The DIP2A Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human A-549 lung adenocarcinoma epithelial cell line. This product provides a heterogeneous pool of cells with targeted disruption of the DIP2A gene, enabling loss-of-function studies without selecting single-cell clones. The polyclonal population minimizes clonal artifacts and captures editing diversity, facilitating robust phenotypic screening in cancer biology and signal transduction.
The A-549 host cell line originates from a human lung adenocarcinoma and possesses characteristics of alveolar basal epithelial cells. Widely used in cancer research, A-549 cells express epithelial markers, form tight junctions, and respond to growth factors. They are a standard model for studying lung cancer biology, drug resistance, and epithelial?Cmesenchymal transition. Their well-characterized signaling landscape makes them an ideal system for interrogating DIP2A function in non-small cell lung cancer.
DIP2A encodes a cell-surface receptor for the secreted glycoprotein FSTL1. Ligand binding triggers intracellular signaling via AKT, a key kinase in the PI3K-AKT pathway. Activated AKT phosphorylates downstream targets such as mTOR, BAD, and Caspase-9, thereby promoting cell survival, proliferation, and inhibition of apoptosis. The FSTL1-DIP2A axis thus transduces extracellular cues into critical growth decisions. Mechanistically, FSTL1 serves as an upstream regulator, while DIP2A interacts with AKT, positioning this receptor as an essential mediator of the pathway.
In A-549 cells, endogenous DIP2A supports FSTL1-driven AKT activation, contributing to the malignant phenotype. Disrupting DIP2A in this context provides a valuable tool to dissect FSTL1-dependent and independent roles in lung tumorigenesis. Given DIP2A??s involvement in gastric cancer, colorectal cancer, neurodevelopmental disorders, and congenital heart defects, this polyclonal knockout model enables exploration of broader disease mechanisms. The loss-of-function approach can reveal compensatory signaling changes and therapeutic vulnerabilities specific to lung adenocarcinoma.
This polyclonal knockout cell population is suitable for diverse applications, including western blotting and RT-qPCR for confirmation of DIP2A disruption, as well as functional assays for proliferation, apoptosis, and drug sensitivity. It facilitates detailed analysis of FSTL1-DIP2A signaling effects on cell migration and viability. Additionally, the model aids in identifying downstream targets and screening modulators of the PI3K-AKT-mTOR cascade. For further information or custom requests, please contact Ascent Research.
