Abstract
Galectins are a family of proteins that bind β-galactose residues through a highly conserved carbohydrate recognition domain. They regulate several important biological functions, including cell proliferation, adhesion, migration, and invasion, and play critical roles during embryonic development and cell differentiation. In adults, different galectin members are expressed depending on the tissue type and can be altered during pathological processes. Numerous reports have shown the involvement of galectins in diseases, mostly inflammation and cancer. Here, we review the state-of-the-art of the role that different galectin family members play in pancreatic cancer. This tumor is predicted to become the second leading cause of cancer-related deaths in the next decade as there is still no effective treatment nor accurate diagnosis for it. We also discuss the possible translation of recent results about galectin expression and functions in pancreatic cancer into clinical interventions (i.e., diagnosis, prediction of prognosis and/or therapy) for this fatal disease.
Highlights
Cancer Research Program, Hospital del Mar Medical Research Institute (IMIM), Unidad Asociada IIBB-CSIC, Department of Gastroenterolgy, Hospital del Mar-IMIM, 08003 Barcelona, Spain; Department of Medical Oncology, Hospital del Mar-IMIM-CIBERONC, 08003 Barcelona, Spain; Institute of Biomedical Research of Barcelona (IIBB-CSIC), 08036 Barcelona, Spain
extracellular matrix (ECM) and secreted factors from activated pancreatic stellate cells (PSCs) lead to increased pancreatic tumor cell motility, proliferation, metastasis, and chemoresistance, highlighting the relevance of tumor-stroma crosstalk in pancreatic ductal adenocarcinoma (PDA) progression [8,9,10]
Galectins are a family of proteins that bind to carbohydrates, and in particular to β-galactose residues
Summary
The most common type of pancreatic cancer is pancreatic ductal adenocarcinoma (PDA), which is an aggressive disease with a devastating prognosis [1]. ECM and secreted factors from activated PSCs lead to increased pancreatic tumor cell motility, proliferation, metastasis, and chemoresistance, highlighting the relevance of tumor-stroma crosstalk in PDA progression [8,9,10]. Pancreatic cells contribute to immune system evasion by expressing and secreting immunosuppressive factors, such as TGF-β, IL-10, IL-6, VEGF, and the Fas ligand, among others [13,15]. Together, these processes lead to failed immune surveillance, which could explain the low rate of response to immunotherapy [9,14,15]
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