The DHRS11 Knockout AGS Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the AGS human gastric adenocarcinoma cell line, featuring targeted disruption of the DHRS11 gene. This polyclonal knockout model provides a heterogeneous collection of edited cells, enabling robust functional studies without the selection biases inherent to monoclonal isolates. This model is instrumental for investigating the biological roles of DHRS11 in cancer metabolism and signaling.
The AGS cell line is a widely employed human gastric adenocarcinoma epithelial line established from a primary tumor of a female patient. These cells exhibit epithelial morphology and possess inherent metastatic potential, making them a classic model for gastric cancer research. AGS cells are particularly valued for studies on Helicobacter pylori pathogenesis, oncogenic signaling, and therapeutic drug responses, providing a physiologically relevant background for gene-editing applications. Their well-characterized molecular features and robust growth in culture further enhance their utility.
The DHRS11 gene encodes an NADPH-dependent short-chain dehydrogenase/reductase that reduces carbonyl substrates, including retinaldehyde and steroids, thereby participating in retinoid metabolism, steroid hormone biosynthesis, and prostaglandin metabolic processes. Its expression is regulated by NRF2, PPAR??, and estrogen receptor, and influenced by cytokines such as IL-1?? and TNF. DHRS11 acts upstream of retinoic acid receptors RAR?? and RXR?? and cooperates with pathway components like RDH10, ALDH1A1, and CYP26A1. This enzymatic activity is critical for cellular redox homeostasis and hormonal signaling.
In AGS gastric cancer cells, loss of DHRS11 disrupts retinoic acid signaling and steroid hormone metabolism, pathways frequently dysregulated in gastric carcinogenesis. This knockout model enables the investigation of how altered retinoid processing affects cancer cell proliferation, differentiation, and survival. Additionally, DHRS11 deficiency may perturb the cellular redox state, potentially sensitizing cells to oxidative stress and influencing metabolic adaptations characteristic of malignant cells. Thus, these polyclonal knockout cells provide a relevant system to explore the metabolic dependencies of gastric adenocarcinoma.
This DHRS11 knockout polyclonal cell population is applicable to a variety of functional genomics and cancer metabolism studies. Researchers can perform Western blotting and RT-qPCR to verify gene disruption and examine pathway activation, while cell viability and migration/invasion assays provide functional readouts of cancer cell behavior. Global analyses via metabolic profiling and RNA-seq reveal comprehensive molecular changes, and retinoic acid reporter assays offer direct measurement of retinoic acid signaling activity. These cells are especially relevant for gastric cancer research, retinoid pathway investigation, and drug target discovery. For further assistance, please contact Ascent Research.
