The JADE1 Knockout A-549 Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal knockout population derived from the A-549 human lung adenocarcinoma epithelial cell line, with disrupted JADE1 gene function across a heterogeneous cell pool. This polyclonal format preserves cellular diversity and avoids clonal artifacts, offering a representative loss-of-function model for functional studies. The population is generated through targeted gene disruption using CRISPR/Cas9 technology, ensuring efficient inactivation while maintaining the parental line??s genomic heterogeneity. These cells are validated for standard culture conditions and advanced biomedical research.
The A-549 cell line was derived from a lung carcinoma of a 58-year-old Caucasian male and is a well-characterized model of human lung adenocarcinoma, displaying features of alveolar type II pneumocytes. These adherent epithelial cells form polarized monolayers and retain wild-type TP53, making them suitable for studying p53-dependent regulation. A-549 cells have been extensively employed in oncogenic signaling, drug metabolism, and epigenetic analyses, providing a consistent background for gene editing and functional investigation.
JADE1 is an essential scaffold in the HBO1 (KAT7) histone acetyltransferase complex, interacting with ING4/5, BRPF1/2, and MEAF6 to direct histone H4 acetylation at lysines 5, 8, and 12. This activity facilitates p53- and E2F1-mediated transcription of downstream targets including p21/CDKN1A, BAX, PUMA, NOXA, and GADD45A, thereby linking histone acetylation to the p53/p21 tumor suppressor axis. JADE1 function is further modulated by upstream regulators MYC and p53, positioning it as a critical node between chromatin remodeling and cell fate decisions.
In A-549 lung cancer cells, JADE1 knockout impairs HBO1 complex function and reduces histone H4 acetylation, attenuating p53 target gene induction. Consequently, these polyclonal cells show diminished p21/CDKN1A expression and reduced pro-apoptotic factor levels, leading to altered cell cycle control and apoptosis. This phenotype recapitulates epigenetic silencing of tumor suppressor networks seen in non-small cell lung cancer, making the model valuable for studying chromatin-mediated oncogenic mechanisms and testing therapeutic interventions that restore acetylation.
These JADE1 knockout polyclonal cells are amenable to a broad range of assays, including ChIP-qPCR for H4K5ac/H4K8ac mapping, RT-qPCR and western blotting for p21, BAX, and PUMA quantification, and functional analyses via proliferation, colony formation, and flow cytometry-based cell cycle and apoptosis measurements. The mixed population is also suitable for RNA-seq to identify JADE1-dependent transcriptomic changes. Applications span epigenetic regulation in lung cancer, p53 network dissection, chromatin biology of tumor suppression, and preclinical evaluation of HBO1-targeting compounds. Please contact Ascent Research for more information.
