The ABHD16A Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from human A-549 lung adenocarcinoma epithelial cells, featuring targeted disruption of the ABHD16A gene. This loss-of-function model enables investigation of ABHD16A-dependent lipid signaling and autophagy regulation without the need for monoclonal isolation. The polyclonal format preserves genetic diversity while delivering robust gene disruption, making it ideal for functional genomic studies in a cancer-relevant context.
A-549 cells, a well-established model of type II alveolar epithelium, are widely used to study lung adenocarcinoma biology. They exhibit key tumorigenic properties, including rapid proliferation and sensitivity to inflammatory mediators. This background is particularly suited for examining lipid metabolism and autophagy, as these processes are frequently dysregulated in lung tumors. The ABHD16A knockout thus provides a physiologically relevant platform for dissecting lipid-driven signaling in pulmonary cancer.
ABHD16A encodes a phosphatidylserine lipase that converts phosphatidylserine (PS) to lysophosphatidylserine (LysoPS), a bioactive lipid agonist of the GPR34 receptor. LysoPS-GPR34 signaling activates downstream kinases Akt and ERK, influencing cell survival and inflammation. ABHD16A expression is induced by TNF, IL-1??, and LPS; its disruption reduces LysoPS production, attenuating GPR34-mediated phosphorylation cascades and altering autophagy markers such as LC3B and p62. Consequently, ABHD16A knockout cells exhibit impaired lipid homeostasis and defective adaptive responses to stress.
In A-549 cells, loss of ABHD16A perturbs the LysoPS-GPR34 axis, offering a unique system to study how lipid mediators govern tumor cell proliferation, migration, and autophagy. Because A-549 cells rely on autophagy for metabolic adaptation, the knockout model reveals critical links between lipid signaling and cancer cell fitness. The polyclonal population ensures averaged phenotypes that reflect diverse edit outcomes, strengthening biological conclusions.
Applications include lipidomic quantification of LysoPS, GPR34 functional assays, and phospho-flow cytometry to monitor Akt/ERK activity. Western blot analysis of LC3B and p62 enables autophagy flux measurements, while cell proliferation, migration, and invasion assays assess metastatic potential. Transcriptomic and cytokine profiling further elucidate downstream consequences of ABHD16A deficiency. These tools support cancer signaling research and drug target screening. For technical inquiries, contact Ascent Research.
