The DTD1 Knockout HGC-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the HGC-27 human gastric adenocarcinoma cell line, offering a loss-of-function model to study D-aminoacyl-tRNA deacylase (DTD1). This pooled cell population carries targeted disruptions in the DTD1 gene, enabling functional studies without clonal selection bias and better reflecting tumor heterogeneity.
HGC-27 is a well-characterized epithelial cell line established from a lymph node metastasis of a poorly differentiated gastric carcinoma. It retains key features of gastric adenocarcinoma, including aberrant proliferation and invasive potential, making it a clinically relevant platform for investigating cancer cell biology and the impact of DTD1 loss on tumor phenotypes.
DTD1 hydrolyzes D-aminoacylated tRNAs to prevent misincorporation of D-amino acids into proteins, thereby maintaining translational fidelity and proteome integrity. Its activity is regulated by upstream signals such as ATF4 of the integrated stress response and translational demand, and it interacts with tRNA molecules and ribosome-associated quality control factors. DTD1 functions within a network that includes aminoacyl-tRNA synthetases, ribosomes, and elongation factors. Knockout leads to accumulation of D-aminoacyl-tRNAs and potential synthesis of aberrant proteins, causing proteotoxic stress.
Disruption of DTD1 in HGC-27 cells creates a valuable model for dissecting the role of translational quality control in gastric cancer. Given the high protein synthesis demand of cancer cells, DTD1 loss may accentuate disease phenotypes such as proliferation, migration, and invasion. This allows exploration of how translational infidelity contributes to gastric adenocarcinoma progression and whether it generates exploitable therapeutic vulnerabilities.
Applications include mistranslation reporter assays, proliferation (MTT/XTT) and colony formation assays, migration/invasion studies, and proteomic detection of D-amino acid-containing proteins. The model also supports drug sensitivity screening to identify compounds targeting cells with compromised translational fidelity. For inquiries, please contact Ascent Research.
