The L1CAM Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated from the A-549 human lung adenocarcinoma cell line, in which the L1CAM gene has been disrupted to create a loss-of-function model. This polyclonal population provides a genetically diverse pool of cells with L1CAM deficiency, enabling robust assessment of L1CAM-dependent phenotypes without clonal bias. The product is intended for advanced biomedical research applications focusing on cell adhesion, migration, invasion, and signaling in cancer and neurobiology.
A-549 cells are an established epithelial cell line originally isolated from a 58-year-old Caucasian male with lung adenocarcinoma. They exhibit characteristics of type II alveolar epithelial cells and are widely used as an in vitro model for lung adenocarcinoma biology and respiratory epithelium function. The cells maintain key epithelial features and are amenable to genetic manipulation, making them a suitable host for CRISPR/Cas9-mediated gene disruption. This background is particularly relevant for studying L1CAM in the context of non-small cell lung cancer progression and metastasis.
L1CAM encodes a transmembrane cell adhesion molecule of the immunoglobulin superfamily that plays critical roles in neuronal development, axon guidance, and tumor cell migration. In signaling, L1CAM engages in homophilic interactions and heterophilic binding with partners such as integrins, neuropilins, and contactin. It is regulated by upstream factors including Reelin, ephrinB, and semaphorin3A. Proteolytic cleavage by ADAM10 or ADAM17 releases the L1 intracellular domain (L1-ICD), which translocates to the nucleus and functions as a coactivator for ??-catenin/TCF transcription, promoting expression of genes like MMP2/9 and ITGA5. Additionally, L1CAM activates Src/FAK signaling, leading to ERK1/2 and PI3K/Akt pathway activation. Thus, L1CAM integrates extracellular cues to drive proliferation, survival, and motility.
In the A-549 lung adenocarcinoma cell line, L1CAM expression is associated with enhanced invasive and metastatic potential. Knockout of L1CAM in this model enables dissection of its contribution to epithelial-to-mesenchymal transition, cell migration, and tumor cell dissemination. This polyclonal knockout population is particularly valuable for studying how L1CAM-mediated signaling interacts with oncogenic drivers in lung cancer. It allows researchers to analyze the impact of L1CAM loss on downstream effectors such as ERK, Akt, and ??-catenin in a lung epithelial context, providing insights into potential therapeutic targets for metastatic lung adenocarcinoma.
Researchers can employ this product in a variety of assays, including Western blotting and RT-qPCR to confirm L1CAM knockout, immunofluorescence and flow cytometry to assess residual protein expression, and functional assays such as Boyden chamber migration/invasion assays to evaluate motility. The cells are suitable for xenograft metastasis models to study in vivo tumor spread, and for drug sensitivity studies to test L1CAM-targeted therapeutic candidates. Co-immunoprecipitation and phospho-ERK analysis can be used to probe the L1CAM interactome and downstream signaling. For additional information and technical support, please contact Ascent Research.
