The BCL11B Knockout 143B Polyclonal Cells represent a genetically engineered loss-of-function model generated by CRISPR/Cas9-mediated disruption of the BCL11B gene in the human 143B osteosarcoma cell line. This product is supplied as a polyclonal knockout cell population, providing a heterogeneous pool of edited cells suitable for experiments where clonal isolation is not required. The targeted gene disruption enables functional interrogation of BCL11B-dependent transcriptional networks and cellular phenotypes within a bone cancer context.
The parental 143B cell line is a highly tumorigenic and metastatic human osteosarcoma model originally derived from a patient with osteosarcoma. These malignant bone-forming cells are extensively used to study the molecular mechanisms driving osteosarcoma pathogenesis, invasion, and metastatic dissemination. Their aggressive behavior in vitro and in vivo makes them a robust platform for evaluating gene function and therapeutic interventions relevant to bone oncology.
BCL11B encodes a zinc finger transcription factor with pleiotropic roles in cell fate determination. It acts downstream of Notch and TCF7, is regulated by GATA3 and IL-7 signaling, and exerts transcriptional control over key downstream targets including CDKN1A, BCL2L1, CD4, CD8, and RUNX3. BCL11B interacts with cofactors such as BCL11A, HDAC1, HDAC2, CTBP1, and COUP-TF II to modulate chromatin state and gene expression. These molecular connections position BCL11B as a nodal regulator integrating signals from T-cell receptor signaling, Notch signaling, and the p53 pathway to influence cell cycle progression, apoptosis, and differentiation programs.
In the 143B osteosarcoma context, loss of BCL11B likely disrupts its ability to regulate cell proliferation and survival genes, potentially impairing tumor cell growth and sensitizing cells to apoptotic stimuli. The knockout may also alter differentiation-related gene expression, providing a system to dissect how BCL11B’s transcriptional activity contributes to osteosarcoma maintenance. This model is particularly relevant for investigating the proposed tumor suppressor functions of BCL11B in non-hematopoietic malignancies, as it overrides endogenous expression in a bone cancer environment.
Researchers can apply this polyclonal knockout population to a wide range of studies, including mechanistic investigations of BCL11B in osteosarcoma cell biology, functional analyses of its role in transcriptional regulation, and comparative assessments of cell proliferation and apoptosis via MTT, BrdU, Annexin V, or caspase-3 assays. The model supports drug screening efforts targeting BCL11B-related pathways, as well as migration and invasion assays. Downstream molecular phenotyping can be performed using Western blotting for BCL11B and its targets, RT-qPCR for gene expression, RNA-seq for transcriptomic profiling, and ChIP-qPCR to validate direct target gene occupancy. For further details on integrating this model into your osteosarcoma research program, please contact Ascent Research.
