The GPSM2 Knockout SK-HEP-1 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal population of the human hepatic adenocarcinoma SK-HEP-1 cell line with targeted disruption of the GPSM2 gene. This loss-of-function model allows population-level studies of GPSM2 without clonal isolation, maintaining the biological diversity of the parental line while abolishing functional protein expression.
SK-HEP-1 cells were derived from the ascitic fluid of a liver adenocarcinoma patient and display a mixed epithelial?Cendothelial phenotype, making them a distinctive model for hepatic tumor biology, including vasculogenic mimicry and metastatic potential. They are extensively used in hepatocellular carcinoma research and drug sensitivity screening, offering a robust platform for mechanistic and therapeutic studies.
GPSM2 (LGN) is a receptor-independent G protein modulator that orchestrates mitotic spindle orientation and cell polarity. It associates with the plasma membrane via G??i??GDP (GNAI family) and recruits NUMA1 and the dynein-dynactin complex, which exert pulling forces on astral microtubules. Upstream, the PARD3?CPARD6A?CaPKC polarity complex and INSC regulate GPSM2 localization, while it also interacts with DLG1 and FRMPD2, integrating G protein signaling with cytoskeletal dynamics.
In SK-HEP-1 cells, GPSM2 knockout likely disrupts spindle positioning and asymmetric division, impacting cell fate and polarity. This is particularly relevant to hepatocarcinogenesis, where aberrant G protein signaling and loss of polarity are common. Furthermore, GPSM2 mutations cause Chudley-McCullough syndrome (deafness, brain malformations), highlighting the gene’s developmental importance and providing a platform for modeling disease pathways in vitro.
Researchers can employ this knockout model to investigate mitotic spindle morphology via immunofluorescence, assess cell cycle changes by flow cytometry, and study protein complexes using co-immunoprecipitation of GPSM2 partners such as GNAI and NUMA1. Migration, invasion, and drug sensitivity assays are suited for liver cancer research, while RT-qPCR and Sanger sequencing enable genetic validation. For additional information, contact Ascent Research.
