Galectin-3's Complex Interactions in Pancreatic Ductal Adenocarcinoma: From Cellular Signaling to Therapeutic Potential

Milica Dimitrijevic Stojanovic; Bojan Stojanovic; Ivan Radosavljevic; Vojin Kovacevic; Ivan Jovanovic; Bojana S Stojanovic; Nikola Prodanovic; Vesna Stankovic; Miodrag Jocic; Marina Jovanovic

doi:10.3390/biom13101500

Galectin-3's Complex Interactions in Pancreatic Ductal Adenocarcinoma: From Cellular Signaling to Therapeutic Potential

Biomolecules. 2023 Oct 10;13(10):1500. doi: 10.3390/biom13101500.

Authors

Affiliations

¹ Department of Pathology, Faculty of Medical Sciences, University of Kragujevac, 34000 Kragujevac, Serbia.
² Center for Molecular Medicine and Stem Cell Research, Faculty of Medical Sciences, University of Kragujevac, 34000 Kragujevac, Serbia.
³ Department of Surgery, Faculty of Medical Sciences, University of Kragujevac, 34000 Kragujevac, Serbia.
⁴ Department of Pathophysiology, Faculty of Medical Sciences, University of Kragujevac, 34000 Kragujevac, Serbia.
⁵ Institute for Transfusiology and Haemobiology, Military Medical Academy, 11000 Belgrade, Serbia.
⁶ Department of Internal Medicine, Faculty of Medical Sciences, University of Kragujevac, 34000 Kragujevac, Serbia.

Abstract

Galectin-3 (Gal-3) plays a multifaceted role in the development, progression, and prognosis of pancreatic ductal adenocarcinoma (PDAC). This review offers a comprehensive examination of its expression in PDAC, its interaction with various immune cells, signaling pathways, effects on apoptosis, and therapeutic resistance. Additionally, the prognostic significance of serum levels of Gal-3 is discussed, providing insights into its potential utilization as a biomarker. Critical analysis is also extended to the inhibitors of Gal-3 and their potential therapeutic applications in PDAC, offering new avenues for targeted treatments. The intricate nature of Gal-3's role in PDAC reveals a complex landscape that demands a nuanced understanding for potential therapeutic interventions and monitoring.

Keywords: Gal-3 inhibitors; Galectin-3; biomarker; immune interaction; pancreatic ductal adenocarcinoma; prognosis; signaling pathways.

Publication types

Review
Research Support, Non-U.S. Gov't

MeSH terms

Carcinoma, Pancreatic Ductal* / drug therapy
Carcinoma, Pancreatic Ductal* / metabolism
Galectin 3 / genetics
Galectin 3 / metabolism
Humans
Pancreatic Neoplasms* / metabolism
Signal Transduction

Substances

Galectin 3

Grants and funding

This research received financial support from the Faculty of Medical Sciences at the University of Kragujevac, Serbia, via grants JP02/20, JP11/18, and JP15/19. Additional backing was provided by the Ministry of Science, Technological Development, and Innovation of the Republic of Serbia, under contract number 451-03-47/2023-01/200111.