The BRD8 Knockout 143B Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human osteosarcoma 143B cell line, in which the BRD8 gene has been disrupted by CRISPR/Cas9-mediated gene disruption. This heterogeneous population serves as a loss-of-function model for investigating BRD8-dependent roles in chromatin remodeling, transcriptional regulation, and cancer cell biology.
The 143B cell line is a widely used model of human osteosarcoma, originally derived from a HOS (TE-85) tumor. These adherent cells carry a TP53 mutation, rendering them deficient in wild-type p53 function, and are tumorigenic in nude mice. The TP53-mutant background makes 143B cells particularly useful for studying p53-independent mechanisms and for evaluating therapeutic strategies in bone cancer.
BRD8 encodes a bromodomain-containing subunit of the NuA4/TIP60 histone acetyltransferase and SRCAP chromatin remodeling complexes. Its bromodomain recognizes acetylated histone H4, facilitating complex targeting to chromatin. BRD8 functions as a transcriptional coactivator for SREBP-1a, driving expression of lipogenic genes such as FASN and SCD1 during adipogenesis. In the DNA damage response, BRD8 participates in ATM/ATR signaling, modulating p53 acetylation and stability, and consequently influencing CDKN1A expression. Additional interacting partners include TIP60, EP400, TRRAP, MORF4L1, and H2A.Z, linking BRD8 to histone modification, H2A.Z deposition, and DNA double-strand break repair.
In the TP53-mutant 143B background, BRD8 knockout allows dissection of p53-independent functions in tumor cell proliferation, metabolic reprogramming, and genomic maintenance. Disruption of BRD8 is expected to impair SREBP-1a-mediated lipogenesis, potentially perturbing membrane lipid synthesis and sensitizing cells to metabolic stress. Additionally, loss of BRD8 may alter NuA4/TIP60 complex activity, leading to changes in histone H4 acetylation and H2A.Z deposition, which can affect DNA repair and senescence pathways independently of p53. This model is thus valuable for studying the intersection of chromatin remodeling, metabolism, and DNA damage responses in osteosarcoma and broader cancer contexts.
This polyclonal knockout cell product is designed for diverse research applications, including cancer cell proliferation and colony formation assays, adipogenic differentiation evaluated by Oil Red O staining, and DNA damage response studies using flow cytometry and apoptosis assays. It is also suitable for ChIP-qPCR to profile histone modifications, drug sensitivity screens targeting lipogenesis or DNA repair pathways, and RNA-seq-based transcriptomic analyses to identify BRD8-dependent gene networks. For further technical information, pricing, or to discuss custom cell engineering, please contact Ascent Research.
