The GNPDA1 Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting the GNPDA1 gene in the human SK-HEP-1 hepatic adenocarcinoma cell line. This polyclonal product provides a heterogeneous loss-of-function model for studying glucosamine-6-phosphate deaminase 1 function in hexosamine metabolism. CRISPR/Cas9-mediated gene disruption generates a versatile tool for investigating metabolic flux, protein O-GlcNAcylation, and proliferation without single-cell cloning.
SK-HEP-1 is an immortalized hepatocellular carcinoma cell line derived from liver adenocarcinoma, widely used in cancer metabolism research. These cells exhibit active glycolysis and hexosamine pathway flux, making them a relevant context for examining GNPDA1-dependent metabolic reprogramming. Their well-characterized signaling networks facilitate mechanistic studies on amino sugar metabolism.
GNPDA1 deaminates glucosamine-6-phosphate to fructose-6-phosphate, linking hexosamine salvage to central carbon metabolism. It operates within a network including GFPT1, GNPNAT1, PGM3, and UAP1, with OGT and OGA as downstream effectors of protein O-GlcNAcylation. Glucose availability and insulin signaling regulate this axis through GFPT1-mediated hexosamine flux. Downstream targets include fructose-6-phosphate and glycolytic intermediates, connecting to energy metabolism. Knockout is expected to reduce UDP-GlcNAc pools and impair O-GlcNAcylation of proteins involved in metabolic regulation and cell cycle progression.
In hepatocellular carcinoma, dysregulated hexosamine metabolism contributes to malignant phenotypes. GNPDA1 disruption in SK-HEP-1 cells creates a model to explore how glucosamine-6-phosphate deamination impacts HCC proliferation and metabolic homeostasis. This model allows dissection of hexosamine salvage dependency in HCC and validation of GNPDA1 as a potential metabolic vulnerability. The polyclonal knockout population enables assessment of altered glycolytic flux, diminished O-GlcNAc signaling, and reduced proliferative capacity in a relevant liver cancer background.
This model supports hexosamine pathway analysis, O-GlcNAcylation research, and metabolic reprogramming studies. Applications include western blot for O-GlcNAc and OGT/OGA, metabolomic profiling of hexosamine intermediates, UDP-GlcNAc quantification, proliferation and glucose uptake assays, and Seahorse analysis. RT-qPCR and lectin blotting complement functional readouts, enabling comprehensive investigation of amino sugar metabolism in cancer. For further technical information or custom inquiries, please contact Ascent Research.
