DYNC2H1 Knockout HGC-27 Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal knockout cell population generated in the human gastric carcinoma cell line HGC-27. This loss-of-function model disrupts the DYNC2H1 gene, encoding a dynein-2 heavy chain, across a heterogeneous cell pool, offering a robust platform for studying gene function in a metastatic gastric adenocarcinoma context without the constraints of clonal selection.
HGC-27 cells, derived from a lymph node metastasis of a human gastric adenocarcinoma, retain characteristic epithelial morphology and serve as a standard model for advanced gastric cancer research. They are extensively used to evaluate cellular processes such as proliferation, migration, invasion, and pharmacological response. By introducing DYNC2H1 disruption, this product enables targeted investigations into the contributions of primary cilia and ciliary signaling to the malignant features of gastric cancer.
DYNC2H1 encodes the heavy chain of cytoplasmic dynein-2, the motor for retrograde intraflagellar transport (IFT) in primary cilia. It powers the return of IFT particles and ciliary cargo, a process critical for cilium assembly. Dynein-2 interacts with IFT-A (IFT144, IFT139), IFT-B (IFT88, IFT172), kinesin-2, the BBSome, and DYNC2LI1, and its expression is regulated by RFX3 and FoxJ1. Downstream of Hedgehog pathway activation, DYNC2H1 mediates retrograde trafficking of signaling components. Knockout disrupts this transport, impairing processing of Gli transcription factors and reducing expression of targets such as PTCH1 and HHIP, revealing a central role in Hedgehog signal transduction.
In the HGC-27 gastric carcinoma background, DYNC2H1 knockout abrogates primary cilium formation and attenuates Hedgehog signaling, a pathway implicated in gastric tumorigenesis and cancer stem cells. This model allows dissection of ciliary dysfunction effects on cell migration, invasion, and drug sensitivity. It provides a clinically relevant platform to study how impaired IFT-dependent trafficking of molecules like Smoothened and Patched alters oncogenic signaling in metastatic gastric epithelial cells.
Key research applications encompass the investigation of primary cilia roles in gastric cancer cell motility and invasiveness, analysis of Hedgehog pathway activation through Gli1 and Gli3 processing, and evaluation of drug sensitivity to Hedgehog inhibitors. Representative assays include immunofluorescence staining for ciliary markers (Arl13b, acetylated tubulin), Western blotting for Gli protein isoforms, and RT-qPCR for Hedgehog target genes (PTCH1, HHIP). These polyclonal knockout cells are also suitable for functional rescue experiments and high-content screening. For additional product information and technical support, please contact Ascent Research.
