The DPYSL5 Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-engineered polyclonal knockout cell population derived from the A-549 human lung adenocarcinoma cell line. This product introduces targeted disruption of the DPYSL5 (CRMP5) gene, generating a heterogeneous mixture of edited cells that collectively model loss of CRMP5 function. As a polyclonal population, it mitigates clonal biases and represents a versatile tool for functional genomics studies, particularly investigations into cell migration, cytoskeletal dynamics, and cancer-related signaling.
The parental A-549 cell line is an established model of human lung adenocarcinoma, originally isolated from the tumor tissue of a 58-year-old Caucasian male. A-549 cells exhibit adherent epithelial morphology and are widely employed in cancer research for studying tumor biology, drug responsiveness, and metastatic mechanisms. Their well-documented characteristics make them an ideal host for gene-editing approaches aimed at elucidating molecular drivers of lung cancer progression.
DPYSL5 encodes collapsin response mediator protein 5 (CRMP5), a cytosolic phosphoprotein implicated in Semaphorin and Reelin signaling pathways. In A-549 cells, CRMP5 acts downstream of receptors such as Neuropilin-1 and ApoER2, interacting with tubulin, actin, and kinesin light chain to regulate microtubule stability and actin filament organization. Its activity is modulated by kinases including GSK-3?? and Cdk5, which phosphorylate CRMP5 in response to extracellular cues like Semaphorin3A and Reelin. Through these interactions, CRMP5 coordinates cytoskeletal remodeling, filopodia formation, and cell migration. Disruption of DPYSL5 thereby compromises these signaling axes, altering the cell’s motile and invasive properties.
In the context of lung adenocarcinoma, DPYSL5 knockout in A-549 cells serves as a critical loss-of-function model for dissecting the contribution of CRMP5 to cancer cell motility and metastasis. Since cytoskeletal reorganization is essential for tumor cell invasion, this polyclonal knockout system enables analysis of how CRMP5-mediated signaling integrates with oncogenic pathways. Researchers can use this model to explore the role of neurodevelopmental guidance molecules in non-neuronal cancer cells and to assess the impact of CRMP5 depletion on metastatic potential, potentially revealing therapeutic vulnerabilities.
This knockout product is suited for a range of functional assays, including wound healing and transwell migration/invasion studies to quantify cell motility, immunofluorescence and western blotting to monitor cytoskeletal architecture and CRMP5 expression, and RNA sequencing to profile transcriptomic changes. It facilitates screening of small-molecule inhibitors of cell migration and supports mechanistic studies of Semaphorin and Reelin pathway components in lung cancer. For further information, please contact Ascent Research.
