GPER1 Knockout AsPC-1 Cell Line

The choice depends on whether you are studying GPER1 (GPR30, G protein-coupled estrogen receptor 1)'s role as a non-canonical estrogen-responsive membrane GPCR or its functions in pancreatic cancer biology. The Knockout line is the standard tool for asking whether GPER1 is required for non-genomic estrogen signaling — GPER1 is a seven-transmembrane GPCR activated by 17β-estradiol that initiates rapid non-genomic estrogen signaling (cAMP, ERK, EGFR transactivation) distinct from classical ESR1/ESR2 nuclear receptor signaling. Overexpression is useful for studying GPER1 in heterologous expression contexts. For pancreatic cancer research, the EDITGENE GPER1 Knockout in AsPC-1 is highly relevant — AsPC-1 is a pancreatic ductal adenocarcinoma cell line, and GPER1 has been implicated in pancreatic cancer biology with both pro- and anti-tumor effects reported. Rescue with wild-type or signaling-deficient GPER1 enables structure-function studies. The knockout is a critical specificity control for GPER1 agonist G-1 (LNS8801, in clinical development for various cancers), GPER1 antagonist G-15, and emerging GPER1-targeted cancer therapeutics.

Primary applications: • Non-genomic estrogen signaling: rapid cAMP and phospho-ERK analysis following 17β-estradiol stimulation in GPER1-null cells. • Pancreatic cancer biology: proliferation, migration, and survival assays given GPER1's role in pancreatic cancer. • G-1 agonist specificity: critical genetic control for G-1 (LNS8801, in clinical development for various cancers) — G-1 should have no effect in GPER1-null cells. • GPER1 antagonist studies: G-15, G-36 antagonist specificity testing. EDITGENE recommends this AsPC-1-based model for researchers investigating GPER1 biology, non-genomic estrogen signaling, and GPER1-targeted pancreatic cancer therapeutic development.

Yes. GPER1 rescue experiments require attention to GPCR architecture: • Construct design: use a codon-modified GPER1 sequence with a small intracellular C-terminal tag (FLAG, HA). GPER1 is a seven-transmembrane GPCR — preserve estrogen-binding pocket and intracellular signaling regions. • Signaling-deficient rescue: DRY motif mutations disrupt G-protein coupling. • Surface localization validation: confirm plasma membrane localization by cell surface staining; GPER1 is partially intracellular in some contexts. • Functional readout: rescue should restore 17β-estradiol-induced cAMP elevation and rapid ERK activation. AsPC-1-specific considerations: • AsPC-1 is a human pancreatic ductal adenocarcinoma cell line (KRAS-mutant, derived from ascites of a patient with metastatic disease) — a relevant model for pancreatic cancer biology. • Lentiviral transduction is supported with moderate efficiency. • AsPC-1's metastatic origin and KRAS-mutant background make it valuable for pancreatic cancer mechanism studies.