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Lactate metabolism reprogramming in PDAC: Potential for tumor therapy
Fan Gao1, Kang Sun2, Sicheng Wang2
1Department of Hepatobiliary and Pancreatic Surgery, the First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310003, Zhejiang, China; Zhejiang Provincial Key Laboratory of Pancreatic Disease, the First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310009, Zhejiang, China; Shangyu People's Hospital of Shaoxing, Shaoxing University, Shaoxing 312300, Zhejiang, China.
Pancreatic ductal adenocarcinoma (PDAC) relies on enhanced glycolysis, increasing lactate. This lactate fuels tumor growth and suppresses immune cells, highlighting its critical role in cancer progression.
Area of Science:
- Oncology
- Cancer Metabolism
- Immunology
Background:
- Pancreatic ductal adenocarcinoma (PDAC) is a highly lethal cancer.
- Metabolic reprogramming, particularly enhanced glycolysis and lactate production, is a hallmark of PDAC.
- Lactate accumulation impacts tumor proliferation, immune evasion, and the tumor immune microenvironment.
Purpose of the Study:
- To elucidate the role of lactate in pancreatic ductal adenocarcinoma progression.
- To investigate the impact of lactate on immune cell function within the tumor microenvironment.
- To explore the therapeutic potential of targeting lactate-related pathways in PDAC.
Main Methods:
- Analysis of metabolic reprogramming in PDAC.
- Investigation of glycolysis and lactate production mechanisms.
- Assessment of lactate's effects on immune cell phenotypes.
- Evaluation of pharmacological agents targeting lactate pathways.
Main Results:
- Elevated glycolysis and subsequent lactate accumulation are significant features in PDAC.
- Lactate promotes tumor growth and survival.
- Lactate induces an immune-suppressive phenotype in immune cells within the tumor microenvironment.
Conclusions:
- Lactate plays a multifaceted role in promoting PDAC progression and immune evasion.
- Targeting lactate generation, accumulation, and related pathways presents a promising therapeutic strategy for PDAC.
