The BAP1 Knockout KYSE-150 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population designed for targeted disruption of the BAP1 gene in human KYSE-150 esophageal squamous cell carcinoma cells. This polyclonal format provides a heterogeneous loss-of-function model derived from a well-characterized cancer cell line, intended for rigorous investigation of BAP1 tumor suppressor functions.
KYSE-150 is a human esophageal squamous cell carcinoma cell line established from a well-differentiated primary tumor, exhibiting adherent epithelial morphology. As a model of esophageal epithelial cancer, this cell line retains key features of malignant transformation and is widely used to study molecular mechanisms underlying esophageal carcinogenesis, including genomic instability, aberrant signaling, and therapeutic resistance.
BAP1 functions as a nuclear deubiquitinase enzyme that specifically removes monoubiquitin from lysine 119 of histone H2A (H2A-K119ub1), a modification critical for regulating gene expression and chromatin structure. Acting as a tumor suppressor, BAP1 coordinates DNA repair through interactions with BRCA1 and the Polycomb repressive complex, facilitating homologous recombination and transcriptional control. BAP1 forms multiprotein complexes with ASXL1/2, FOXK1/2, HCFC1, and other chromatin-associated factors, and its activity is responsive to DNA damage signals mediated by ATM and ATR kinases. Downstream, BAP1 modulates targets including the chromatin remodeler INO80 and cell cycle regulators such as p21, thereby influencing DNA repair fidelity, apoptosis, and cell cycle progression.
In esophageal squamous cell carcinoma, BAP1 loss or inactivation is associated with impaired DNA damage response and increased genomic instability, promoting tumor progression. The KYSE-150 polyclonal knockout model enables the dissection of BAP1-dependent mechanisms in a relevant esophageal cancer background, where BAP1??s role in chromatin remodeling and DNA repair can be directly examined. This model is particularly valuable for investigating how BAP1 deficiency alters sensitivity to DNA-damaging agents, such as platinum-based chemotherapeutics, and for exploring synthetic lethal interactions with other DNA repair pathways.
Researchers can employ this knockout cell population for a range of functional assays, including Western blotting, RT-qPCR, and RNA-seq to validate protein expression and transcriptional changes. Chromatin immunoprecipitation with qPCR (ChIP-qPCR) and co-immunoprecipitation enable analysis of BAP1-containing complexes and histone modification dynamics. Drug sensitivity assays, such as cisplatin treatment followed by flow cytometry for apoptosis or cell cycle analysis, facilitate evaluation of chemotherapeutic response. Additionally, migration and invasion assays provide insights into BAP1-dependent metastatic potential. These applications support advanced studies in tumor suppressor biology, DNA repair, and drug discovery. For further information, please contact Ascent Research.
