The HRH1 Knockout HGC-27 Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal knockout cell population derived from HGC-27, a human gastric cancer cell line. This product features targeted disruption of the HRH1 gene, eliminating histamine H1 receptor expression in a genetically heterogeneous format that maintains the host cell??s intrinsic properties. The polyclonal knockout pool provides a reliable loss-of-function model without relying on single-cell clones, enabling robust and reproducible experimental outcomes in gastric cancer research.
HGC-27 cells are an established model of gastric adenocarcinoma, originally isolated from a metastatic lymph node of a gastric carcinoma patient. These cells display undifferentiated carcinoma morphology and are widely employed to study gastric tumor biology, including proliferation, invasion, and signal transduction. Their metastatic origin makes them particularly relevant for investigating pathways that drive cancer progression and dissemination.
HRH1 encodes the histamine H1 receptor, a Gq/11-coupled GPCR central to allergic and inflammatory signaling. Upon histamine binding, the receptor activates G??q/11, which stimulates PLC?? to generate IP3 and DAG, leading to intracellular Ca2+ release and PKC activation. This cascade triggers MAPK pathways (ERK, p38) and NF-??B, promoting transcription of pro-inflammatory mediators (IL-8, COX-2). Receptor regulation involves interacting proteins such as ??-arrestin1/2 and GRK2/3, which mediate desensitization and internalization. Key upstream regulators include histamine, IL-4, IL-13, and TNF-??.
In the gastric tumor microenvironment, histamine signaling through HRH1 may drive proliferation, migration, and inflammatory responses. By ablating HRH1 in HGC-27 cells, researchers can dissect H1-specific contributions to gastric adenocarcinoma behavior, separate from other histamine receptors. This knockout model is valuable for evaluating H1 receptor antagonists as potential anti-cancer agents and for exploring crosstalk between GPCR signaling and oncogenic pathways in gastric epithelial cells.
Applications include calcium flux assays (Fluo-4 AM) to measure H1-dependent Ca2+ mobilization, Western blotting for phospho-ERK/p38, CCK-8 proliferation assays, transwell migration assays, and IL-8 ELISA. Radioligand binding can confirm receptor loss. These tools support investigation of histamine-driven mechanisms in gastric cancer, validation of H1 antagonists, and GPCR signaling studies. For additional information, please contact Ascent Research.
