BAP1 Knockout CAL-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the CAL-27 human tongue squamous cell carcinoma cell line. This heterogeneous pool contains cells with diverse disruptions in the BAP1 gene, generating a loss-of-function model for studying the tumor suppressor deubiquitinase BAP1. The polyclonal format preserves genetic diversity and avoids clonal selection, making it suitable for experiments where a mixed knockout population is advantageous.
The CAL-27 cell line is an established epithelial model derived from a male patient with tongue squamous cell carcinoma. These adherent cells exhibit epithelial-like morphology and are widely used in cancer research, including studies of tumor biology, metastasis, and drug sensitivity. The CAL-27 background provides a physiologically relevant platform for investigating the impact of BAP1 loss in the context of head and neck squamous cell carcinoma, a malignancy in which BAP1 alterations have been implicated. The cells retain key characteristics of the original tumor and are ideal for in vitro functional assays.
BAP1 functions as a nuclear deubiquitinase that specifically removes monoubiquitin from histone H2A at lysine 119 (H2AK119ub), a mark deposited by the Polycomb repressive complex 1. By deubiquitinating H2AK119ub, BAP1 relieves transcriptional repression and promotes the expression of genes critical for DNA repair (e.g., BRCA1, RAD51), cell cycle arrest (e.g., CDKN2A), and apoptosis (e.g., BCL2L11). BAP1 activity is regulated upstream by BRCA1, p53, and ATM, and it forms multi-protein complexes with ASXL1, ASXL2, HCF-1, and FOXK1/2, among others. Additionally, BAP1 interacts with BARD1 and OGT, which modulate its deubiquitinase function and substrate targeting. Loss of BAP1 results in accumulation of H2AK119ub, leading to epigenetic silencing of tumor suppressor genes, impaired DNA damage repair, and increased genomic instability, thereby promoting oncogenesis.
In the CAL-27 tongue carcinoma model, disruption of BAP1 provides a powerful system to dissect its tumor-suppressive roles in an epithelial malignancy context. Given that BAP1 mutations are prevalent in aggressive cancers such as uveal melanoma, malignant mesothelioma, and clear cell renal cell carcinoma, this knockout model helps delineate conserved mechanisms of BAP1-driven tumorigenesis. Researchers can utilize this model to explore how BAP1 loss alters chromatin dynamics, DNA damage responses, and apoptotic thresholds in squamous cell carcinoma, which may inform therapeutic strategies targeting BAP1-deficient tumors. The combination of the CAL-27 background with BAP1 knockout enables investigations into synthetic lethal interactions and drug sensitivity profiles relevant to head and neck cancers and beyond.
This polyclonal BAP1 knockout pool supports a variety of research applications, including functional genomics, cancer cell biology, tumor suppressor studies, and DNA repair analysis. Representative assays include Western blotting, RT-qPCR, immunofluorescence, ChIP-qPCR, flow cytometry, proliferation, clonogenic, migration, and comet assays, as well as co-immunoprecipitation and drug sensitivity testing. For further details, please contact Ascent Research.
