The Role of Epithelial Signalling Pathways on Tumour Progression

A special issue of Cancers (ISSN 2072-6694).

Deadline for manuscript submissions: closed (15 August 2023) | Viewed by 256

Special Issue Editor

1. First Department of Medicine, University Hospital Schleswig-Holstein (UKSH), Campus Lübeck, Ratzeburger Allee 160, 23538 Lübeck, Germany
2. Department of General and Thoracic Surgery, University Hospital Schleswig-Holstein (UKSH), Campus Kiel, Arnold-Heller Str. 7, 24105 Kiel, Germany
Interests: TGF-beta signaling and its crosstalk with other signaling pathways; cell migration and invasion; mechanisms of metastasis; tumor biology; pancreatic tumors, small GTPases
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Special Issue Information

Dear Colleagues,

Almost 80% of malignant tumors are derived from the epithelial tissues of different organs. In the early tumor stages, normal epithelial cells and cancer cells have cohesive cell–cell junctions that inhibit their movements, and therefore, they do not have migratory and/or invasive properties. Upon the overexpression of mesenchymal factors, the epithelial tumor cells exhibit mesenchymal features and eventually become motile and invasive. Many carcinomas., i.e., pancreatic ductal adenocarcinomas, are a heterogeneous group that consist of different subtypes, and those with epithelial/classical differentiation have a better prognosis than those with (quasi)mesenchymal characteristics. The loss or gain of epithelial traits is associated with embryonic programs such as the epithelial–mesenchymal transition (EMT) or mesenchymal–epithelial transition (MET), respectively. Over the course of EMT, cells lose their epithelial characteristics, such as their collective mode of cell migration, cell–cell and cell–extracellular matrix interactions, and epithelial polarity. Concomitantly, they develop mesenchymal traits, such as high invasive capabilities that may result in tumor cell dissemination to distant sites in the body. Although MET is increasingly recognized as the principal mechanism for establishing metastasis following the distant colonization of circulating tumor cells, it has received much less attention than EMT. MET involves the re-expression of epithelial cell markers and the accompanying inhibition of mesenchymal markers. The current paradigm states that EMT drives carcinoma cells to disseminate from the primary tumor, while MET drives disseminated carcinoma cells to adopt an epithelial appearance and reinitiate the proliferative programs that are necessary for the formation of secondary tumors. The ability of disseminated tumor cells to reestablish epithelial phenotypes via MET programs may in fact represent the rate-limiting step in the metastatic cascade. EMT and MET programs are modulated at different levels of control, such as receptor-mediated signaling, transcriptional and translational regulation, epigenetic modifications, alternative splicing, and microRNA-mediated gene silencing. In addition, cancer cells that have undergone EMT have increased resistance to apoptosis and chemotherapy, which may ultimately cause cancer recurrence. Hence, epithelial–mesenchymal plasticity (EMP) has been proposed as a promising therapeutic target. For instance, shifting mesenchymal cells back to the epithelial state or converting mesenchymal or E/M hybrid cells to the original epithelial precursor can potentially prevent metastasis and stem cell generation. EMP is regulated by many signaling pathways, i.e., the Ras-ERK, MAPK, and TGFβ pathways via the control of the activation of the transcription factors that serve as master regulators of epithelial or mesenchymal differentiation. This Special Issue will discuss the different aspects of EMP and will focus on the signaling pathways in the cancer cells involved in reestablishing epithelial (or blocking mesenchymal) differentiation, thereby promoting a less malignant phenotype. It will cover both basic and more (pre)clinical aspects that advance our understanding of targeting these pathways in human tumors to overcome drug resistance and metastasis.

Prof. Dr. Hendrik Ungefroren
Guest Editor

Manuscript Submission Information

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Published Papers

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