Special Issue "Mesenchymal-Epithelial Transition in Cellular Reprogramming and Cancer"
Deadline for manuscript submissions: 31 December 2021.
Interests: cancer; evolution; ecology; comparative oncology; drug resistance; metastasis; prostate cancer; sarcoma; systems biology; molecular biology
Interests: metastasis; mathematical oncology; systems biology; computational biology; phenotypic plasticity; cellular decision-making; cancer stem cells; epithelial-mesenchymal transition
Special Issues and Collections in MDPI journals
Cellular lineages are determined by coordinated gene expression programs that direct cells toward a given fate. While almost all cells in the body maintain their lineages, some cells undergo reversible plasticity, which enables the cells to convert to a different phenotype. This phenotypic plasticity occurs during both the normal processes of development and wound healing, as well as in pathologic conditions of fibrosis and cancer metastasis. In the context of metastasis, cancer cells undergo phenotypic conversions known as epithelial plasticity. Epithelial plasticity leads to a loss of epithelial-like characteristics and a gain of either hybrid epithelial/mesenchymal/stem-like properties or a mesenchymal-like phenotype. Epithelial plasticity underlies many of the processes of metastasis. For example, phenotypic switching from epithelial to mesenchymal by way of an epithelial–mesenchymal transition (EMT) facilitates migration, invasion, and dissemination. In addition, epithelial plasticity has also been shown to be critical for the development of therapy resistance. Similarly, a reversion back to an epithelial-like state via mesenchymal–epithelial transition (MET) is thought to enable disseminated cancer cells to re-awaken the proliferative signals needed to colonize secondary sites. While the role of partial or complete EMT in metastatic dissemination and therapy resistance is well-established, the importance of a partial or complete MET as a driver of metastatic colonization and therapy resistance remains poorly understood. Recent studies have also indicated that MET is not simply a mirror image of EMT; these can be asymmetric processes in a high-dimensional molecular and/or morphological space through which the cells navigate.
In this Special Issue, we are soliciting articles from an interdisciplinary group of experts who study MET in cancer progression and other normal and pathologic processes, such as development, wound healing, and fibrosis. Articles will cover topics focused on the biomolecular and microenvironmental factors that govern EMT/MET dynamics across a range of cancers. We feel this Issue will fill an important gap in our understanding of the mechanisms underlying metastatic spread, and eventually contribute to identify new therapeutic vulnerabilities.
Dr. Jason A. Somarelli
Dr. Mohit Kumar Jolly
Manuscript Submission Information
Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.
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. Cancers is an international peer-reviewed open access semimonthly 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 2200 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.
- epithelial–mesenchymal transition
- mesenchymal–epithelial transition
- lineage reprogramming
- phenotypic plasticity
- tumor microenvironment
- soluble factors
- biomolecular drivers of plasticity
- gene expression networks of plasticity
- mathematical models of epithelial plasticity