scholarly journals MicroRNAs in Ocular Infection

2019 ◽  
Vol 7 (9) ◽  
pp. 359 ◽  
Author(s):  
Shunbin Xu ◽  
Linda D. Hazlett
Keyword(s):  
Molecular Mechanisms ◽  
Gene Expression Regulation ◽  
Current Status ◽  
Ocular Infection ◽  
Rna Molecules ◽  
Novel Mirna ◽  
Organ Systems ◽  
A Cell ◽  
And Function ◽  
Treatment And Diagnosis

MicroRNAs (miRNAs) are small, non-coding, regulatory RNA molecules and constitute a newly recognized, important layer of gene-expression regulation at post-transcriptional levels. miRNAs quantitatively fine tune the expression of their downstream genes in a cell type- and developmental stage-specific fashion. miRNAs have been proven to play important roles in the normal development and function as well as in the pathogenesis of diseases in all tissues and organ systems. miRNAs have emerged as new therapeutic targets and biomarkers for treatment and diagnosis of various diseases. Although miRNA research in ocular infection remains in its early stages, a handful of pioneering studies have provided insight into the roles of miRNAs in the pathogenesis of parasitic, fungal, bacterial, and viral ocular infections. Here, we review the current status of research in miRNAs in several major ocular infectious diseases. We predict that the field of miRNAs in ocular infection will greatly expand with the discovery of novel miRNA-involved molecular mechanisms that will inform development of new therapies and identify novel diagnostic biomarkers.

scholarly journals miRador: a fast and precise tool for the prediction of plant miRNAs

2021 ◽  
Author(s):  
Reza K Hammond ◽  
Parth Patel ◽  
Pallavi Gupta ◽  
Blake C. Meyers
Keyword(s):  
Stress Responses ◽  
Target Prediction ◽  
Accurate Identification ◽  
Rna Molecules ◽  
Prediction Tools ◽  
Novel Mirna ◽  
Precise Tool ◽  
Computationally Intensive ◽  
And Function ◽  
Post Transcriptional Regulation

Plant microRNAs (miRNAs) are short, non-coding RNA molecules that restrict gene expression via post-transcriptional regulation and function in several essential pathways including development, growth, and stress responses. Accurately identifying miRNAs in populations of small RNA (sRNA) sequencing libraries is a computationally intensive process which has resulted in the misidentification of inaccurately annotated miRNA sequences. In recent years, criteria for miRNA annotation have been refined to reduce these misannotations. Here, we describe miRador, a novel miRNA identification tool that utilizes the most up-to-date, community-established criteria for accurate identification of miRNAs in plants. We combine target prediction and Parallel Analysis of RNA Ends (PARE) data to assess the precision of the miRNAs identified by miRador. We compare miRador to other commonly used miRNA prediction tools and we find that miRador is at least as precise as other prediction tools while being significantly faster than other tools.

scholarly journals Targeting Mechanotransduction in Osteosarcoma: A Comparative Oncology Perspective

2020 ◽  
Vol 21 (20) ◽  
pp. 7595
Author(s):  
Anita K. Luu ◽  
Alicia M. Viloria-Petit
Keyword(s):  
Tumour Progression ◽  
Cell Signalling ◽  
Bone Tumour ◽  
Mechanical Stimuli ◽  
Current State ◽  
Organ Systems ◽  
A Cell ◽  
Canine Models ◽  
Improved Design ◽  
And Function

Mechanotransduction is the process in which cells can convert extracellular mechanical stimuli into biochemical changes within a cell. While this a normal process for physiological development and function in many organ systems, tumour cells can exploit this process to promote tumour progression. Here we summarise the current state of knowledge of mechanotransduction in osteosarcoma (OSA), the most common primary bone tumour, referencing both human and canine models and other similar mesenchymal malignancies (e.g., Ewing sarcoma). Specifically, we discuss the mechanical properties of OSA cells, the pathways that these cells utilise to respond to external mechanical cues, and mechanotransduction-targeting strategies tested in OSA so far. We point out gaps in the literature and propose avenues to address them. Understanding how the physical microenvironment influences cell signalling and behaviour will lead to the improved design of strategies to target the mechanical vulnerabilities of OSA cells.

