The GPER1 Knockout CAL-27 Polyclonal Cells are a polyclonal population of human oral squamous cell carcinoma cells engineered by CRISPR/Cas9-mediated disruption of the GPER1 gene. This loss-of-function model is provided as a non-clonal knockout pool, preserving the genetic heterogeneity inherent to tumor cell populations. By eliminating GPER1 expression, these cells enable precise dissection of rapid estrogen signaling pathways independent of clonal artifacts.
The parental CAL-27 line originates from a human tongue squamous cell carcinoma obtained before therapy and maintains an epithelial phenotype. It is widely utilized as a robust model for investigating oral cancer cell biology, including proliferation, migration, invasion, and response to pharmacological agents. This background is ideal for examining GPER1??s role in head and neck squamous cell carcinoma.
GPER1 is a membrane-bound estrogen receptor that triggers non-genomic signaling cascades. Stimulation by 17??-estradiol or the selective agonist G-1 promotes coupling to G??s, activating adenylyl cyclase and elevating cAMP levels, which in turn activate PKA. Concurrently, GPER1 transactivates EGFR, initiating the Ras?CRaf?CMEK?CERK1/2 phosphorylation cascade, and directly engages the PI3K?CAKT pathway. Downstream consequences include phosphorylation of ERK1/2 and AKT, transcriptional upregulation of c-Fos and Cyclin D1, and increased production of matrix metalloproteinases, collectively enhancing cell cycle progression and invasive capacity.
Knockout of GPER1 in CAL-27 cells ablates estrogen-mediated activation of MAPK/ERK and PI3K/AKT signaling, resulting in impaired proliferation, migration, and invasion. This polyclonal model thus provides a powerful tool for distinguishing GPER1-specific contributions from those of nuclear estrogen receptors in squamous cell carcinoma of the head and neck. It is particularly suited for studies on EGFR transactivation and the interplay between estrogenic stimuli and tumor progression.
These polyclonal knockout cells are applicable to functional genomics studies of estrogen action in oral cancer, detailed analysis of GPER1-driven cell motility and invasiveness, and high-throughput screening of GPER1-targeted therapeutics. They facilitate the investigation of receptor crosstalk and the validation of putative biomarkers. Compatible assays include western blotting for phosphorylated ERK1/2 and AKT, RT-qPCR for GPER1 and downstream effectors, MTT or BrdU proliferation assays, Transwell migration and invasion tests, immunofluorescence, RNA-seq, and rescue experiments with GPER1 agonist G-1. For technical inquiries and ordering, please contact Ascent Research.
