The ITGB2 Knockout A-549 Polyclonal Cells product comprises a CRISPR/Cas9-edited polyclonal knockout cell population derived from the A-549 human lung adenocarcinoma cell line. This model features disruption of the ITGB2 gene, encoding the integrin beta-2 subunit (CD18), a critical component of leukocyte adhesion receptors. The polyclonal format provides a heterogeneous population of cells with targeted gene disruption, allowing researchers to assess ITGB2 loss-of-function phenotypes without clonal selection biases. This product is suitable for studying beta-2 integrin-mediated processes in a cancer-relevant context.
The A-549 host cell line is a widely employed epithelial model established from a 58-year-old male with lung adenocarcinoma. These cells exhibit hypotriploid karyotype and retain features of type II alveolar epithelium, making them a standard system for investigating lung cancer biology, drug responses, and epithelial-mesenchymal transition. The A-549 background offers a robust platform for examining the role of integrin beta-2 in non-hematopoietic cells, which express CD18 under certain inflammatory or oncogenic conditions.
ITGB2 encodes integrin beta-2 (CD18), which pairs with alpha chains (CD11a, CD11b, CD11c, CD11d) to form heterodimers such as LFA-1 and Mac-1. These receptors are activated by inside-out signals involving Rap1-GTP, talin, and kindlin-3, in response to upstream regulators like TNF-??, IL-1, and chemokines. Upon activation, they bind ICAM-1, VCAM-1, or fibrinogen, linking to downstream effectors including FAK, Src kinases, and Rho GTPases. ITGB2 knockout thus disrupts surface CD18 expression, abolishing beta-2 integrin-dependent adhesion and signaling cascades.
In the A-549 lung carcinoma model, ITGB2 disruption eliminates CD18-dependent adhesion and signaling pathways, providing a loss-of-function system to dissect the contributions of beta-2 integrins outside the hematopoietic lineage. Although A-549 cells are epithelial, they can express CD18 under certain conditions, and forced expression models demonstrate its potential roles in tumor cell adhesion to the endothelium and extracellular matrix. This knockout model is therefore instrumental for studying how beta-2 integrins may facilitate metastatic dissemination, tumor-immune cell interactions, or inflammatory cytokine responsiveness in lung cancer biology.
Applications include flow cytometric verification of CD18 loss, adhesion assays to ICAM-1-coated substrates, and cell migration analyses to evaluate integrin-mediated motility. Western blotting and immunofluorescence can assess downstream signaling, such as FAK phosphorylation. The model is suited for drug target validation, screening integrin inhibitors, and investigating the roles of beta-2 integrins in cancer metastasis and inflammatory disorders. For additional information or to discuss your application, please contact Ascent Research.
