The BICC1 Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population in which the BICC1 gene has been disrupted. This polyclonal pool provides a loss-of-function model for studying BICC1-dependent processes without single-cell cloning, offering a heterogeneous knockout background suitable for pooled screening applications.
HAP1 is a human near-haploid cell line derived from the chronic myeloid leukemia line KBM-7. It displays adherent, fibroblast-like morphology and is widely used in functional genomics because its near-haploid karyotype eliminates diploid genetic compensation, enabling unambiguous assessment of gene function in signaling studies and drug target validation.
The BICC1 gene encodes an RNA-binding protein that functions as a translational repressor of DVL2 mRNA by binding its 3?? UTR, thereby limiting DVL2 protein synthesis. DVL2 is a key cytoplasmic phosphoprotein transducing signals from Frizzled receptors in both Wnt/??-catenin and planar cell polarity (PCP) pathways. Consequently, BICC1 negatively regulates Wnt5a-induced ??-catenin nuclear accumulation and PCP components such as Vangl2 and Prickle. BICC1 interacts with Dishevelled isoforms (DVL1/2/3) and the RNA-binding protein DAZAP1, integrating signals from upstream factors like TGF-??1 and HNF1??. Loss of BICC1 results in elevated DVL2, sustained ??-catenin activity, and disruption of PCP-dependent processes.
In the HAP1 near-haploid leukemia background, BICC1 disruption provides a direct model to investigate how aberrant Wnt/PCP signaling contributes to oncogenic processes. Given BICC1’s roles in renal development and colorectal cancer, these knockout cells bridge developmental signaling and cancer biology. The near-haploid state ensures that gene disruption effects are not masked by a second allele, facilitating quantitative assessment of DVL2 protein changes, ??-catenin transcriptional activity, and sensitivity to Wnt pathway modulators.
These polyclonal BICC1-knockout HAP1 cells are suitable for functional dissection of Wnt/PCP signaling, investigation of DVL2-dependent gene expression, and drug sensitivity profiling with Wnt inhibitors. Representative assays include western blotting for DVL2 and ??-catenin, RT-qPCR for DVL2 mRNA, TOPFlash luciferase reporter assays, immunofluorescence detection of DVL2, wound healing migration assays, and apoptosis or viability assays with small-molecule Wnt antagonists. The polyclonal format facilitates high-throughput genetic and chemical screens. For additional information, please contact Ascent Research.
