The DPCD Knockout AGS Polyclonal Cells product comprises a CRISPR/Cas9-edited polyclonal knockout cell population derived from the AGS human gastric adenocarcinoma cell line. This product delivers a heterogeneous pool of AGS cells carrying targeted disruptions in the DPCD locus, enabling robust loss-of-function studies without the clonal bias inherent in single-cell-derived lines. The polyclonal format maintains cellular heterogeneity, reducing potential artifacts from clonal selection and providing a physiologically relevant population for functional assays. This knockout model is designed to facilitate investigation of DPCD-dependent mechanisms in gastric epithelial biology, including ciliary function and tumorigenic processes.
The host cell line, AGS, is a widely used human gastric adenocarcinoma cell line with adherent epithelial morphology. Derived from a primary gastric adenocarcinoma, AGS cells harbor a mutant p53 background, making them a valuable model for studying gastric cancer pathogenesis and mucosal responses. AGS cells exhibit key characteristics of gastric epithelium and are commonly employed in research on gastric cancer cell signaling, drug response, and host-pathogen interactions. Their well-characterized growth properties and suitability for genetic manipulation make AGS cells an ideal platform for CRISPR/Cas9-mediated gene disruption.
DPCD encodes a cytoplasmic protein that plays a critical role in the preassembly of dynein arm complexes, which are essential for the motility of cilia and flagella. DPCD functions within a multi-protein assembly network, interacting with co-chaperones and assembly factors such as DNAAF2, DNAAF3, DNAAF4, HEATR2, LRRC6, and ZMYND10. Its activity is transcriptionally regulated by upstream factors including FOXJ1, RFX transcription factors, and NOTCH signaling. DPCD is necessary for the proper assembly of outer dynein arms, and its disruption leads to impaired ciliary beat frequency and defective mucociliary clearance. Representative downstream targets affected by DPCD loss include dynein axonemal heavy chain components like DNAH5, DNAH11, and the intermediate chain DNAI1, as well as radial spoke protein RSPH4A.
In the context of AGS gastric cancer cells, DPCD knockout provides a unique model to dissect the interplay between ciliary function and gastric epithelial malignancy. Although AGS cells are not traditionally considered ciliated, recent evidence indicates that cancer cells can express components of the ciliary machinery, and dysregulation of ciliogenesis genes is increasingly linked to tumorigenesis and drug resistance. Disruption of DPCD in AGS cells may alter cellular behaviors such as proliferation, migration, and sensitivity to chemotherapeutic agents, mimicking aspects of primary ciliary dyskinesia at the cellular level. This model thus enables exploration of how ciliary protein networks contribute to gastric cancer biology beyond their classical roles in motile cilia.
This knockout cell population supports a range of experimental applications. Researchers can employ RT-qPCR and immunofluorescence to assess DPCD disruption and ciliary gene expression profiles. Western blotting allows detection of dynein arm proteins and interacting partners. Functional assays, including cell proliferation, wound healing, and drug sensitivity tests, can uncover DPCD-dependent phenotypes in gastric cancer progression and treatment response. The polyclonal nature of the product is particularly suited for pooled screening approaches and studies requiring diverse genetic backgrounds. For further technical information or to inquire about custom gene-editing services, please contact Ascent Research.
