BICC1 Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population featuring targeted disruption of the BICC1 gene in the human A-549 lung adenocarcinoma cell line. This polyclonal pool contains numerous edited clones, offering a versatile loss-of-function model for investigating BICC1-dependent cellular processes without the need for clonal isolation.
The A-549 host cell line was derived from a human lung adenocarcinoma and is a standard in vitro model for non-small cell lung cancer. These epithelial cells harbor common mutations such as KRAS and STK11 and are routinely used to study oncogenic signaling, cell migration, invasion, and therapeutic responses. Their stable growth and extensive characterization provide a robust background for gene knockout experiments.
BICC1 codes for a conserved RNA-binding protein that post-transcriptionally regulates gene expression by binding to the 3′ UTRs of specific mRNAs, controlling their translation and stability. Critical downstream targets include DAB2 and E-cadherin (CDH1). BICC1-mediated regulation of DAB2 mRNA influences TGF-?? signaling, as DAB2 facilitates TGF-?? receptor-mediated phosphorylation of SMAD2 and SMAD3, leading to transcriptional activation. Additionally, BICC1 modulates the Wnt/??-catenin pathway by affecting components such as Dishevelled and AXIN, thereby impacting ??-catenin stability and TCF/LEF-mediated transcription. Upstream factors controlling BICC1 expression encompass promoter methylation and transcriptional regulation, and the protein interacts with translational regulatory complexes and DAB2 mRNA.
In A-549 adenocarcinoma cells, disruption of BICC1 is anticipated to profoundly alter post-transcriptional control of adhesion and signaling molecules. Reduced DAB2 levels can attenuate TGF-??/SMAD signaling, while diminished E-cadherin expression may weaken intercellular adhesion and promote a migratory phenotype. This polyclonal knockout model enables examination of BICC1’s contribution to lung cancer progression, especially regarding aberrant Wnt and TGF-?? pathway activity, without the confounding effects of clonal selection.
These cells are designed for a broad range of research applications, including studies of mRNA regulatory networks, crosstalk between TGF-?? and Wnt pathways, and functional genomic screens to identify drug sensitivity modulators. Assay-ready applications include Western blotting for DAB2 and E-cadherin, RT-qPCR for target mRNAs, RNA immunoprecipitation, RNA-seq, migration and invasion assays, colony formation, immunofluorescence for EMT markers, and reporter assays for Wnt/??-catenin and TGF-??/SMAD transcriptional activity. For further information, please contact Ascent Research.
