The EFEMP1 Knockout SK-HEP-1 Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal knockout cell population in which the EFEMP1 gene has been disrupted. This product enables loss-of-function studies of fibulin-3 in a hepatic cancer model without selection of single-cell clones, preserving genetic heterogeneity for robust experimental analysis.
SK-HEP-1 is a human cell line established from the ascites of a patient with liver adenocarcinoma, displaying epithelial morphology and serving as a widely used model for hepatocellular carcinoma research. The cells are amenable to standard culture conditions and support assays for adhesion, migration, and invasion.
EFEMP1 encodes fibulin-3, an extracellular matrix glycoprotein that participates in cell adhesion, migration, and matrix organization through interactions with integrins and EGFR. Fibulin-3 modulates EGFR signaling and matrix metalloproteinase activity, acting downstream of EGF and TGF-?? stimulation and upstream of MMP2, MMP9, and TIMP3. It also influences the PI3K-Akt pathway and is regulated by SP1 and DNA methylation. In the ECM, fibulin-3 forms complexes with TIMP3 and integrins, thereby affecting pericellular proteolysis and growth factor receptor activation. Key signaling nodes include EGFR, AKT, ERK1/2, MMP2, and TIMP3.
In the context of SK-HEP-1 liver adenocarcinoma cells, EFEMP1 disruption is expected to alter integrin-mediated adhesion and growth factor receptor-dependent signaling, potentially affecting cell migration and invasion. Given the context-dependent tumor-suppressive or promoting roles of fibulin-3, this polyclonal knockout model enables investigation of its dual functions in hepatocellular carcinoma progression. Disruption of EFEMP1 may also impact the balance of MMPs and TIMP3, thereby modifying ECM remodeling and metastatic behavior.
This knockout cell population is suitable for a range of experimental applications, including migration/invasion assays, wound healing studies, ECM adhesion assays, and transcriptomic analysis via RNA-seq. Researchers can employ Western blotting and RT-qPCR to verify target gene disruption and downstream effector changes. The model supports studies of EGFR- and TGF-??-mediated signaling, drug response profiling, and evaluation of fibulin-3 as a therapeutic target in liver cancer. For detailed protocols, validation data, or ordering information, please contact Ascent Research.
