The ARID1B Knockout A-549 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population in which the ARID1B gene has been disrupted to generate a loss-of-function model. Developed on the A-549 human lung adenocarcinoma epithelial cell background, this polyclonal knockout cell pool is an ideal tool for dissecting the functional roles of ARID1B, a key DNA-binding subunit of the SWI/SNF chromatin remodeling complex. The heterogeneous nature of the polyclonal population enables robust and reproducible interrogation of ARID1B-dependent phenotypes without the clonal artifacts that can arise from single-cell-derived lines.
A-549 cells were originally derived from a 58-year-old Caucasian male with lung adenocarcinoma and serve as a widely recognized in vitro model of human lung adenocarcinoma. These adherent epithelial cells retain characteristic features of the tumor type, including oncogenic signaling pathways and a stable karyotype, making them particularly suitable for studying the molecular underpinnings of non-small cell lung cancer. Their use in this knockout product provides a clinically relevant context in which to examine the impact of ARID1B loss on cancer cell biology.
ARID1B functions as a sequence-specific DNA-binding subunit that directs the SWI/SNF complex to target genomic loci, where it utilizes ATP hydrolysis to reposition nucleosomes and modulate transcription. Within this complex, ARID1B interacts with core catalytic subunits such as SMARCA4 (BRG1) and SMARCB1 (SNF5), as well as with its paralog ARID1A, and it cooperates with ??-catenin to regulate Wnt-responsive promoters. ARID1B transcriptionally controls key downstream effectors including MYC and CCND1, and its knockout disrupts SWI/SNF-mediated chromatin remodeling, leading to deregulated expression of cell cycle and Wnt target genes with potential consequences for proliferation and differentiation.
In the A-549 lung adenocarcinoma context, ARID1B knockout provides a powerful model for investigating the role of SWI/SNF complex dysfunction in cancer. Loss of ARID1B has been implicated in Coffin-Siris syndrome and various malignancies, and its disruption in these cells may alter tumorigenic properties by affecting pathways critical for cell growth and survival. This model thus enables the dissection of ARID1B-specific contributions to oncogenic transcription programs and their dependence on chromatin remodeling, offering insights into the molecular mechanisms that drive lung adenocarcinoma progression.
This product is designed for a broad range of functional studies, including detailed analysis of SWI/SNF complex activity, investigation of chromatin remodeling in cancer, and profiling of drug sensitivity. Researchers can employ assays such as western blotting and RT-qPCR to confirm target disruption, ChIP-qPCR to assess chromatin occupancy, cell proliferation and flow cytometry assays to evaluate phenotypic changes, and RNA-seq for global transcriptomic analysis. Furthermore, ??-catenin reporter assays and drug sensitivity testing enable exploration of Wnt signaling and therapeutic vulnerabilities. For further information, please contact Ascent Research.
