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Non-coding RNAs (ncRNAs), and in particular microRNAs are rapidly becoming the focus of research interest in numerous basic and translational fields, including brain research; and their importance for many aspects in brain functioning merits special discussion. The wide-scope, multi-targeted and highly efficient manner of ncRNA regulatory activities draws attention to this topic by many, but the available research and analysis tools and experimental protocols are still at their infancy, and calls for special discussion given their importance for many aspects in brain functioning. This eBook is correspondingly focused on the search for, identification and exploration of those non-coding RNAs whose activities modulate the multi-leveled functions of the eukaryotic brain. The different articles strive to cover novel approaches for identifying and establishing ncRNA-target relationships, provide state of the art reports of the affected neurotransmission pathways, describe inherited and acquired changes in ncRNA functioning and cover the use of ncRNA mimics and blockade tools for interference with their functions in health and disease of the brain. Non-coding RNAs are here to stay, and this exciting eBook provides a glimpse into their impact on our brain’s functioning at the physiology, cell biology, behavior and immune levels.

MicroRNAs --- long non-coding RNAs --- Central Nervous System --- cholinergic signaling --- Schizophrenia --- Epilepsy --- ischemic stroke --- Alzheimer

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The epithelial-to-mesenchymal transition (EMT) is a highly dynamic process with multiple transitional states, by which epithelial cells can convert into a mesenchymal phenotype. This process involves loss of cellular adhesion and cellular polarity, and an improvement in migratory and invasive properties. It occurs during normal embryonic development, tissue regeneration, organ fibrosis, and wound healing. It is also involved in tumor progression with metastatic expansion, and plays a major role in resistance to cancer treatment. In cancers, EMT inducers are hypoxia, cytokines and growth factors secreted by the tumor microenvironment, stroma crosstalk, metabolic changes, innate and adaptive immune responses, and treatment with antitumor drugs. Switch in gene expression from epithelial to mesenchymal phenotype is triggered by complex regulatory networks involving transcriptional control, non-coding RNAs, chromatin remodeling and epigenetic modifications, alternative splicing, post-translational regulation, protein stability and subcellular localization. Reversion of EMT, the mesenchymal-to-epithelial transition (MET), affects circulating cancer cells when they reach a desirable metastatic niche to develop secondary tumors. More knowledge and control of EMT to MET is necessary and will be beneficial for patients for cancer treatment. This current Special Issue entitled “Epithelial to Mesenchymal Transition in Cancer” will address these questions.

Epithelial-to-mesenchymal transition (EMT) --- cancer --- metastasis --- chemoresistance --- cancer therapy, epigenetics --- non-coding RNAs --- TGF-beta --- PLK1 --- CK2, exosomes --- epithelial-to-pericyte transition (EPT)

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Transcriptional regulation is a critical biological process involved in the response of a cell, a tissue or an organism to a variety of intra- and extra-cellular signals. Besides, it controls the establishment and maintenance of cell identity throughout developmental and differentiation programs. This highly complex and dynamic process is orchestrated by a huge number of molecules and protein networks and occurs through multiple temporal and functional steps. Of note, many human disorders are characterized by misregulation of global transcription since most of the signaling pathways ultimately target components of transcription machinery. This book includes a selection of papers that illustrate recent advances in our understanding of transcriptional regulation and focuses on many important topics, from cis-regulatory elements to transcription factors, chromatin regulators and non-coding RNAs, other than several transcriptome studies and computational analyses.

major depressive disorder --- glioblastoma --- differentially expressed genes --- transcriptomics --- common pathway --- mouse --- miR-25-3p --- Akt1 --- AP-2? --- promoter --- cell metabolism --- p57Kip2 --- CDKN1C --- epigenetics --- disease --- cell differentiation --- placenta --- long non-coding RNA (lncRNA) --- human --- pregnancy --- high-throughput RNA sequencing (RNA-Seq) --- transcriptome --- Rsh regulon --- Novosphingobium pentaromativorans US6-1 --- sphingomonads --- RNA-seq --- N-acyl-l-homoserine lactone --- ppGpp --- selenium --- selenocysteine --- selenoproteins --- selenocysteine insertion sequence --- nonsense-mediated decay --- G-quadruplex --- transcriptional regulation --- promoter --- CRISPR/Cas9 --- PRDM gene family --- TCGA data analysis --- somatic mutations --- transcriptome profiling --- human malignancies --- tristetraprolin (TTP) --- tumorigenesis --- posttranscriptional regulation --- adenosine and uridine-rich elements (AREs) --- circRNA-disease associations --- pathway --- heterogeneous network --- Patau Syndrome --- cytogenetics --- FOXO1 --- transcription factor --- molecular pathways --- bioinformatics --- molecular docking --- and drug design --- transcription regulation --- gene expression --- causal inference --- enhancer activity --- insect --- transcription factors --- structures and functions --- research methods --- progress and prospects --- Pax3 --- Pteria penguin (Röding, 1798) --- tyrosinase --- melanin --- RNA interference --- liquid chromatograph-tandem mass spectrometer (LC-MS/MS) --- epigenetics --- gene expression --- nutrition --- transcription --- disorders --- mechanisms --- Crassostrea gigas --- Pacific oyster --- pediveliger larvae --- bioadhesive --- transcriptome --- gene expression --- interactome --- microscopy --- fertilization --- self-incompatibility --- transcriptome --- tea --- long non-coding RNAs --- cancer --- acute leukemia --- therapeutic targets --- Adiponectin --- cancer --- Adiponectin receptors --- obesity --- inflammatory response --- inflammation --- nutritional status --- n/a