scholarly journals β-catenin stabilization enhances SS18-SSX2-driven synovial sarcomagenesis and blocks the mesenchymal to epithelial transition

Oncotarget ◽  
2015 ◽  
Vol 6 (26) ◽  
pp. 22758-22766 ◽  
Author(s):  
Jared J. Barrott ◽  
Benjamin E. Illum ◽  
Huifeng Jin ◽  
Ju-Fen Zhu ◽  
Tim Mosbruger ◽  
...  
Keyword(s):  
Mesenchymal To Epithelial Transition

scholarly journals Molecular mechanisms underpinning sarcomas and implications for current and future therapy

2021 ◽  
Vol 6 (1) ◽  
Author(s):  
Victoria Damerell ◽  
Michael S. Pepper ◽  
Sharon Prince
Keyword(s):  
Molecular Mechanisms ◽  
Epithelial To Mesenchymal Transition ◽  
Treatment Strategies ◽  
Mesenchymal Transition ◽  
Mesenchymal To Epithelial Transition ◽  
Cells Of Origin ◽  
Novel Treatment Strategies ◽  
Future Therapy

AbstractSarcomas are complex mesenchymal neoplasms with a poor prognosis. Their clinical management is highly challenging due to their heterogeneity and insensitivity to current treatments. Although there have been advances in understanding specific genomic alterations and genetic mutations driving sarcomagenesis, the underlying molecular mechanisms, which are likely to be unique for each sarcoma subtype, are not fully understood. This is in part due to a lack of consensus on the cells of origin, but there is now mounting evidence that they originate from mesenchymal stromal/stem cells (MSCs). To identify novel treatment strategies for sarcomas, research in recent years has adopted a mechanism-based search for molecular markers for targeted therapy which has included recapitulating sarcomagenesis using in vitro and in vivo MSC models. This review provides a comprehensive up to date overview of the molecular mechanisms that underpin sarcomagenesis, the contribution of MSCs to modelling sarcomagenesis in vivo, as well as novel topics such as the role of epithelial-to-mesenchymal-transition (EMT)/mesenchymal-to-epithelial-transition (MET) plasticity, exosomes, and microRNAs in sarcomagenesis. It also reviews current therapeutic options including ongoing pre-clinical and clinical studies for targeted sarcoma therapy and discusses new therapeutic avenues such as targeting recently identified molecular pathways and key transcription factors.

scholarly journals miRNA proxy approach reveals hidden functions of glycosylation

2015 ◽  
Vol 112 (23) ◽  
pp. 7327-7332 ◽  
Author(s):  
Tomasz Kurcon ◽  
Zhongyin Liu ◽  
Anika V. Paradkar ◽  
Christopher A. Vaiana ◽  
Sujeethraj Koppolu ◽  
...  
Keyword(s):  
Posttranslational Modification ◽  
Epithelial To Mesenchymal Transition ◽  
Biological Function ◽  
Regulatory Elements ◽  
Rapid Identification ◽  
Mesenchymal Transition ◽  
Disease States ◽  
Mesenchymal To Epithelial Transition ◽  
Genes Encoding ◽  
Target Network

Glycosylation, the most abundant posttranslational modification, holds an unprecedented capacity for altering biological function. Our ability to harness glycosylation as a means to control biological systems is hampered by our inability to pinpoint the specific glycans and corresponding biosynthetic enzymes underlying a biological process. Herein we identify glycosylation enzymes acting as regulatory elements within a pathway using microRNA (miRNA) as a proxy. Leveraging the target network of the miRNA-200 family (miR-200f), regulators of epithelial-to-mesenchymal transition (EMT), we pinpoint genes encoding multiple promesenchymal glycosylation enzymes (glycogenes). We focus on three enzymes, beta-1,3-glucosyltransferase (B3GLCT), beta-galactoside alpha-2,3-sialyltransferase 5 (ST3GAL5), and (alpha-N-acetyl-neuraminyl-2,3-beta-galactosyl-1,3)-N-acetylgalactosaminide alpha-2,6-sialyltransferase 5 (ST6GALNAC5), encoding glycans that are difficult to analyze by traditional methods. Silencing these glycogenes phenocopied the effect of miR-200f, inducing mesenchymal-to-epithelial transition. In addition, all three are up-regulated in TGF-β–induced EMT, suggesting tight integration within the EMT-signaling network. Our work indicates that miRNA can act as a relatively simple proxy to decrypt which glycogenes, including those encoding difficult-to-analyze structures (e.g., proteoglycans, glycolipids), are functionally important in a biological pathway, setting the stage for the rapid identification of glycosylation enzymes driving disease states.

Salivary peptide histatin 1 mediated cell adhesion: a possible role in mesenchymal-epithelial transition and in pathologies

2018 ◽  
Vol 399 (12) ◽  
pp. 1409-1419 ◽  
Author(s):  
Irene A. van Dijk ◽  
Enno C.I. Veerman ◽  
Eric A.J. Reits ◽  
Jan G.M. Bolscher ◽  
Jan Stap
Keyword(s):  
Cell Adhesion ◽  
Oral Cavity ◽  
Potential Function ◽  
Clinical Applications ◽  
Epithelial Barrier ◽  
Salivary Peptide ◽  
Mesenchymal To Epithelial Transition ◽  
Mesenchymal Epithelial Transition

Abstract Histatins are histidine-rich peptides present in the saliva of humans and higher primates and have been implicated in the protection of the oral cavity. Histatin 1 is one of the most abundant histatins and recent reports show that it has a stimulating effect on cellular adherence, thereby suggesting a role in maintaining the quality of the epithelial barrier and stimulating mesenchymal-to-epithelial transition. Here we summarize these findings and discuss them in the context of previous reports. The recent findings also provide new insights in the physiological functions of histatin 1, which are discussed here. Furthermore, we put forward a possible role of histatin 1 in various pathologies and its potential function in clinical applications.

Mesenchymal to Epithelial Transition in Development and Disease

2007 ◽  
Vol 185 (1-3) ◽  
pp. 7-19 ◽  
Author(s):  
Christine L. Chaffer ◽  
Erik W. Thompson ◽  
Elizabeth D. Williams
Keyword(s):  
Mesenchymal To Epithelial Transition

357 ZSTK474, a Specific PI3K Inhibitor, Induces Mesenchymal to Epithelial Transition in Vivo

2012 ◽  
Vol 48 ◽  
pp. 109
Author(s):  
M. Okamura ◽  
S. Dan ◽  
H. Yoshimi ◽  
T. Yamori
Keyword(s):  
Pi3k Inhibitor ◽  
Mesenchymal To Epithelial Transition

scholarly journals Aspirin blocks growth of breast tumor cells and tumor-initiating cells and induces reprogramming factors of mesenchymal to epithelial transition

2015 ◽  
Vol 95 (7) ◽  
pp. 702-717 ◽  
Author(s):  
Gargi Maity ◽  
Archana De ◽  
Amlan Das ◽  
Snigdha Banerjee ◽  
Sandipto Sarkar ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Breast Tumor ◽  
Tumor Initiating Cells ◽  
Breast Tumor Cells ◽  
Mesenchymal To Epithelial Transition ◽  
Reprogramming Factors
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