The HRH1 Knockout KYSE-150 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed for targeted disruption of the human HRH1 gene. This product comprises a heterogeneous pool of edited cells derived from the KYSE-150 host line, offering a loss-of-function model without clonal selection. The polyclonal format enables researchers to assess bulk gene disruption effects while mitigating clonal variation, making it suitable for functional genomics and drug response studies. The cells are provided as a ready-to-use knockout system for investigating histamine H1 receptor biology in esophageal cancer.
The parental KYSE-150 cell line originates from a poorly differentiated human esophageal squamous cell carcinoma. This epithelial cancer model is widely employed in cancer biology to study tumor cell proliferation, drug sensitivity, and oncogenic signaling. KYSE-150 cells retain molecular features of the original malignancy, offering a clinically relevant platform for esophageal cancer research. The line??s robust in vitro growth properties facilitate reproducible experimental setups, including inhibitor treatments and genetic perturbation assays.
The HRH1 gene encodes the histamine H1 receptor, a G??q/11-coupled GPCR that mediates allergic and inflammatory responses. Upon histamine binding, the receptor activates phospholipase C?? (PLC??) through G??q/11, generating inositol trisphosphate (IP3) and diacylglycerol (DAG). IP3 triggers calcium release from the endoplasmic reticulum, while DAG activates protein kinase C (PKC). Downstream, the mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) and nuclear factor-??B (NF-??B) cascades become engaged, driving transcription of pro-inflammatory genes such as IL-8, c-Fos, and COX-2. Interacting factors including ??-arrestin, G protein-coupled receptor kinase (GRK), and calmodulin modulate receptor desensitization and trafficking. The HRH1 signaling network therefore integrates G protein-dependent and -independent pathways critical for calcium mobilization, transcriptional regulation, and cytokine secretion.
In esophageal squamous cell carcinoma, aberrant HRH1 expression may contribute to tumor-associated inflammation and microenvironmental signaling. The KYSE-150 model enables dissection of histamine-mediated pathways that could influence cancer cell proliferation, migration, and resistance to apoptosis. Disruption of HRH1 in these cells can clarify the receptor??s role in tumor-promoting signaling, including PI3K-Akt and MAPK cascades, as well as its interplay with NF-??B-dependent expression of angiogenic factors like VEGF. This polyclonal knockout population thus serves as a powerful tool to differentiate H1R-dependent effects from other histamine receptor subtypes in the context of esophageal malignancy.
Researchers can utilize this cell product in a variety of functional assays. Calcium flux measurements using fluorescent indicators assess IP3-induced store mobilization. Western blotting for phospho-ERK and phospho-NF-??B monitors signaling outputs, while RT-qPCR quantifies induction of IL-8 and c-Fos transcripts. Flow cytometry confirms HRH1 surface loss. Additional applications include wound healing and transwell invasion assays to study migration and invasion, MTT proliferation assays, and NF-??B luciferase reporter systems. Cytokine ELISA can profile HRH1-dependent secretory changes. For further experimental guidance and technical support, please contact Ascent Research.
