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Significance Pancreatic ductal adenocarcinoma (PDAC) is the most common form of pancreatic cancer and is one of the most deadly cancer types, with a 5-y survival rate below 10%. One reason for this high mortality rate is that PDAC cells have an enhanced ability to survive and proliferate despite existing in nutrient-deprived environments. Understanding the metabolic rewiring that enables nutrient scavenging and rapid metabolic processing of PDAC cells can provide new strategies to develop effective treatment options for this intractable disease. In this study, convergent findings reveal that UGP2 has a central role in the growth and metabolism of PDAC cells through the regulation of glycogen synthesis and protein N-glycosylation, highlighting therapeutic possibilities for this deadly cancer.

UDP-glucose pyrophosphorylase 2, a regulator of glycogen synthesis and glycosylation, is critical for pancreatic cancer growth