JADE3 Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population for studying JADE3 in epigenetic regulation and lung cancer. The polyclonal pool of A-549 cells harbors CRISPR-mediated gene disruption, enabling analysis of JADE3-dependent phenotypes without clonal bias. This loss-of-function model is suitable for investigating histone acetylation, chromatin remodeling, and transcriptional networks in a human alveolar epithelial context.
The A-549 cell line is derived from lung carcinoma tissue of a 58-year-old Caucasian male, exhibiting adherent epithelial morphology. As a model for type II alveolar epithelial cells, they produce pulmonary surfactant and mediate ion transport. A-549 cells are a standard non-small cell lung cancer (NSCLC) model, retaining molecular features of adenocarcinoma and providing a tumor-relevant background for epigenetic studies.
JADE3 functions as a scaffold in the HBO1 (KAT7) histone acetyltransferase complex, where it interacts with ING4/5, MEAF6, and KAT7 to catalyze acetylation of histones H3 and H4. This activity is dependent on acetyl-CoA and is regulated by cell cycle and proliferation signals. Resulting histone acetylation promotes chromatin relaxation and transcriptional activation of proliferation-related genes. JADE3 knockout disrupts complex integrity, reducing histone acetylation and likely reprogramming gene expression, thus linking JADE3 to fundamental epigenetic and growth control mechanisms.
In A-549 lung carcinoma cells, JADE3 loss-of-function provides a direct means to examine how the HBO1 complex contributes to oncogenic epigenetic states. Disruption of JADE3 may alter histone modification landscapes at genes controlling cell proliferation and survival, offering insights into epigenetic dysregulation in NSCLC. This model facilitates dissection of JADE3-dependent pathways and assessment of their roles in lung cancer cell growth and drug responses.
This knockout model is compatible with multiple assays: western blot for acetyl-H3/H4, RT-qPCR and RNA-seq for transcriptomic profiling, ChIP-qPCR for chromatin occupancy, and cell proliferation assays. It is suited for drug target validation of HAT inhibitors and mechanistic studies of histone acetylation in cancer. Researchers investigating epigenetic therapy or chromatin dynamics will benefit from this tool. For further details or to discuss custom applications, please contact Ascent Research.
