The APOA2 Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population generated from the A-549 human lung adenocarcinoma cell line, with targeted disruption of the APOA2 gene. This polyclonal format provides a mixed loss-of-function model that avoids clonal adaptation biases. APOA2 encodes apolipoprotein A-II, a major structural component of HDL particles, and its genetic ablation in these cells enables systematic study of HDL-mediated lipid transport and cholesterol metabolism in a lung epithelial model. The product is supplied as a polyclonal pool ready for expansion and assays.
The parental A-549 cell line originates from lung adenocarcinoma tissue of a 58-year-old male and is widely used as an alveolar type II epithelial model. These cells exhibit features of type II pneumocytes and represent a well-characterized lung cancer line. A-549 cells express lipid metabolism components and respond to lipoprotein signals, making them a suitable system for studying cholesterol homeostasis in lung cancer. The APOA2 knockout in this background provides a physiologically relevant model to dissect apolipoprotein A-II function in lipid trafficking within the tumor microenvironment.
APOA2 plays a central role in HDL biogenesis and remodeling. Apolipoprotein A-II forms homodimers and associates with HDL particles, interacting with APOA1, LCAT, CETP, PLTP, and SCARB1. It promotes cholesterol efflux by facilitating LCAT-mediated cholesterol esterification and modulating ABCA1 expression. Upstream, APOA2 expression is regulated by nuclear receptors HNF4A, PPARA, LXRA, and RXRA, and is responsive to insulin and glucose. Downstream, APOA2 influences AMPK phosphorylation and AKT signaling, linking HDL to cellular energy sensing. The knockout disrupts these interactions, enabling analysis of HDL deficiency on signaling.
In A-549 lung adenocarcinoma cells, loss of APOA2 impairs HDL-mediated cholesterol efflux, leading to altered intracellular cholesterol distribution and perturbed lipid raft formation. This disruption is expected to modulate AMPK signaling, a key regulator of energy homeostasis, thereby impacting cancer cell proliferation and survival. The APOA2 knockout model thus provides a powerful system to explore the interplay between HDL components and metabolic reprogramming in lung cancer.
These polyclonal knockout cells are suited for lipoprotein metabolism studies, cholesterol transport research, cancer lipid metabolism investigations, and drug screening for lipid-modulating therapies. Representative assays include western blotting for LCAT, ABCA1, AMPK, and AKT, RT-qPCR, cholesterol efflux and HDL particle sizing, cell proliferation (MTT) and migration assays, and metabolic flux analysis (Seahorse). The product facilitates mechanistic studies of HDL in lung cancer and biomarker discovery in cardiovascular and metabolic diseases. For further details, please contact Ascent Research.
