The DIP2A Knockout AGS Polyclonal Cells product is a CRISPR/Cas9-edited polyclonal knockout cell population derived from the AGS human gastric adenocarcinoma cell line, designed to disrupt expression of the DIP2A gene. This pooled polyclonal population provides a heterogeneous loss-of-function model that enables robust investigation of DIP2A-dependent cellular processes without the clonal selection biases inherent to monoclonal lines.
AGS is an adherent epithelial cell line originating from a human gastric adenocarcinoma, widely utilized as an in vitro model for gastric cancer research. These cells harbor a mutant TP53 tumor suppressor, reflecting the genomic instability commonly observed in gastric malignancies. The line??s well-characterized signaling landscape and reproducible growth characteristics make it a reliable host for gene-editing studies focused on cancer cell biology, invasion, and therapeutic response.
DIP2A functions as an intracellular mediator of netrin-1/DCC signaling, which governs axon guidance, cell adhesion, migration, and apoptosis. Mechanistically, DIP2A interacts with the DCC receptor and downstream effectors such as FADD and caspase-8 to transduce apoptotic signals, while also engaging the Rac1/PI3K/Akt pathway to regulate cytoskeletal dynamics and survival. DIP2A is regulated by netrin-1 and DCC, and influences the activity of Rac1, Cdc42, PI3K, Akt, MAPK, and caspase-8, positioning it as a critical node in both attractive and repulsive guidance responses.
In the AGS gastric cancer context, DIP2A loss is predicted to disrupt netrin-1-dependent adhesion and apoptosis, potentially promoting a more migratory and proliferative phenotype. Given the TP53-deficient background of AGS cells, this knockout model may reveal synergistic effects on cell survival and DNA damage responses. Consequently, the DIP2A knockout population offers a physiologically relevant system to study tumor suppressor-like functions and the molecular basis of gastric cancer progression.
Researchers can apply this polyclonal knockout model to interrogate DIP2A??s role in gastric cancer biology, netrin-1 signaling, cell migration and invasion, and apoptosis regulation. Representative experimental approaches include western blotting and RT-qPCR for expression validation, immunofluorescence for subcellular localization, Transwell assays to assess motility, Annexin V staining for apoptosis quantification, co-immunoprecipitation with DCC to probe protein interactions, and phospho-Akt/Erk analysis to map downstream signaling. Drug sensitivity profiling, for instance with cisplatin, can also be performed to evaluate chemoresistance mechanisms. For further information, please contact Ascent Research.
