DTWD1 Knockout HGC-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human gastric carcinoma epithelial cell line HGC-27, engineered for targeted disruption of the DTWD1 gene. This heterogeneous pool of edited cells, generated via CRISPR/Cas9-mediated gene disruption, serves as a loss-of-function model to investigate the biological role of DTWD1. The polyclonal format avoids clone-specific artifacts and represents a range of editing events, enabling robust functional genomic studies without selection for a single clonal genotype. This ready-to-use cell population features efficient target-gene disruption validated at the population level, suitable for immediate downstream applications.
The parental HGC-27 cell line was originally established from the lymph node metastasis of a gastric adenocarcinoma patient and exhibits stable epithelial morphology. As a widely utilized model in gastric cancer research, HGC-27 cells recapitulate key features of metastatic gastric carcinoma, including invasive growth properties and relevant oncogenic signaling networks. This cell line enables investigations into gastric cancer progression, metastasis, and therapeutic responses, providing a clinically relevant background for functional genomics studies. The knockout cells retain these fundamental characteristics, facilitating the dissection of gene-specific contributions to gastric adenocarcinoma biology.
DTWD1 encodes a poorly characterized protein containing a DTW domain, a structural feature commonly associated with enzymes involved in RNA modification, particularly within the tRNA modification machinery. Bioinformatic predictions and domain homology suggest DTWD1 may participate in the regulation of RNA metabolism and cell proliferation, though its direct substrates and interaction partners remain unknown. DTWD1 likely functions in tRNA modification pathways that impact translational fidelity and cell cycle progression. With no known upstream regulators, downstream effectors, or interacting factors, the knockout model offers a critical tool for mapping DTWD1??s molecular functions through unbiased transcriptomic and proteomic profiling.
In the context of the HGC-27 gastric adenocarcinoma model, loss of DTWD1 function permits systematic evaluation of its contribution to oncogenic phenotypes. The metastatic origin of the host cells provides a unique platform to study how DTWD1-mediated RNA modifications may affect processes such as cell migration, invasion, and metastatic colonization. Additionally, the polyclonal knockout population can be used to assess the overall impact of DTWD1 disruption on cellular fitness and proliferation in a gastric cancer background, enabling dissection of RNA metabolism??s role in tumor biology. Comparative analyses between parental and knockout populations can reveal DTWD1-dependent changes in gene expression and cellular behavior.
This knockout product supports a broad range of research applications, including functional characterization of DTWD1 in gastric adenocarcinoma, investigation of tRNA modification dynamics through specialized profiling techniques, and assessment of cell proliferation, migration, and invasion via standard in vitro assays. Researchers may use Western blotting and RT?qPCR to confirm target-gene disruption and quantify downstream effects, while RNA?seq and tRNA modification profiling provide global insights into RNA metabolism alterations. Clonogenic assays and drug sensitivity studies further extend the utility for preclinical evaluation of therapeutic vulnerabilities. For inquiries, additional product specifications, or support, please contact Ascent Research.
