The CCDC120 Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population targeting the CCDC120 gene in the human A-549 lung adenocarcinoma epithelial line. This loss-of-function model utilizes CRISPR/Cas9-mediated gene disruption to eliminate CCDC120 protein expression across a heterogeneous pool, enabling population-level functional studies without clonal selection. It is ideal for investigating CCDC120-dependent signaling in a lung cancer context.
A-549 cells, derived from a 58-year-old male with lung adenocarcinoma, model respiratory epithelial biology and non-small cell lung cancer. Widely used for transfection, infection, and drug discovery studies, these adherent cells exhibit alveolar type II pneumocyte features. Their robust growth and genetic tractability facilitate examination of oncogenic pathways and therapeutic responses, providing a physiologically relevant platform for knockout analyses.
CCDC120 modulates TRAF2- and TRAF6-mediated JNK and NF-??B signaling by binding these adaptors and influencing their ubiquitination. Downstream of TNF, IL-1, and Toll-like receptors, CCDC120 regulates MAP3Ks and MAP2Ks leading to JNK and IKK phosphorylation, activating AP-1 and NF-??B. This coordinates expression of genes controlling apoptosis (e.g., BCL2 family) and inflammation, positioning CCDC120 as a key regulator of stress-responsive pathways.
In lung adenocarcinoma, NF-??B and JNK hyperactivation drive proliferation, chemoresistance, and immune escape. A-549 CCDC120 knockout cells allow dissection of how CCDC120-TRAF interactions shape these pathways in an epithelial tumor setting. This model is pertinent to research on inflammatory disorders, autoimmune conditions, and cancer, where CCDC120 may modulate disease-relevant signaling networks.
Applications include Western blotting for phospho-JNK/NF-??B, NF-??B luciferase reporter assays, TRAF2/6 co-immunoprecipitation, Annexin V/PI apoptosis assays, cytokine ELISA, and RT-qPCR for inflammatory targets. These cells support signal transduction, apoptosis, and cancer biology studies. For further information, please contact Ascent Research.
