The GPRIN1 knockout SK-HEP-1 polyclonal cells constitute a CRISPR/Cas9-edited polyclonal knockout population, in which the GPRIN1 gene has been disrupted. As a polyclonal knockout model, this product comprises a heterogeneous cell pool with diverse editing outcomes at the targeted locus, avoiding clonal selection. This loss-of-function system is tailored for examining GPRIN1-dependent processes in hepatic adenocarcinoma.
SK-HEP-1 cells originate from the ascites of a liver adenocarcinoma patient and serve as a well-characterized hepatocellular carcinoma model. These adherent epithelial cells are valued for their rapid growth and invasive behavior, reflecting the aggressive features of liver tumors. Their wide application in cancer research includes signaling studies, drug testing, and metastasis assays.
GPRIN1 operates as a scaffolding/effector protein downstream of GPCRs, binding G??o (GNAO1) and G??i (GNAI) subunits, 14-3-3 proteins, and tubulin. It mediates GTPase signaling and cytoskeletal dynamics, regulating effectors such as ERK1/2, AKT, CDC42, RAC1, cyclin D1, and p21. Consequently, GPRIN1 intersects the MAPK/ERK cascade, PI3K/AKT pathway, and cell cycle machinery. Its expression is influenced by transcription factors CREB and AP-1. In knockout cells, disruption of GPRIN1 likely impairs GPCR-driven signaling, diminishing downstream pathway activity.
Within SK-HEP-1 liver adenocarcinoma cells, GPRIN1 knockout provides a relevant platform to dissect GPCR-mediated oncogenic mechanisms. Aberrant MAPK and PI3K/AKT signaling frequently drives hepatocellular carcinoma progression; thus, this model enables exploration of GPRIN1??s impact on proliferation, migration, and apoptosis. By attenuating AKT and ERK1/2 signaling and altering cyclin D1 and p21 expression, the knockout cells permit quantitative analysis of tumorigenic traits and evaluation of GPCR-directed therapeutics.
Key applications include studying GPCR signaling in liver cancer, investigating GPRIN1??s role in hepatocellular carcinoma, screening drugs targeting GPCR pathways, and biomarker identification. Compatible assays span Western blotting, RT-qPCR, proliferation (MTT/CCK8), Transwell migration/invasion, immunofluorescence, cAMP accumulation, apoptosis (Annexin V/PI), and GPCR activity reporters. For further information, contact Ascent Research.
