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Engauge digitizer hazard ratio12/29/2023 In terms of GLUT1, previous studies investigating the relationship between GLUT1 expression and clinical outcomes of patients with pancreatic cancer have yet yielded conflicting results. It has been well demonstrated that these glycolysis enzymes contribute to biological behaviors of cancer.Īlthough emerging evidence has focused on the correlation between various glycolysis markers and pancreatic cancer, the conclusions remain controversial. Moreover, ENO1, also known as alpha-enolase, a critical glycolytic enzyme that dehydrates 2-phosphoglycerate to phosphoenolpyruvate, is present both in cell surface and cytoplasm ( 13). PKM2 is the key rate-limiting enzyme involved in the final step of the glycolysis pathway and catalyzes the last irreversible step in glycolysis, the conversion of phosphoenolpyruvate to pyruvate, while ADP is phosphorylated to form ATP ( 12). As the most influential functional enzyme of glycolysis, overexpression of HK2 promotes glycolysis process by catalyzing phosphorylation of glucose to glucose-6-phosphate ( 11). Besides cellular membrane transporters, several enzymes located in cytoplasmic fractions also contribute to glycolytic flux. Since enhanced glycolysis is associated with lactate production, tumor cells must eliminate excessive lactate out of the cell to prevent cellular acidification, which is achieved by the upregulation of MCT4, a proton-coupled lactate transporter ( 10). Increased rate of glucose uptake in malignant cells is associated with elevated expression of GLUTs, especially GLUT1 ( 9). Transport of glucose across the plasma membrane is an important regulator of glucose metabolism and is mediated by glucose transporter (GLUT) family proteins. Previous studies have shown that multiple key glycolytic enzymes such as glucose transporter 1 (GLUT1), monocarboxylate transporter 4 (MCT4), hexokinase 2 (HK2), pyruvate kinase M2 (PKM2) and enolase 1 (ENO1) are usually overexpressed in tumors and play critical roles in glycolysis pathway ( 8). The enhancement of glycolysis has been demonstrated to play critical roles in pancreatic tumorigenesis and development ( 6, 7). It has been well known that tumor cells tend to increase their glucose uptake and lactate production even in the presence of ample oxygen, which is described as the “aerobic glycolysis” or “Warburg effect” ( 5). Malignant proliferating cancer cells usually rewire energy metabolism manners to meet the requirements of rapid cell growth, division, invasion, and migration, which is an emerging hallmark of cancer known as “energy metabolism reprogramming” ( 4). ![]() The worse clinical outcomes of PDAC are due to the lack of early typical symptoms and the highly aggressive biological characteristics, emphasizing the urgent need for searching promising prognostic markers for clinical practice. Pancreatic ductal adenocarcinoma (PDAC), the most common type of pancreatic cancer, is the deadliest malignancy with a 5-year survival rate of less than 8% ( 3). Pancreatic cancer is the seventh leading cause of cancer-related death worldwide due to its poor prognosis with almost as many deaths (n=466,003) as cases (n=495,773) ( 1), which was estimated to become the second most common cause of cancer-related death by 2030 in the U.S ( 2).
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