Abstract

Epithelial to mesenchymal transition (EMT) is a physiologic process that allows morphological and genetic changes of carcinoma cells from an epithelial to a mesenchymal phenotype, which is the basis of the high metastatic potential of pancreatic cancer cells. EMT is triggered by various tumor microenvironmental factors, including cytokines, growth factors, and chemotherapeutic agents. This review summarizes the state-of-the-art knowledge on the molecular mechanisms that support pancreatic cancer EMT and the evidences that support its involvement in invasiveness/aggressiveness, and the drug resistance of pancreatic cancer cells.

Highlights

  • Epithelial-to-mesenchymal transition (EMT) is the collection of events that allows the conversion of adherent epithelial cells, tightly bound to each other within an organized tissue, into independent fibroblastic cells possessing migratory properties and the ability to invade the extracellular matrix

  • Clinicopathological analysis shows that TGFβ1 expression is significantly correlated with lymph node metastasis and the depth of invasion, indicating that TGFβ protumoral action prevails in pancreatic cancer

  • EMT is at the basis of the most hassling features of pancreatic cancer cells, which are their great invasiveness and drug resistance

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Summary

INTRODUCTION

Epithelial-to-mesenchymal transition (EMT) is the collection of events that allows the conversion of adherent epithelial cells, tightly bound to each other within an organized tissue, into independent fibroblastic cells possessing migratory properties and the ability to invade the extracellular matrix. In the early 1990s, EMT attracted the attention of cancer researchers after the discovery of its strong association with growth, invasion, and metastasis of cancer cells[2,3]. Tumor cells convert from low- to high-grade malignancy partly through EMT[4,5]. A great help to the understanding of pancreatic adenocarcinoma has come from the development and analysis of mutant mice that very closely reproduce the human disease. Both the human observations and the targeting of EMT-related pathways in murine models have shown the crucial role of EMT in the aggressiveness and lethality of pancreatic cancer. EMT was already deeply reviewed elsewhere[6], in this review, after overviewing basic EMT concepts, we would like to focus on the recent findings on EMT of pancreatic cancer cells

EMT BASICS
Cell Adhesion
EMT AND DRUG RESISTANCE IN PANCREATIC CANCER
Findings
CONCLUSION
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