The INO80D Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human A-549 lung adenocarcinoma epithelial cell line. This model features targeted disruption of the INO80D gene, creating a loss-of-function system to dissect INO80D-dependent cellular processes. The polyclonal format encompasses a heterogeneous pool of gene-edited cells with diverse CRISPR/Cas9-mediated modifications, minimizing clonal bias and ensuring statistically robust phenotypic outputs. These cells are supplied as a ready-to-use culture for functional genomics and drug discovery applications.
The A-549 host cell line was established from a 58-year-old male patient with lung adenocarcinoma and is a classic model of alveolar type II epithelium. These adherent epithelial cells retain key characteristics of type II pneumocytes and are extensively employed in respiratory oncology research. Their well-defined genetic profile and predictable responses to DNA-damaging agents make them an optimal background for studying DNA repair pathway dependencies and therapeutic vulnerabilities in lung adenocarcinoma.
INO80D is a core subunit of the INO80 chromatin remodeling complex essential for homologous recombination repair of DNA double-strand breaks. Upon DNA damage, ATM/ATR-mediated ??-H2AX signaling recruits the complex to lesion sites, where INO80D promotes nucleosome eviction and DNA end resection. This facilitates loading of RAD51 and BRCA1, critical for homologous recombination. INO80D interacts with ACTL6A, ARP5, RUVBL1, and RUVBL2 to coordinate chromatin remodeling. INO80D also functions in transcription regulation and cell cycle checkpoints, and its loss compromises DNA repair and elevates genotoxic sensitivity.
In the A-549 lung adenocarcinoma context, INO80D knockout cells reveal roles for chromatin remodeling in tumor cell fitness and therapeutic response. Elevated endogenous DNA damage in lung adenocarcinoma cells creates a reliance on homologous recombination, which is compromised upon INO80D loss. This hypomorphic repair phenotype supports synthetic lethality screening with PARP inhibitors or cisplatin and dissection of INO80D-specific repair functions. The model thus enables investigation of repair kinetics, replication stress tolerance, and drug resistance mechanisms.
INO80D Knockout A-549 Polyclonal Cells support diverse assays including ??-H2AX foci immunofluorescence, comet assays, ChIP-qPCR, and homologous recombination reporters. Clonogenic survival assays after treatment with PARP inhibitors, cisplatin, or irradiation reveal drug sensitivity profiles. They are also compatible with flow cytometry for cell cycle and apoptosis, RT-qPCR, Western blotting, and synthetic lethality screens. For additional information, please contact Ascent Research.
