The ISOC1 Knockout SK-HEP-1 Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal population of SK-HEP-1 human liver adenocarcinoma cells with targeted disruption of the ISOC1 gene. As a non-clonal pool, these cells circumvent the genetic drift and selection effects inherent to monoclonal lines, offering a more representative model for functional studies of ISOC1 in hepatocellular carcinoma contexts.
The parental SK-HEP-1 cell line was established from the ascites of a patient with liver adenocarcinoma and is widely employed as an epithelial model for hepatic cancer and endothelial biology. Its tumorigenic properties and well-characterized signaling landscape make it an appropriate host for interrogating liver cancer-specific gene functions.
ISOC1 encodes a putative mitochondrial protein with an isochorismatase-like domain and has been implicated in mitochondrial energy metabolism and cell proliferation through activation of PI3K/Akt signaling. Mechanistically, ISOC1 functions downstream of transcriptional regulators such as PPARGC1A (PGC-1??), NRF1, and HIF-1??, and upstream of AKT and mTOR. It interacts with mitochondrial ribosomal proteins (MRPLs and MRPSs) and electron transport chain subunits, and its activity converges on pathway components including PIK3CA, AKT1, MTOR, NDUFV1, and SDHB. ISOC1-mediated signaling promotes hepatocellular carcinoma cell proliferation, and its disruption attenuates Akt phosphorylation and impairs mitochondrial respiratory chain function.
In the SK-HEP-1 background, knockout of ISOC1 disrupts mitochondrial homeostasis, reduces Akt activation, and suppresses cell growth, mirroring the phenotype observed in other hepatic cancer models. This polyclonal knockout system serves as a robust platform for dissecting the ISOC1-dependent link between mitochondrial metabolism and oncogenic signaling in hepatocellular carcinoma, and for probing interactions with metabolic regulators such as PGC-1?? and mTOR.
Potential applications include mechanistic studies of liver cancer cell proliferation, apoptosis resistance, metabolic reprogramming, and drug sensitivity. The knockout cells are suitable for western blotting (ISOC1, phosphorylated Akt, cleaved caspase-3), RT-qPCR, MTT and colony formation assays, Seahorse mitochondrial stress tests, and flow cytometry-based cell cycle and apoptosis analyses. Researchers can leverage this model to identify vulnerabilities in ISOC1-driven tumors or to validate downstream effectors. For further details, please contact Ascent Research.
