IMR Press / FBL / Volume 17 / Issue 5 / DOI: 10.2741/4017

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.

Hyperglycemia as a mechanism of pancreatic cancer metastasis
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1 Department of Hepatobiliary Surgery, First Affiliated Hospital of Medical College, Xi'an Jiaotong University, 277 West Yanta Road, Xi'an 710061, Shaanxi Province, China
2 Department of Gastrointestinal Medical Oncology, the University of Texas MD Anderson Cancer Center, Houston, Texas, USA
3 Department of Pharmaceutical Sciences, NDSU, Sudro Hall 203, Fargo, ND 58105, USA
Front. Biosci. (Landmark Ed) 2012, 17(5), 1761–1774;
Published: 1 January 2012

As a vital step in the progression of cancer, metastasis poses the largest problem in cancer treatment and is the main cause of death of cancer patients. In pancreatic cancer, almost 80% of patients have locally deteriorated or metastatic disease and thus are not appropriate for resection at the time of diagnosis. Due to the high rate of incidence and mortality, it is crucial to study the molecular mechanisms of metastasis to clarify therapeutic targets to hinder the spread of cancer. Diabetes mellitus has long been considered a potential risk factor for pancreatic cancer. In this review, we comprehensively describe the role of hyperglycemia in governing critical steps of the metastatic process. In particular, we focus on the hyperglycemia-dependent aspects of the Epithelial-Mesenchymal Transition (EMT) and vascular dysfunction. Furthermore, we discuss how hyperglycemia-related production of reactive oxygen species (ROS) may play an important role in these two processes. A deep understanding of metastasis mechanisms will identify novel targets for therapeutic intervention.

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