The DCPS Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population, produced by targeted disruption of the DCPS gene in the HT29 human colorectal adenocarcinoma cell line. This gene-edited product provides a loss-of-function model for studying the scavenger decapping enzyme DCPS in mRNA decay and gene regulation.
HT29 is a human colorectal adenocarcinoma cell line with epithelial morphology, commonly used to study intestinal epithelial biology, drug transport, and colorectal cancer mechanisms. It serves as a relevant host for investigating RNA metabolism in the context of intestinal tumorigenesis.
DCPS encodes a scavenger decapping enzyme that hydrolyzes the m7GpppN cap remnant after DCP2-mediated decapping, enabling cap recycling and 5???3?? mRNA degradation by XRN1. It interacts with the exon junction complex and nuclear cap-binding complex, and functions in nonsense-mediated decay and pre-mRNA splicing. Upstream, it is regulated by stress-responsive transcription factors and proliferation signals; downstream, it affects global mRNA stability and post-transcriptional control. It works within a network including DCP1A, DCP2, the LSM1-7 complex, and CCR4-NOT.
In HT29 cells, DCPS knockout disrupts mRNA turnover, potentially altering proliferation and stress responses. This model helps elucidate how defective RNA quality control contributes to colorectal cancer, particularly via exon junction complex and nonsense-mediated decay pathways. DCPS relevance to neurological disorders also allows cross-disease studies of RNA metabolism defects.
Applications include mRNA stability assays (RT-qPCR), RNA-seq, proliferation/apoptosis assays, drug sensitivity profiling, and synthetic lethal screens. Immunofluorescence and Western blotting can track DCPS and interacting proteins. This tool supports mechanistic and translational research. For further information, contact Ascent Research.
