The ECHDC1 Knockout 786-O Polyclonal Cells product comprises a CRISPR/Cas9-edited polyclonal knockout cell population in which the ECHDC1 gene has been disrupted in the 786-O human renal cell adenocarcinoma line. ECHDC1 encodes a mitochondrial enoyl-CoA hydratase that performs the second step of fatty acid ??-oxidation. This polyclonal population provides a heterogeneous collection of gene-edited cells, avoiding clonal biases and enabling robust functional investigations of mitochondrial lipid metabolism in a cancer context.
786-O is a well-characterized cell line derived from a primary clear cell renal cell carcinoma of a 58-year-old male. This line serves as a standard in vitro model for ccRCC, a tumor type notable for metabolic reprogramming including altered fatty acid oxidation and mitochondrial function. The inherent VHL mutation in 786-O cells links hypoxia signaling to metabolic adaptation, making it an appropriate host to study how ECHDC1 loss impacts cancer cell energetics.
ECHDC1 catalyzes the hydration of trans-2-enoyl-CoA to 3-hydroxyacyl-CoA within the mitochondrial ??-oxidation spiral. It functions in concert with interacting factors such as acyl-CoA dehydrogenases (ACADs) and the mitochondrial trifunctional protein (HADHA/HADHB), and is transcriptionally regulated by PPARA and PPARGC1A in response to fatty acid availability. Downstream, ECHDC1 activity generates acetyl-CoA, NADH, and FADH2 to drive ATP production and mitochondrial respiration. Knockout of ECHDC1 thus disrupts this metabolic cycle, likely leading to energetic stress and accumulation of intermediate metabolites.
In 786-O ccRCC cells, ECHDC1 disruption is particularly relevant because renal carcinomas often exhibit heightened reliance on fatty acid metabolism for growth and survival. This knockout model enables dissection of how mitochondrial ??-oxidation contributes to ccRCC proliferation, metabolic flexibility, and drug response. It also permits exploration of compensatory metabolic shifts toward glycolysis or glutaminolysis upon fatty acid oxidation impairment.
This polyclonal knockout population is suited for biochemical and functional assays including RT-qPCR, Western blotting, 14C-palmitate oxidation assays, Seahorse metabolic flux analysis, and cell proliferation measurements. It offers a versatile platform for research in cancer metabolism, mitochondrial dysfunction, and metabolic disorders. For further information, please contact Ascent Research.
