The CCPG1 Knockout A-549 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the A-549 human lung adenocarcinoma epithelial cell line. This product provides a loss-of-function model for the CCPG1 gene, generated through targeted genome disruption using the CRISPR/Cas9 system, and is supplied as a mixed population of edited cells. The polyclonal format enables direct study of gene function without the selection bottleneck associated with clonal isolation, making it suitable for experiments where population-level effects are desired.
A-549 cells are an established model of human lung adenocarcinoma, originally isolated from the lung tumor tissue of a 58-year-old Caucasian male. They harbor an activating KRAS G12S mutation, rendering them a relevant substrate for investigating oncogenic signaling and drug metabolism in non-small cell lung cancer (NSCLC). These adherent epithelial cells are widely employed in cancer biology research, including studies of proliferation, apoptosis, and chemosensitivity.
CCPG1 functions as a regulator of cell cycle progression, specifically at the G1/S transition checkpoint. Its activity is influenced by upstream regulators including p53 and E2F transcription factors, which integrate signals from EGFR-mediated pathways. CCPG1 interacts with and modulates the activity of the cyclin D1-CDK4 complex, and its loss disrupts normal transcriptional programs governed by the TP53-CCND1-CDK4/6-RB1-E2F1 axis. Knockout of CCPG1 in A-549 cells leads to dysregulation of p53-mediated transcription and aberrant E2F activity, resulting in impaired G1/S transition, suppressed expression of cyclin D1 and other downstream G1/S phase genes, and ultimately attenuated cell proliferation.
In the context of A-549 cells bearing the KRAS G12S mutation, CCPG1 disruption serves as a relevant model for examining cell cycle checkpoint control in lung adenocarcinoma. The interplay between oncogenic KRAS signaling and the G1/S regulatory machinery, including CCPG1, cyclin D1, and CDK4, is critical to the proliferative phenotype of NSCLC. This knockout system enables dissection of how loss of CCPG1 cooperates with or counteracts KRAS-driven tumorigenic pathways, potentially revealing vulnerabilities that can be targeted pharmacologically.
This polyclonal knockout cell product is suited for a range of experimental applications, including profiling cell cycle marker expression by Western blot, quantifying CCPG1 transcript levels via RT-qPCR, and assessing cell cycle distribution through flow cytometry. Proliferation and viability can be evaluated with MTT and colony formation assays, while migration assays provide insights into invasive potential. Additionally, the mixed population allows transcriptome-wide analyses via RNA-seq to identify compensatory pathways or off-target effects. For technical inquiries and ordering details, please contact Ascent Research.
