The ALCAM Knockout A-549 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human A-549 lung adenocarcinoma cell line, engineered to disrupt the ALCAM (CD166) gene. This loss-of-function model is supplied as a heterogeneous pool of cells containing diverse ALCAM-targeting edits, enabling robust investigation of ALCAM-dependent processes without clonal selection artifacts.
The parental A-549 cell line originates from alveolar basal epithelial adenocarcinoma tissue of a 58-year-old male and is widely utilized as an in vitro model of lung adenocarcinoma and alveolar type II epithelium. These cells retain key epithelial characteristics and serve as a versatile platform for respiratory biology, drug metabolism, and cancer research, including studies on tumor cell invasion and the lung microenvironment.
ALCAM, an immunoglobulin superfamily adhesion molecule, mediates homophilic and heterophilic (with CD6) interactions, contributing to immune cell trafficking, T-cell activation, and neuronal development. In cancer, ALCAM promotes metastasis by enhancing adhesion, migration, and invasion through PI3K/Akt and MAPK/ERK signaling, and by regulating MMP-2 and MMP-9 expression and cytoskeletal dynamics. Upstream regulators include WNT/??-catenin, TNF-??, IL-1??, TGF-??, and NF-??B, while downstream targets include ERK1/2 and Akt phosphorylation, RhoA activation, and AP-1 transcription. ALCAM interacts with LFA-1 and ERM proteins to reorganize the actin cytoskeleton.
In the A-549 lung adenocarcinoma context, ALCAM knockout disrupts cell adhesion, migration, and invasion pathways frequently deregulated in non-small cell lung cancer metastasis. This polyclonal knockout pool enables the study of ALCAM??s contribution to lung cancer progression, immune evasion, and therapeutic resistance, and provides a physiologically relevant system for dissecting ALCAM-driven PI3K/Akt and MAPK signaling crosstalk.
Researchers can employ this knockout model in scratch wound migration and Boyden chamber invasion assays to quantify motility and invasiveness, or use cell adhesion assays and co-immunoprecipitation with CD6 to study ALCAM-dependent adhesion. Phospho-ERK/Akt ELISA, MMP activity assays, and RNA-seq enable signaling and transcriptomic profiling. These cells are suited for evaluating ALCAM as a therapeutic target, screening adhesion inhibitors, and testing anti-metastatic compounds. For additional information, please contact Ascent Research.
