Special Issue "TGF-Beta Signaling in Tissue Fibrosis and Cancer"
Deadline for manuscript submissions: 31 August 2021.
Interests: EGFR transactivation; TGF-β signaling; gene regulation; tumor progression; fibroproliferative disease; EMT; skin cancer; cell motility; PAI-1
Special Issues and Collections in MDPI journals
Interests: hippo signaling; renal fibrosis; kidney cancer; EGFR transactivation; non-SMAD TGF-β pathway; tumor suppressor deregulation in fibrosis
Special Issues and Collections in MDPI journals
TGF-β is a major contributor to fibrotic and neoplastic diseases in both humans and animals. Although this pleiotropic cytokine promotes epithelial cell plasticity/dedifferentiation/pEMT, cellular stemness, migration/invasion, and stimulates acquisition of a profibrotic phenotype within the tumor microenvironment (i.e., myofibroblasts and cancer-associated fibroblasts/CAFs), translation of emerging knowledge to successfully target TGF-β1 remains an unrealized clinical challenge. This Special Issue welcomes original research articles as well as state-of-the-art reviews that address the following topics to further our understanding of the mechanistic and pathological basis of TGF-β involvement in organ fibrosis and cancer.
- TGF-β-mediated transcriptional (both SMAD and non-SMAD) networks, genetic reprogramming and phenotypic responses (e.g., cell plasticity/stemness, cell cycle arrest, proliferation, migration) related to the onset or progression of fibrotic and neoplastic diseases.
- Nontranscriptional (e.g., microRNA, lncRNA, epigenetic) control of TGF-β1 signaling.
- TGF-β crosstalk with other receptors (e.g., tyrosine kinases and serine/threonine kinases) or tumor suppressors (e.g., p53, PTEN) in promoting or suppressing fibrotic and oncogenic behavior.
- Novel positive (e.g., inducers) and negative regulators (e.g., suppressors) of TGF-β1 pathways.
- Novel or potential therapeutic approaches (TGF-β ligand traps and neutralizing antibodies, signaling networks, or TGF-β collateral networks) to target aberrant TGF-β signaling in organ fibrosis and cancer.
- TGF-β1-induced metabolic alterations (e.g., glycolysis, Krebs cycle, oxidative phosphorylation, fatty acid oxidation) in tissue fibrosis and cancer.
- TGF-β1 control of inflammatory networks.
- Tissue or organ specificity of TGF-signaling.
- Evaluation of TGF-β1 signal transducers as biomarkers of cancer and fibrosis progression in animal models and humans.
Prof. Paul J. Higgins
Dr. Rohan Samarakoon
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. Biomolecules 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 2000 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.
The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.
Title: TGF-β1 Signaling in Gut Fibrosis and Cancer
Author: Carmine Stolfi, Edoardo Troncone, Irene Marafini, Giovanni Monteleone
Affiliations: Department of Systems Medicine, University of Rome "Tor Vergata"
Abstract: The human gastrointestinal tract contains the largest population of immune cells in the body and this is a reflection of the fact that it is continuously exposed to a myriad of dietary and bacterial antigens. Although these cells produce a variety of inflammatory cytokines that could potentially promote tissue damage, in normal conditions the mucosal immune response is tightly controlled by counter-regulatory factors, which help induce and maintain gut homeostasis and tolerance. One such a molecules is transforming growth factor (TGF)-β1, a cytokine produced by multiple lineages of leukocytes, stromal cells and epithelial cells and virtually targeting all the gut mucosal cell types. Indeed, studies in animals and humans have shown that defects in TGF-β1 production and/or signaling can lead to the development of immune-inflammatory pathologies, fibrosis and cancer in the gut. Here, we review and discuss the available evidence about the role of TGF-β1 and Smad7, an inhibitor of TGF-β1 activity, in gut fibrosis and cancer with particular regard to the contribution of these two molecules in the pathogenesis of fibrogenesis in patients with inflammatory bowel diseases and the initiation and progression of colon cancer.
Title: Organ fibrosis and autoimmunity: the role of inflammation in TGFbeta-dependent EMT
Author: Margherita Sisto, Domenico Ribatti and Sabrina Lisi
Affiliations: Department of Basic Medical Science, Neurosciences and sense Organs, Section of Human Anatomy, University of Bari Medical School
Abstract: Recent advances in our understanding of the molecular pathways that control the link of inflammation with organ fibrosis and autoimmune diseases point to the epithelial to mesenchymal transition (EMT) as the common association in the progression of these diseases characterized by intensive inflammatory response. EMT, a process in which epithelial cells gradually change to mesenchymal ones, is a major contributor in the pathogenesis of fibrosis. Importantly, the chronic inflammatory microenvironment emerges as a decisive factor in the induction of the pathological EMT. Transforming growth factor-β (TGF-β), a multifunctional cytokine, plays a crucial role in the induction of fibrosis, often associated with chronic phases of inflammatory diseases contributing to marked fibrotic changes that severely impair normal tissue architecture and function. The understanding of molecular mechanisms underlying EMT-dependent fibrosis has both a basic and a translational relevance, since it may be useful for setup of therapies aimed at counteracting the organs deterioration and failure. To this end, we review the recent literature to better elucidate the molecular response to inflammatory/fibrogenic signals in autoimmune diseases to guarantee the specific regulation of EMT-dependent fibrosis for more targeted therapies.