The BRD8 Knockout SK-OV-3 Polyclonal Cells product comprises a polyclonal population of SK-OV-3 ovarian adenocarcinoma cells engineered by CRISPR/Cas9-mediated disruption of the BRD8 gene. This heterogeneous cell pool provides a versatile loss-of-function model for investigating BRD8-dependent processes without the bias of clonal selection, enabling robust functional studies in a disease-relevant context.
SK-OV-3 is a well-characterized human ovarian adenocarcinoma cell line originally isolated from ascitic fluid of a patient with ovarian cancer. Widely employed as a model for ovarian cancer research, this cell line recapitulates key features of tumor biology, including proliferation, invasion, and chemoresistance. Its epithelial origin and genomic landscape render it a suitable host for examining epigenetic regulators implicated in ovarian malignancy.
BRD8 encodes a bromodomain-containing scaffold protein that functions as an integral subunit of the NuA4/TIP60 histone acetyltransferase complex. Within this multiprotein assembly, BRD8 interacts directly with EP400, TRRAP, KAT5 (TIP60), RUVBL1, RUVBL2, and YEATS4 to coordinate the acetylation of histone H4 and H2A.Z. This activity promotes an open chromatin conformation and facilitates the transcriptional activation of genes governing cell cycle progression and DNA damage repair. Upstream signals from transcriptional activators and cell cycle regulators converge on the complex, while downstream consequences include elevated histone H4 acetylation and enhanced expression of proliferation-associated genes. Disruption of BRD8 via CRISPR/Cas9 impairs NuA4 complex integrity, leading to diminished histone acetylation and proliferative defects.
In the SK-OV-3 ovarian cancer background, BRD8 knockout allows dissection of epigenetic dependencies that sustain malignant phenotypes. Loss of BRD8 function reduces histone H4 acetylation, potentially sensitizing cells to DNA-damaging agents or inducing growth arrest. This model thus links NuA4-mediated chromatin remodeling directly to ovarian cancer cell fitness, providing a platform to explore BRD8 as a therapeutic vulnerability.
Researchers can utilize this polyclonal knockout population for diverse experimental applications, including chromatin immunoprecipitation (ChIP) to assess histone H4 acetylation occupancy, western blotting to monitor changes in acetylation marks, RT-qPCR to quantify expression of BRD8 target genes, proliferation assays, and flow cytometry-based cell cycle analysis. The model also supports drug target validation and investigation of chemoresistance mechanisms. For further information or technical assistance, please contact Ascent Research.
