The interactive role of inflammatory mediators and metabolic reprogramming in pancreatic cancer

Pancreatic ductal adenocarcinoma (PDAC) is characterized by its highly reactive inflammatory desmoplastic stroma with evidence of an extensive tumor stromal interaction largely mediated by inflammatory factors. KRAS mutation and inflammatory signaling promote protumorigenic events, including metabolic reprogramming with several inter-regulatory crosstalks to fulfill the high demand of energy and regulate oxidative stress for tumor growth and progression. Notably, the more aggressive molecular subtype of PDAC enhances influx of glycolytic intermediates. This review focuses on the interactive role of inflammatory signaling and metabolic reprogramming with emerging evidence of crosstalk, which supports the development, progression, and therapeutic resistance of PDAC. Understanding the emerging crosstalk between inflammation and metabolic adaptations may identify potential targets and develop novel therapeutic approaches for PDAC.

Automated summary

Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive tumor type, with development intricately linked to inflammatory signaling and metabolic reprogramming. Understanding the interaction of these factors may provide new insights for the treatment of PDAC.