The DNTTIP1 Knockout AGS Polyclonal Cells are a polyclonal population of AGS gastric epithelial cells that have been engineered via CRISPR/Cas9-mediated disruption of the DNTTIP1 gene. This loss-of-function model is designed for studies of DNTTIP1 within the NuRD complex, enabling interrogation of chromatin remodeling and transcriptional repression in a gastric cancer background. As a polyclonal knockout pool, it supports bulk analyses of DNTTIP1-dependent effects without clonal selection.
The parental AGS cell line is a well-characterized human gastric adenocarcinoma epithelial model derived from a patient with gastric cancer. AGS cells are extensively employed to investigate gastric cancer biology, including proliferation, metastasis, and drug sensitivity, as well as Helicobacter pylori pathogenesis. Their adherent epithelial morphology and robust growth render them amenable to numerous functional assays.
DNTTIP1 is a core subunit of the nucleosome remodeling and deacetylase (NuRD) complex, which couples ATP-dependent chromatin remodeling with histone deacetylation to establish repressive chromatin states. It interacts with multiple NuRD components, including histone deacetylases HDAC1 and HDAC2, metastasis-associated proteins MTA1 and MTA2, chromatin remodelers CHD3 and CHD4, and scaffold proteins such as RBBP4, RBBP7, MBD2, MBD3, GATAD2A, and GATAD2B. Through these interactions, DNTTIP1 facilitates NuRD targeting to genomic loci, leading to deacetylation of histones H3 and H4 and subsequent silencing of downstream targets such as tumor suppressor genes and cell cycle regulators. Recruitment of NuRD by transcription factors and regulation by MTA proteins further link DNTTIP1 to pathways controlling proliferation and apoptosis.
In AGS gastric cancer cells, DNTTIP1 disruption is expected to impair NuRD complex integrity, resulting in derepression of genes governing cell cycle progression, apoptosis, and metastatic potential. This makes the knockout model highly relevant for studying epigenetic dysregulation in gastric adenocarcinoma and for understanding how H. pylori-driven chromatin alterations contribute to host cell transformation. It provides a valuable platform to dissect NuRD-mediated transcriptional silencing in tumorigenesis.
This DNTTIP1 knockout model is suitable for diverse applications, including characterization of transcriptional programs via RT-qPCR and ChIP-qPCR for histone modifications, and assessment of NuRD complex composition by co-immunoprecipitation. Functional assays can include cell viability and proliferation measurements, wound healing, Transwell migration and invasion assays, and flow cytometry-based apoptosis analyses. The polyclonal cells also serve in drug sensitivity screens and immunofluorescence studies. These experiments can aid in identifying therapeutic targets in gastric and other adenocarcinomas. For further information or technical support, please contact Ascent Research.
