The BCL11B Knockout A2780 Polyclonal Cells are a CRISPR/Cas9-mediated polyclonal knockout cell population derived from the human ovarian carcinoma cell line A2780. This product enables loss-of-function studies for BCL11B, a C2H2-type zinc finger transcription factor that acts as a context-dependent transcriptional repressor or activator. The polyclonal population consists of a heterogeneous pool of cells with targeted gene disruption introduced by CRISPR/Cas9 editing, providing a robust model for investigating BCL11B function without the selection biases of single-cell cloning. This knockout model is designed for use in a variety of downstream molecular and cellular assays relevant to cancer biology and signal transduction research.
The A2780 host cell line is an epithelial cell line originally derived from an untreated patient with ovarian carcinoma. It is widely adopted as a model system for studying ovarian cancer biology, including drug resistance mechanisms and sensitivity to chemotherapeutic agents. A2780 cells exhibit adherent growth and maintain key signaling pathways that are frequently dysregulated in ovarian cancer, making them a suitable background for probing the function of tumor-associated genes.
BCL11B is a critical transcription factor that operates downstream of the Notch signaling pathway, where it is activated by the Notch1 intracellular domain and relays signals to modulate gene expression programs. It also intersects with the Wnt, T-cell receptor, TGF-beta, and MAPK pathways. BCL11B interacts with several co-regulators, including components of the NuRD complex, HDAC1/2, SIRT1, SATB1, and RUNX1, to mediate transcriptional repression or activation. Key downstream targets directly or indirectly regulated by BCL11B include the cell cycle regulator CDKN1A (p21), the anti-apoptotic factor BCL2L1, the pro-apoptotic BAX, and the immune cytokine IL2. Through these molecular interactions, BCL11B shapes cellular outcomes such as proliferation, apoptosis, and differentiation.
In the A2780 ovarian carcinoma background, knockout of BCL11B is expected to perturb the transcriptional networks controlling cell cycle progression and apoptotic thresholds. Loss of BCL11B may lead to altered expression of CDKN1A and BCL2L1, thereby modulating sensitivity to DNA-damaging chemotherapeutics and other apoptotic stimuli. This model thus provides a valuable tool for dissecting BCL11B??s potential tumor suppressor functions in ovarian cancer and for exploring its role in Notch-dependent drug resistance mechanisms. The polyclonal nature of the knockout population allows for the assessment of heterogeneous cellular responses, mimicking tumor heterogeneity.
Researchers can employ this knockout model in a range of experimental workflows to study BCL11B-dependent processes. Applications include investigating transcription factor function in ovarian cancer, Notch signaling dynamics, apoptosis regulation, and drug sensitivity mechanisms. Compatible assays include Western blotting to confirm BCL11B protein loss, RT-qPCR for transcriptional changes of downstream targets such as CDKN1A and BCL2L1, flow cytometry for apoptosis markers, MTT-based proliferation assays, drug sensitivity testing, and transcriptome-wide profiling by RNA-seq. Chromatin immunoprecipitation (ChIP-qPCR) can be used to examine BCL11B binding at target loci in wild-type controls. For researchers seeking a robust polyclonal knockout model to advance ovarian cancer studies, Ascent Research welcomes inquiries about this product.
