The GNRH1 Knockout KYSE-150 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the KYSE-150 human esophageal squamous cell carcinoma line. This product provides a loss-of-function model for the GNRH1 gene, which encodes gonadotropin-releasing hormone 1, enabling researchers to dissect the autocrine and paracrine roles of GnRH signaling in esophageal cancer biology. The polyclonal pool retains the genetic heterogeneity typical of a non-clonal knockout population, suitable for pooled functional assays and multi-parametric analyses.
The KYSE-150 cell line was established from a poorly differentiated esophageal squamous cell carcinoma and is widely used as a model for esophageal cancer research. It exhibits representative epithelial characteristics and retains key oncogenic properties, including dysregulated proliferation and migration. Its derivation from a squamous cell carcinoma makes it particularly relevant for studying signaling pathways implicated in the progression of esophageal squamous cell cancers.
GNRH1 encodes the precursor of GnRH, a decapeptide that binds with high affinity to its receptor GNRHR, a G protein-coupled receptor. Ligand?Creceptor engagement triggers Gq/11-mediated activation of phospholipase C (PLCB), leading to generation of inositol trisphosphate (IP3) and diacylglycerol (DAG), mobilization of intracellular calcium, and activation of protein kinase C (PRKCA). These events converge on multiple mitogen-activated protein kinase (MAPK) cascades, including ERK1/2 (MAPK1/3), JNK (MAPK8/9), and p38 (MAPK14), as well as transcription factors such as CREB, ELK1, and AP-1 components. The GnRH system is classically controlled by upstream regulators such as kisspeptin, neurokinin B, and sex steroids, and transduces signals through interacting partners including beta-arrestin and calmodulin.
In KYSE-150 cells, endogenous GNRH1 expression may establish an autocrine/paracrine loop that fuels cancer cell proliferation, survival, and motility via the GNRHR-mediated pathways. Disruption of this loop through knockout of GNRH1 allows systematic investigation of how loss of GnRH signaling alters MAPK activity, calcium flux, and gene transcription, thereby modulating key malignant phenotypes. The knockout model thus provides a defined genetic background for comparative studies of GnRH-dependent and -independent mechanisms in esophageal cancer progression.
Typical applications include analyzing the role of GnRH autocrine signaling in cell proliferation using MTS/MTT assays, migration and invasion in transwell chambers, and apoptosis via flow cytometry. The knockout cells are also suited for phospho-ERK and other MAPK activation studies by western blot, RT-qPCR profiling of downstream targets such as GNRHR and MAPK-regulated genes, and global transcriptomic analysis via RNA-seq. Additionally, the model enables screening of GnRH analogs and small-molecule inhibitors for their anticancer efficacy in esophageal carcinoma. For further information or to request a quote, please contact Ascent Research.
