Special Issue "The regulators of metastasis related signalling targets in cancer cells"

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Medical Biology".

Deadline for manuscript submissions: 31 August 2021.

Special Issue Editors

Dr. Pinar Uysal Onganer
Guest Editor
University of Westminster, Cancer Research Group, School of Life Sciences, College of Liberal Arts & Sciences, London, United Kingdom
Interests: microRNAs; Wnt signalling; cancer metastasis; cancer stem cells; breast cancer
Special Issues and Collections in MDPI journals
Dr. Elif Damla Arisan
Guest Editor
Gebze Technical University, Turkey
Interests: cell signalling; apoptosis; mTOR; AMPK
Dr. Alwyn Dart
Guest Editor
St George's, University of London, UK
Interests: metastasis; bone; microRNA; androgens

Special Issue Information

Dear Colleagues,

Cell signalling pathways, which regulate cell growth, proliferation and survival mechanisms in cancer cells, are also crucial for the poor progression of disease.  Abnormal activation of these targets drives tumorigenesis with unlimited alterations in the tumour microenvironment and leads to metastasis through changing fundamental characteristics of cancer cells. A number of critical players have been identified, with their multiple roles in cell survival and metastasis-related cancer progression. Thus, the clarification of the responsible pathways and related biomarkers is currently under way using specific inhibitors and/or receptor blockers and promises to help identify potential therapeutic targets to develop successful cancer treatments. These research efforts are crucial to achieve new targeted therapy options with less adverse effects, which increase the life quality of patients.

The aim of this Special Issue is to evaluate the current therapeutic targets as well as to identify new key regulators of cell signalling pathways that are involved in cell survival and metastatic cascades.

Dr. Pinar Uysal Onganer
Dr. Elif Damla Arisan
Dr. Alwyn Dart
Guest Editors

Manuscript Submission Information

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biology is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1500 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.


  • cancer 
  • signalling 
  • pathway 
  • receptor 
  • crosstalk 
  • growth 
  • apoptosis metastasis

Published Papers (1 paper)

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Open AccessArticle
Inhibition on JNK Mimics Silencing of Wnt-11 Mediated Cellular Response in Androgen-Independent Prostate Cancer Cells
Biology 2020, 9(7), 142; https://doi.org/10.3390/biology9070142 - 27 Jun 2020
Prostate cancer (PCa) is one of the most common cancers among men, and one of the leading causes of cancer death for men. The c-Jun N-terminal kinase (JNK) pathway is required for several cellular functions, such as survival, proliferation, differentiation, and migration. Wnt-11, [...] Read more.
Prostate cancer (PCa) is one of the most common cancers among men, and one of the leading causes of cancer death for men. The c-Jun N-terminal kinase (JNK) pathway is required for several cellular functions, such as survival, proliferation, differentiation, and migration. Wnt-11, a member of the Wnt family, has been identified for its upregulation in PCa; however, downstream signalling of Wnt-11 remains to be fully characterized. In this study, we investigated the role of the JNK pathway as a potential downstream factor for Wnt-11 signalling. For this purpose, LNCaP, DU145, and PC-3 PCa cells and normal epithelial PNT1A cells were treated with a specific JNK kinase inhibitor: JNKVIII. Our results showed that JNK inhibition decreased mitochondrial membrane potential and promoted cell death in a cell type-dependent manner. We found that JNK inhibition led to an increase in autophagy and prevented epithelial–mesenchymal transition (EMT) in independently growing androgen cells. JNK inhibition and the silencing of Wnt-11 showed similar responses in DU145 and PC-3 cells and decreased metastasis-related biomarkers, cell migration, and invasion. Overall, our results suggest that JNK signalling plays a significant role in the pathophysiology of PCa by mediating Wnt-11 induced signals. Our data highlights that both the JNK pathway and Wnt-11 could be a useful therapeutic target for the combinatory application of current PCa. Full article
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