The BCL11B Knockout Ca Ski Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population in the Ca Ski human cervical carcinoma epithelial cell line, designed to disrupt the BCL11B gene. This polyclonal knockout model provides a heterogeneous pool of cells with targeted gene disruption, enabling loss-of-function studies of BCL11B in a HPV-driven cervical cancer context. The product is supplied as a live cell population, suitable for immediate culture and downstream assays, and is intended for advanced biomedical research applications requiring a robust genetic knockout system without clonal isolation.
The Ca Ski cell line is an adherent epithelial cell line derived from a metastatic cervical squamous cell carcinoma, maintaining integrated HPV-16 and HPV-18 genomes. This well-characterized model recapitulates key features of HPV-related carcinogenesis, including expression of viral oncoproteins E6 and E7 that inactivate host tumor suppressors p53 and pRb. The HPV-positive background makes Ca Ski cells particularly valuable for studying the interplay between viral oncogenesis and host cell regulatory networks, including those governed by BCL11B.
BCL11B encodes a C2H2-type zinc finger transcription factor that functions primarily as a transcriptional repressor and tumor suppressor. It is regulated by upstream signals including Notch1, IL-7, TGF-??, T-bet, and NF-??B, and it represses transcription of downstream targets such as CDKN1A (p21) and BAX, while also modulating expression of BCL2, IL2, and CCR9. BCL11B interacts with chromatin-modifying complexes containing BCL6, HDAC1, HDAC2, MTA2, SATB1, and the NuRD complex, thereby coordinating histone deacetylation and nucleosome remodeling. Through these interactions, BCL11B integrates signals from the Notch, T-cell receptor, Wnt/??-catenin, and TGF-?? pathways to control apoptosis and cell cycle progression.
In Ca Ski cells, BCL11B knockout ablates its transcriptional repression, leading to derepression of pro-apoptotic (BAX) and cell cycle inhibitor (CDKN1A) genes, as outlined by the representative pathway Notch1??HES1??BCL11B?CDKN1A/BAX. This disruption offers a unique system to dissect BCL11B??s tumor suppressor functions in an HPV-positive cervical cancer model, where its loss may collaborate with viral oncoproteins to promote malignancy. The model further enables investigation of how BCL11B-dependent chromatin regulation affects HPV gene expression and host cell transformation.
This BCL11B knockout model is designed for diverse research applications, including HPV-related cancer gene regulation studies, transcription factor mechanism dissection, drug target validation, and apoptosis pathway analysis. It is compatible with a variety of representative assays such as Western blotting, RT-qPCR, ChIP-qPCR, flow cytometry, apoptosis detection, migration and invasion assays, and colony formation assays. For additional information or custom inquiries, please contact Ascent Research.
