Recent Progress In Epithelial Mesenchymal Transitions

The concept of the epithelial-mesenchymal transition (EMT) provides a basis for understanding complex changes in gene expression, molecular function and cell behaviour. This field has undergone explosive growth in the last few years as the concept has spread from developmental biology to the pathologies of cancer and fibrosis. As scientists are on the verge of being able to control or mitigate the process of EMT in some pathological conditions, understanding of its fundamental mechanisms is of vital importance. This special issue brings together selected reviews and new data from the Boden Conference on Epithelial-Mesenchymal Transitions. The reviews highlight developmental, cancer and pathological EMTs, and are rich in detail at the cell and molecular levels. The publication is aimed at cancer biologists, pathologists and developmental biologists who are interested in why cells begin to move, and the genes and molecules involved in this process.

This book is a printed edition of the Special Issue "The Epithelial-to-Mesenchymal Transition (EMT) in Cancer" that was published in Cancers

This special issue represents a progression through signaling processes, development, fibrosis and cancer, illustrating common underlying mechanisms and highlighting the growing recognition of therapeutic possibilities. Novel molecular pathways are shown in the context of known regulators, and many articles offer specific insights into therapeutic targeting. Not surprisingly, several articles relate to the signaling pathways activated by the common anchor transforming growth factor (TGF)-beta in relation to epithelial-mesenchymal transition (EMT). A number of new mechanisms with therapeutic implications are described, specifically the interplay between the non-Smad PI3 kinase-Akt-mTOR axis and EMT-associated invasion in response to TGF-beta, the unexpected role of c-Abl in repressing TGF-beta1-induced EMT, the cooperativity between oncostatin M, hepatocyte growth factor and TGF-beta1 in lung carcinoma EMT, and the roles of dystroglycan and periostin in developmental EMT associated with gastrulation and palate fusion, respectively. Collectively, the issue presents the full spectrum of interest in EMT today.

The concept of epithelial-mesenchymal transitions (EMT) has brought valuable insights to the study of complex processes involved in early embryo development, wound healing, carcinoma progression or kidney fibrosis. Major advances are reported in identifying new model systems, transcriptional regulators (including chromatin structure and microRNA), specific signaling pathways, and effector molecules. In this special issue, recent developments in the EMT field are reviewed, including the first localizations of Snail proteins in human cancers. Snail signaling and targets are carefully explored in several systems. Another emerging signaling pathway discussed involves TGF-beta. Several new concepts are consolidated including partial EMT, resulting in a metastable phenotype in cancer systems, and reversed EMT, described during bladder cancer progression as a mesenchymal-epithelial transition. Some of the papers focus on the first therapeutic approaches and different microarray analysis approaches specifically targeting the EMT process. Basic and clinical reseachers, clinicians as well as graduate and PhD students in the fields of cell and developmental biology, oncology and nephrology will appreciate this multidisciplinary and up-to-date overview of the EMT process.

Transitions between the epithelial and mesenchymal states are among the most basic of cellular events. They underpin major changes in animal development and in cancer progression. This publication is the second of two special issues of ACTA ANATOMICA presenting recent advances in understanding these transitions. The first volume gave an overview of epithelial-mesenchymal transitions, provided reviews of the molecular systems involved and presented two important developmental examples. The present volume continues and complements this, providing reviews from distinguished researchers exploring novel relationships of protease-like molecules to epithelial-mesenchymal transitions, and detailing such transitions in heart development, in trophoblast invasion, in cancer and in tissue culture model systems, as well as changes in the reverse direction in kidney development. This publication and its predecessor are required reading for cell and developmental biologists and oncologists.

Epithelial phenotype is a dynamic stage of differentiation that can be modulated during several physiological or pathological events. The rapid conversion to a mesenchymal-like phenotype is called an epithelial-mesenchymal transition (EMT). The Rise and Fall of Epithelial Phenotype is the first book to comprehensively introduce the concept of EMT. The first part of this volume describes main examples and models and explains their physiological relevance. These examples include hydra morphogenesis, gastrulation in mouse, drosophila and sea urchin, as well as neural crest cell migration and heart morphogenesis in vertebrates. Part two reviews in detail, specific EMT molecular pathways covering extracellular induction, transduction and transcription response and modulation of cell-cell adhesion structures. It emphasizes new specific pathways with potential medical applications. EMTs can also be linked to pathological events such as wound healing and cancer progression, as detailed in this section of the book.

Targeting Cell Survival Pathways to Enhance Response to Chemotherapy encompasses recently developed molecular targeting agents and approaches that suppress cell survival signaling. Cell survival signaling attenuates the effectiveness of conventional chemotherapy and numerous mechanisms have been described, and continue to be described, which contribute to cell survival in the face of chemotherapy treatment. Key pathways leading to chemoresistance emanate from growth factor receptors, PI3K, STAT3, anti-apoptotic Bcl-2 family members, autophagy, and the DNA damage response pathway. New advances have underscored the potential of targeting each of these cell survival mechanisms to improve responsiveness to chemotherapy. This book reviews these recent advances and provides a foundational background and hints of new opportunities for basic, translational, and clinical investigators focused on improving therapeutic responses to chemotherapy. Presents cutting-edge agents and approaches with proved success in different model systems that can be translated to a different type of cancer Brings updated information to be used to propose new clinical trials investigating innovative strategies for improving responses to chemotherapy Provides mechanistic details to help guide the design of laboratory studies associated with clinical trials