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Special Issue "Pancreatic Fibrosis in Inflammation and Cancer"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: 31 October 2021.

Special Issue Editor

Dr. Antonio Gonzalez
E-Mail Website
Guest Editor
Department of Physiology, Faculty of Veterinary Sciences, University of Extremadura, Caceres, Spain
Interests: melatonin; oxidative stress; pancreas; astrocytes; cancer

Special Issue Information

Dear Colleagues,

Pancreatic fibrosis is a condition that develops in diseases that affect the pancreas such as pancreatitis and cancer. It can evolve starting from changes in the physiology of cells that normally contribute to the homeostasis of the stroma in the tissue. Cells can be abnormally activated by signals from different origins and then can proliferate and contribute to the deposition of extracellular matrix components. The developed fibrotic tissue can impair the functions of pancreas, both exocrine and endocrine. The consequences may vary depending on the extent of the fibrosis but usually enhance the development of inflammatory or cancerous cells within the gland, being a result of major relevance to human health. Over the past few years, and especially at present, researchers are working on the identification of regulators of pancreatic fibrosis. Nowadays, it is accepted that pancreatic stellate cells (PSC) contribute significantly to these pathogenic processes. Moreover, interrelationship with other cell types of the pancreas, including developing cancer cells, is emerging as potential regulator of PSC pathophysiology. Therefore, the understanding of the cellular and molecular basis of cell-to-cell interconnection is of major relevance to the knowledge of pancreatic disease development and the potential discovery of a cure.

Dr. Antonio Gonzalez
Guest Editor

Manuscript Submission Information

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Keywords

  • pancreas
  • fibrosis
  • disease
  • inflammation
  • cancer

Published Papers (2 papers)

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Research

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Article
Melatonin Induces Apoptosis and Modulates Cyclin Expression and MAPK Phosphorylation in Pancreatic Stellate Cells Subjected to Hypoxia
Int. J. Mol. Sci. 2021, 22(11), 5555; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22115555 - 24 May 2021
Cited by 1 | Viewed by 866
Abstract
In certain diseases of the pancreas, pancreatic stellate cells form an important part of fibrosis and are critical for the development of cancer cells. A hypoxic condition develops within the tumor, to which pancreatic stellate cells adapt and are able to proliferate. The [...] Read more.
In certain diseases of the pancreas, pancreatic stellate cells form an important part of fibrosis and are critical for the development of cancer cells. A hypoxic condition develops within the tumor, to which pancreatic stellate cells adapt and are able to proliferate. The consequence is the growth of the tumor. Melatonin, the product of the pineal gland, is gaining attention as an agent with therapeutic potential against pancreatic cancers. Its actions on tumor cells lead, in general, to a reduction in cell viability and proliferation. However, its effects on pancreatic stellate cells subjected to hypoxia are less known. In this study, we evaluated the actions of pharmacological concentrations of melatonin (1 mM–1 µM) on pancreatic stellate cells subjected to hypoxia. The results show that melatonin induced a decrease in cell viability at the highest concentrations tested. Similarly, the incorporation of BrdU into DNA was diminished by melatonin. The expression of cyclins A and D also was decreased in the presence of melatonin. Upon treatment of cells with melatonin, increases in the expression of major markers of ER stress, namely BIP, phospho-eIF2α and ATF-4, were detected. Modulation of apoptosis was noticed as an increase in caspase-3 activation. In addition, changes in the phosphorylated state of p44/42, p38 and JNK MAPKs were detected in cells treated with melatonin. A slight decrease in the content of α-smooth muscle actin was detected in cells treated with melatonin. Finally, treatment of cells with melatonin decreased the expression of matrix metalloproteinases 2, 3, 9 and 13. Our observations suggest that melatonin, at pharmacological concentrations, diminishes the proliferation of pancreatic stellate cells subjected to hypoxia through modulation of cell cycle, apoptosis and the activation of crucial MAPKs. Cellular responses might involve certain ER stress regulator proteins. In view of the results, melatonin could be taken into consideration as a potential therapeutic agent for pancreatic fibrosis. Full article
(This article belongs to the Special Issue Pancreatic Fibrosis in Inflammation and Cancer)
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Review

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Review
Targeting Fibrosis: The Bridge That Connects Pancreatitis and Pancreatic Cancer
Int. J. Mol. Sci. 2021, 22(9), 4970; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22094970 - 07 May 2021
Viewed by 888
Abstract
Pancreatic fibrosis is caused by the excessive deposits of extracellular matrix (ECM) and collagen fibers during repeated necrosis to repair damaged pancreatic tissue. Pancreatic fibrosis is frequently present in chronic pancreatitis (CP) and pancreatic cancer (PC). Clinically, pancreatic fibrosis is a pathological feature [...] Read more.
Pancreatic fibrosis is caused by the excessive deposits of extracellular matrix (ECM) and collagen fibers during repeated necrosis to repair damaged pancreatic tissue. Pancreatic fibrosis is frequently present in chronic pancreatitis (CP) and pancreatic cancer (PC). Clinically, pancreatic fibrosis is a pathological feature of pancreatitis and pancreatic cancer. However, many new studies have found that pancreatic fibrosis is involved in the transformation from pancreatitis to pancreatic cancer. Thus, the role of fibrosis in the crosstalk between pancreatitis and pancreatic cancer is critical and still elusive; therefore, it deserves more attention. Here, we review the development of pancreatic fibrosis in inflammation and cancer, and we discuss the therapeutic strategies for alleviating pancreatic fibrosis. We further propose that cellular stress response might be a key driver that links fibrosis to cancer initiation and progression. Therefore, targeting stress proteins, such as nuclear protein 1 (NUPR1), could be an interesting strategy for pancreatic fibrosis and PC treatment. Full article
(This article belongs to the Special Issue Pancreatic Fibrosis in Inflammation and Cancer)
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