The ABCF2 Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human A-549 lung carcinoma epithelial cell line, featuring targeted disruption of the ABCF2 gene. This loss-of-function model yields a heterogeneous pool of edited cells collectively lacking functional ABCF2 protein, offering a robust representation of editing outcomes for population-level assays. The product is designed for studies in translation control, drug resistance, and cancer cell biology.
The A-549 host cell line is an established adherent epithelial model from a 58-year-old male with lung adenocarcinoma. It is widely used as a representative system for type II alveolar epithelial cells, with well-characterized growth and genetic features relevant to lung cancer biology, toxicology, and drug response studies. Its susceptibility to genetic manipulation makes it an ideal platform for CRISPR/Cas9 knockout generation.
ABCF2 encodes an ATP-binding cassette protein that associates with the ribosome and regulates translation initiation and ribosome recycling. It interacts with the 40S ribosomal subunit and the eIF3 complex, utilizing ATP hydrolysis to modulate translation efficiency. ABCF2 activity is controlled by mTORC1 signaling, linking growth factor and amino acid cues to the mTOR/eIF4E/eIF4G/eIF3/40S ribosome pathway. Knockout of ABCF2 disrupts global protein synthesis and alters downstream targets, notably the BCL2 family of apoptosis regulators, thereby influencing cell proliferation and apoptosis. These interactions place ABCF2 at a nexus of nutrient sensing and protein homeostasis.
In the context of A-549 lung adenocarcinoma cells, ABCF2 knockout provides a model to investigate translational dysregulation in oncogenic phenotypes and therapeutic resistance. ABCF2 is implicated in multidrug resistance and apoptosis evasion, central to lung cancer progression. Disruption of ABCF2 enables dissection of mTOR-driven translation effects on chemosensitivity to cisplatin and paclitaxel. The model facilitates study of ribosome-associated mechanisms underpinning cancer cell proliferation and survival. Comparing edited and parental cells delineates ABCF2’s role in modulating ribosomal landscape and downstream effectors, informing combinatorial strategies against drug resistance.
These polyclonal knockout cells are suited for western blotting with puromycin incorporation to monitor protein synthesis, RT?qPCR for gene expression, MTT/BrdU proliferation assays, and annexin V apoptosis staining. Drug sensitivity profiling with cisplatin or paclitaxel assesses chemoresistance, while ribosome and polysome profiling interrogate translational control. The model supports functional genomics of ABC transporters and target discovery in lung cancer. For further details, contact Ascent Research.
