The DNAL1 Knockout HGC-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population in which the DNAL1 gene has been disrupted in the HGC-27 human gastric adenocarcinoma cell line. This loss-of-function model enables investigation of DNAL1-dependent cellular processes without specifying the exact editing outcome. The polyclonal nature provides a mixed population of edited alleles, representing a versatile tool for functional genomics studies in a cancer-relevant epithelial context.
HGC-27 is an epithelial cell line derived from a primary gastric carcinoma, retaining key characteristics of human stomach adenocarcinoma. These cells are widely employed to model gastric cancer biology and explore mechanisms of tumorigenesis, migration, and apoptosis. Although not classically ciliated, HGC-27 cells express components of the motile ciliary machinery, making them suitable for studying ciliary protein functions in a transformed epithelial background. Their adherent growth and robust culture properties facilitate diverse experimental workflows.
DNAL1 encodes a light chain of the outer dynein arm, a macromolecular motor complex that powers ciliary and flagellar beating through ATP-dependent conformational changes. DNAL1 is transcriptionally regulated by the master ciliogenesis factor FOXJ1 and RFX family transcription factors, which control ciliary gene expression programs. DNAL1 interacts directly with other outer dynein arm subunits, including DNAH5, DNAI1, and DNALI1, and its incorporation is essential for proper axonemal dynein assembly. Disruption of DNAL1 impairs ciliary beat frequency, fluid flow generation, and overall cellular motility, thus compromising mucociliary clearance in epithelial tissues.
In the HGC-27 gastric cancer model, DNAL1 knockout provides a platform to dissect the contributions of motile cilia to epithelial tumor cell behavior. Loss of ciliary motility may influence cell migration and apoptotic responses, processes often dysregulated in gastric adenocarcinoma. This model is particularly relevant for primary ciliary dyskinesia research, as DNAL1 mutations are associated with this disorder. By engineering DNAL1 deficiency in a cancer cell line, researchers can explore cilia-dependent signaling cascades that intersect with oncogenic pathways.
Key applications include modeling primary ciliary dyskinesia at the cellular level, elucidating the biogenesis of outer dynein arms, examining ciliary function in epithelial homeostasis, and interrogating the role of DNAL1 in gastric cancer progression. Standard assays for characterization include western blotting to confirm protein loss, RT-qPCR for transcript analysis, immunofluorescence to visualize dynein arm components, ciliary beat frequency measurement to assess motility, and migration and apoptosis assays to evaluate functional consequences. For additional information or to request a quotation, please contact Ascent Research.
