The HOXC9 Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the human near-haploid HAP1 cell line. Engineered to disrupt the HOXC9 gene, this product provides a loss-of-function model that avoids single-cell cloning biases, enabling robust population-level analysis of HOXC9-mediated processes.
HAP1 cells originate from the KBM-7 chronic myeloid leukemia line and maintain a largely haploid karyotype, which facilitates direct genotype-phenotype correlation. Notably, they lack functional p53, altering apoptosis and cell-cycle checkpoints and making them a valuable platform for cancer biology and genetic dependency studies. The haploid genomic configuration enhances knockout penetrance in the polyclonal pool, as a single CRISPR editing event abolishes gene function in most cells.
HOXC9 is a homeodomain transcription factor that binds AT-rich DNA motifs in complex with PBX and MEIS cofactors, regulating target genes involved in proliferation, migration, and differentiation. Its activity is controlled by retinoic acid, WNT3A, and FGF8 signaling, and it cooperates with CDX1, PBX1, and MEIS1. HOXC9 recruits coactivators CREBBP and EP300 to drive expression of downstream effectors such as CDH2, ITGA5, BDNF, and BCL2, and it may indirectly influence p53 pathways. Disruption of HOXC9 in HAP1 cells accordingly alters cell adhesion, motility, and survival signaling.
HOXC9 dysregulation has been implicated in breast cancer, lung adenocarcinoma, colorectal cancer, and acute myeloid leukemia, where it may exert oncogenic or tumor-suppressive functions. The HAP1 knockout model, with its p53-deficient background, permits investigation of HOXC9-dependent proliferation, migration, and apoptosis without confounding secondary mutations. The near-haploid state ensures that knockout effects are unmasked, providing a sensitive system for dissecting context-specific roles of HOXC9 in tumorigenesis and developmental anomalies.
The polyclonal KO cells are suited for functional genomics, cancer cell biology, and drug target validation. Typical assays include RT-qPCR and RNA-seq for target gene analysis, MTT and BrdU proliferation assays, transwell migration/invasion studies, ChIP-qPCR, and luciferase reporter assays for Wnt/??-catenin and TGF-?? pathway activity. Immunofluorescence and high-content imaging can further characterize subcellular protein distribution. Researchers studying limb development or retinoic acid signaling can also employ the model to explore Hox gene networks. For additional information or to request a quote, please contact Ascent Research.
