The BAIAP2 Knockout A-549 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the A-549 human lung adenocarcinoma epithelial cell line. This product provides a genetic loss-of-function model for investigating the biological role of BAIAP2 (also known as IRSp53). The polyclonal nature ensures a heterogeneous pool of edited cells, ideal for robust functional assays. Validated for target gene disruption, these cells are a reliable tool for studying BAIAP2-mediated signaling pathways without the clonal selection biases inherent in single-cell?Cderived lines.
A-549 cells originate from a lung adenocarcinoma isolated from a 58-year-old Caucasian male and are widely employed in cancer research. This epithelial cell line exhibits key characteristics of non-small cell lung cancer, including rapid proliferation and metastatic potential. Its well-characterized transcriptome and signaling networks make it a suitable platform for examining the molecular mechanisms underlying lung adenocarcinoma progression, drug resistance, and epithelial-mesenchymal transition.
BAIAP2 functions as a scaffolding adaptor protein that links membrane microdomains to the actin cytoskeleton. It is activated by the small GTPases Rac1 and Cdc42 and interacts with the insulin receptor (INSR) and receptor tyrosine kinases. Downstream, BAIAP2 recruits the WAVE complex and N-WASP, promoting actin polymerization through the ARP2/3 complex, which drives filopodia and lamellipodia formation. Additional interacting partners include EPS8, WAVE1, and ENAH. This signaling cascade is essential for cell migration, insulin signaling, and cytoskeletal reorganization.
In the A-549 host cell context, BAIAP2 knockout disrupts actin-dependent membrane protrusion and impedes cell migration and invasion, which are critical steps in cancer metastasis. Furthermore, impaired insulin signaling downstream of BAIAP2 deficiency may alter metabolic and proliferative responses in lung epithelial cells. Consequently, this knockout model is a valuable resource for dissecting the contribution of BAIAP2 to metastatic behavior, epithelial-mesenchymal transition, and the crosstalk between insulin signaling and lung adenocarcinoma biology.
Researchers can utilize these cells in a variety of functional assays, including wound healing and Transwell migration assays to quantify motility, immunofluorescence with phalloidin to visualize F-actin, Western blotting for BAIAP2, WAVE1, and phospho-ERK, and RT-qPCR for EMT markers such as E-cadherin and Vimentin. Drug sensitivity assays with cisplatin or gefitinib allow exploration of BAIAP2’s role in therapeutic resistance. For more information, please contact Ascent Research.
