade invasive bladder tumor. These cells exhibit hallmark features of aggressive urothelial cancer, including robust proliferation, anchorage-independent growth, and tumor formation in xenograft models. UM-UC-3 cells maintain epithelial marker expression and respond to growth factors such as epidermal growth factor (EGF) and hormones, providing a physiologically relevant background for studying genes implicated in bladder cancer initiation, progression, and therapeutic resistance.
HCFC1R1 (HPIP) is a scaffold protein that assembles complexes with HCF-1, ER??, ??-catenin, and SRC to relay signals from estrogen, EGF, Sp1, and miR-148a. It amplifies Wnt/??-catenin signaling by stabilizing ??-catenin and activating TCF/LEF transcription, while concurrently boosting PI3K/AKT and MAPK/Erk activity. These pathways converge to upregulate c-Myc, Cyclin D1, and MMP9, promoting proliferation, survival, and migration. HCFC1R1 thus functions as a master coordinator of tumor-promoting networks.
In UM-UC-3 cells, HCFC1R1 knockout disrupts these oncogenic circuits. It attenuates estrogen- and EGF-induced AKT and Erk phosphorylation, reduces ??-catenin nuclear accumulation and TCF/LEF activity, and downregulates Cyclin D1 and MMP9. Consequently, knockout cells show diminished proliferation and migration in transwell and wound healing assays. This model recapitulates the effects of inhibiting PI3K/AKT and Wnt pathways, underscoring HCFC1R1??s role in sustaining bladder cancer malignancy and providing a platform for preclinical drug testing.
Researchers can employ these polyclonal knockout cells for signaling analysis via Western blot, RT-qPCR, and RNA-seq; functional phenotyping with proliferation, transwell, and wound healing assays; and protein interaction studies using co-immunoprecipitation and immunofluorescence to evaluate HCFC1R1 partners like ??-catenin and ER??. The model supports drug target validation, EMT research, and synthetic lethality screens. The polyclonal nature ensures representative allele coverage, enhancing the reliability of bulk assays. For further technical details, please contact Ascent Research.
