The BRD3 Knockout A-549 Polyclonal Cells product is a CRISPR/Cas9-edited polyclonal knockout cell population targeting the BRD3 gene in the human A-549 lung adenocarcinoma cell line. This loss-of-function model enables the study of BRD3-mediated transcriptional regulation in a cancer-relevant background. The polyclonal format provides a heterogeneous population, avoiding clonal artifacts while maintaining robust gene disruption across the culture.
The A-549 cell line is derived from a human lung adenocarcinoma and is a well-established model in non-small cell lung cancer (NSCLC) research. Its epithelial origin and extensive characterization for drug responses and signaling make it an ideal host for investigating epigenetic regulators like BRD3. The line’s genetic tractability allows efficient CRISPR/Cas9 genome editing to create targeted knockouts.
BRD3 is an acetyl-lysine reader protein that specifically recognizes acetylated histone marks such as H3K27Ac through its dual bromodomains. This recognition recruits transcriptional co-activators including the mediator complex and P-TEFb, facilitating RNA polymerase II elongation at target gene promoters. Consequently, BRD3 drives expression of key proliferative and survival factors, notably MYC, FOSL1, CCND1, and BCL2. Its activity is regulated by upstream acetyltransferases (p300/CBP) and deacetylases (HDACs) and is directly inhibited by BET bromodomain inhibitors like JQ1. CRISPR-mediated knockout of BRD3 abrogates this epigenetic regulation, leading to transcriptional silencing of these oncogenes and impaired cell proliferation.
In the A-549 lung adenocarcinoma context, BRD3 knockout disrupts critical oncogenic pathways including MYC and NF-??B signaling, attenuating cell cycle progression and survival. This model is particularly relevant for investigating resistance to BET inhibitors, as BRD3 is a canonical target of these drugs. The knockout also allows interrogation of compensatory mechanisms that may emerge following BRD3 loss, shedding light on epigenetic vulnerabilities in solid tumors.
This polyclonal BRD3 knockout cell population is suited for a range of molecular and functional assays, including ChIP-qPCR to assess chromatin binding dynamics, RNA-seq for transcriptome analysis, and RT-qPCR or western blotting to confirm target gene modulation. Proliferation and drug sensitivity assays further enable studies of oncogene dependency and therapeutic response in lung cancer. These applications support research in epigenetic regulation, cancer biology, and inhibitor development. For more details or to request a quote, please contact Ascent Research.
