This product consists of a CRISPR/Cas9-edited polyclonal knockout cell population in which the GOPC gene has been disrupted within the human SK-HEP-1 cell line. The polyclonal pool contains a heterogeneous mixture of cells carrying diverse loss-of-function mutations at the GOPC locus, generated by CRISPR/Cas9-mediated gene disruption. This knockout model provides a versatile tool for investigating GOPC-dependent biological processes without the constraints of single-cell clonal selection.
The SK-HEP-1 host cell line was originally derived from the ascitic fluid of a 52-year-old male patient with liver adenocarcinoma. These cells display a hypertriploid karyotype and adherent epithelial morphology, and they serve as a widely used in vitro model for hepatocellular carcinoma (HCC) tumorigenesis, metastasis, and drug response studies. The genetic background and malignant characteristics of SK-HEP-1 make it particularly suitable for examining the roles of trafficking and autophagy regulators in liver cancer progression.
GOPC encodes a Golgi-associated PDZ scaffold that sorts transmembrane proteins into transport vesicles, controlling their surface expression and signaling output. It negatively regulates autophagosome formation through its interaction with Beclin 1 (BECN1), linking vesicular trafficking to autophagy. Key molecular partners include CFTR, Frizzled (FZD) receptors, AMPA receptor subunit GRIA2, neuroligin (NLGN1), STX6, GOLGA2, and acetylated tubulin. GOPC integrates signals from autophagy pathways (BECN1, PIK3C3, ATG14) and Wnt/planar cell polarity signaling (via DVL and FZD), with autophagy-inducing stimuli such as nutrient deprivation or mTORC1 inhibition likely modulating its activity.
In SK-HEP-1 liver adenocarcinoma cells, GOPC loss disrupts trafficking and surface expression of receptors that influence proliferation, migration, and survival. Because GOPC interacts with Frizzled receptors and autophagy components, its knockout may alter Wnt/PCP activity and autophagic flux, both implicated in HCC metastasis and drug resistance. This model enables dissection of GOPC’s role in hepatocellular carcinoma biology and its impact on responses to chemotherapeutics or trafficking/autophagy-targeted inhibitors.
This polyclonal knockout population is suited for functional studies of receptor trafficking, autophagy, and Golgi morphology in liver cancer. Key assays include Western blotting, immunofluorescence (Golgi markers), autophagy flux assays (LC3), co-immunoprecipitation, RT-qPCR, and flow cytometry for surface receptor quantification. Cell migration and drug sensitivity assays enable metastasis and chemoresponse investigations. The model is also valuable for studying GOPC-ROS1 fusion biology and screening autophagy/trafficking-targeted compounds. For technical support, contact Ascent Research.
