The ACYP1 Knockout SK-HEP-1 Polyclonal Cells product is a human liver adenocarcinoma-derived polyclonal cell population engineered by CRISPR/Cas9-mediated disruption of the ACYP1 gene. This polyclonal knockout model provides a physiologically relevant system for studying loss of ACYP1 function in a cancer cell background without the clonal selection biases inherent in single-cell-derived lines. By eliminating acylphosphatase 1 activity, the cells enable researchers to investigate metabolic consequences of ACYP1 deficiency in hepatocellular carcinoma.
The parental SK-HEP-1 line is an epithelial-like cell line originally established from the ascitic fluid of a patient with liver adenocarcinoma. Widely used in hepatocellular carcinoma (HCC) research, SK-HEP-1 cells retain key features of hepatic malignancy, including dysregulated metabolism and proliferative signaling. This background makes the knockout model particularly suitable for investigating the interplay between metabolic pathways and oncogenic processes in liver cancer.
ACYP1 encodes acylphosphatase 1, an enzyme that catalyzes the hydrolysis of carboxyl-phosphate bonds in acyl phosphates, with 1,3-bisphosphoglycerate (1,3-BPG) being a primary substrate. In the glycolytic pathway, 1,3-BPG is generated by glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and is subsequently converted to 3-phosphoglycerate by phosphoglycerate kinase 1 (PGK1) in an ATP-generating step. ACYP1 competes with PGK1 for 1,3-BPG, thereby influencing glycolytic flux and cellular ATP balance. Disruption of ACYP1 leads to accumulation of 1,3-BPG, which can allosterically affect metabolic enzymes and alter flux through glycolysis, pyrimidine metabolism, and carbon metabolism. The loss of acylphosphatase activity disrupts energy homeostasis and may impair the metabolic flexibility typically exploited by cancer cells to adapt to nutrient stress.
In hepatocellular carcinoma, metabolic reprogramming is a hallmark that supports rapid proliferation and survival. SK-HEP-1 cells, like many cancer cells, rely heavily on glycolysis for energy and biosynthetic precursors. ACYP1 knockout in this background serves as a loss-of-function model to dissect the contribution of acylphosphatase 1 to glycolytic control and to evaluate how bypassing the PGK1 step via acylphosphatase activity affects metabolic robustness. This model is particularly relevant for studying mechanisms of metabolic adaptability and drug resistance often observed in liver tumors, where altered glycolytic intermediates can influence signaling and redox balance.
Researchers can utilize these polyclonal cells in a range of experimental workflows, including glycolysis stress tests with Seahorse XF analyzers, lactate production and glucose uptake assays, cell proliferation studies, and targeted metabolomic profiling to quantify changes in glycolytic and related intermediates. Western blotting and RT-qPCR for ACYP1 confirm knockout status, while acylphosphatase activity assays provide functional validation. This product is ideal for investigating hepatocellular carcinoma metabolism, glycolysis inhibition strategies, and metabolic reprogramming associated with drug resistance. For further technical details and ordering information, please contact Ascent Research.
