ECI1 Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated from the SK-HEP-1 human hepatocellular carcinoma cell line, featuring targeted disruption of the ECI1 gene. This polyclonal pool provides a heterogeneous loss-of-function model that mirrors the genetic variability inherent in CRISPR editing, offering researchers a robust tool for investigating ECI1-dependent biology without the limitations of single-clone artifacts.
The parental SK-HEP-1 cell line is a well-characterized human liver adenocarcinoma line, isolated from ascites of a patient with hepatocellular carcinoma. These cells maintain metabolic hallmarks of liver cancer, including active fatty acid oxidation and lipid metabolism, making them an appropriate host for studying the consequences of ECI1 deficiency in a hepatocellular carcinoma context.
ECI1 encodes mitochondrial enoyl-CoA isomerase, a key auxiliary enzyme in the ??-oxidation of unsaturated fatty acids. It catalyzes the isomerization of 3-cis-enoyl-CoA intermediates to the 2-trans-enoyl-CoA form, a critical step that allows complete fatty acid degradation. ECI1 functions downstream of PPARA (PPAR??) and AMPK signaling pathways, and its activity supports the generation of acetyl-CoA for the TCA cycle, mitochondrial ATP production, and ketone body synthesis. Within the ??-oxidation complex, ECI1 physically interacts with ACADVL, HADHA, and HADHB, and its function is integrated with other pathway components such as CPT1, CPT2, and ACADM. By processing unsaturated fatty acyl-CoA species, ECI1 helps maintain efficient energy homeostasis in hepatoma-derived cells.
In SK-HEP-1 hepatocellular carcinoma cells, knockout of ECI1 abolishes enoyl-CoA isomerase activity, resulting in the accumulation of 3-cis-enoyl-CoA intermediates and a selective block in unsaturated fatty acid ??-oxidation. This disruption impairs mitochondrial fatty acid-derived energy production and may induce metabolic reprogramming, shifting cellular reliance toward glycolysis or glutaminolysis. Consequently, these ECI1 knockout cells serve as a valuable model for examining how fatty acid oxidation capacity influences hepatocellular carcinoma proliferation, survival under energetic stress, and sensitivity to metabolic inhibitors.
This polyclonal knockout product is ideally suited for applications in fatty acid metabolism research, hepatocellular carcinoma biology, and metabolic drug screening. Researchers can employ these cells in functional assays such as Seahorse mitochondrial stress tests, 14C-palmitate oxidation measurements, ATP quantification, and acyl-CoA metabolomic profiling to assess metabolic flux changes. Furthermore, the pool is appropriate for investigating PPAR signaling pathway dynamics, AMPK activation, and transcriptional responses to fatty acid oxidation disruption via RT-qPCR and Western blotting for key pathway targets. These ECI1 knockout cells also support lipidomics studies and phenotypic screens for compounds that modulate metabolic flexibility in liver cancer. For additional information or custom requests, please contact Ascent Research.