scholarly journals A Cell-free System to Study Regulation of Focal Adhesions and of the Connected Actin Cytoskeleton

1999 ◽  
Vol 10 (2) ◽  
pp. 373-391 ◽  
Author(s):  
Anna Cattelino ◽  
Chiara Albertinazzi ◽  
Mario Bossi ◽  
David R. Critchley ◽  
Ivan de Curtis
Keyword(s):  
Actin Cytoskeleton ◽  
Actin Polymerization ◽  
Plasma Membranes ◽  
Molecular Mechanisms ◽  
Divalent Cations ◽  
Focal Adhesions ◽  
Free System ◽  
Β1 Integrins ◽  
A Cell ◽  
And Function

Assembly and modulation of focal adhesions during dynamic adhesive processes are poorly understood. We describe here the use of ventral plasma membranes from adherent fibroblasts to explore mechanisms regulating integrin distribution and function in a system that preserves the integration of these receptors into the plasma membrane. We find that partial disruption of the cellular organization responsible for the maintenance of organized adhesive sites allows modulation of integrin distribution by divalent cations. High Ca2+ concentrations induce quasi-reversible diffusion of β1 integrins out of focal adhesions, whereas low Ca2+ concentrations induce irreversible recruitment of β1 receptors along extracellular matrix fibrils, as shown by immunofluorescence and electron microscopy. Both effects are independent from the presence of actin stress fibers in this system. Experiments with cells expressing truncated β1 receptors show that the cytoplasmic portion of β1 is required for low Ca2+-induced recruitment of the receptors to matrix fibrils. Analysis with function-modulating antibodies indicates that divalent cation-mediated receptor distribution within the membrane correlates with changes in the functional state of the receptors. Moreover, reconstitution experiments show that purified α-actinin colocalizes and redistributes with β1 receptors on ventral plasma membranes depleted of actin, implicating binding of α-actinin to the receptors. Finally, we found that recruitment of exogenous actin is specifically restricted to focal adhesions under conditions in which new actin polymerization is inhibited. Our data show that the described system can be exploited to investigate the mechanisms of integrin function in an experimental setup that permits receptor redistribution. The possibility to uncouple, under cell-free conditions, events involved in focal adhesion and actin cytoskeleton assembly should facilitate the comprehension of the underlying molecular mechanisms.

scholarly journals The Emerging Regulatory Role of Circular RNAs in Periodontal Tissues and Cells

2021 ◽  
Vol 22 (9) ◽  
pp. 4636
Author(s):  
Kexin Jiao ◽  
Laurence J. Walsh ◽  
Sašo Ivanovski ◽  
Pingping Han
Keyword(s):  
Rna Binding ◽  
Alveolar Bone ◽  
Circular Rnas ◽  
Rna Molecules ◽  
Periodontal Tissues ◽  
Microbial Dysbiosis ◽  
A Cell ◽  
And Function ◽  
Regulatory Functions

Periodontitis is a chronic complex inflammatory disease associated with a destructive host immune response to microbial dysbiosis, leading to irreversible loss of tooth-supporting tissues. Regeneration of functional periodontal soft (periodontal ligament and gingiva) and hard tissue components (cementum and alveolar bone) to replace lost tissues is the ultimate goal of periodontal treatment, but clinically predictable treatments are lacking. Similarly, the identification of biomarkers that can be used to accurately diagnose periodontitis activity is lacking. A relatively novel category of molecules found in oral tissue, circular RNAs (circRNAs) are single-stranded endogenous, long, non-coding RNA molecules, with covalently circular-closed structures without a 5’ cap and a 3’ tail via non-classic backsplicing. Emerging research indicates that circRNAs are tissue and disease-specific expressed and have crucial regulatory functions in various diseases. CircRNAs can function as microRNA or RNA binding sites or can regulate mRNA. In this review, we explore the biogenesis and function of circRNAs in the context of the emerging role of circRNAs in periodontitis pathogenesis and the differentiation of periodontal cells. CircMAP3K11, circCDK8, circCDR1as, circ_0062491, and circ_0095812 are associated with pathological periodontitis tissues. Furthermore, circRNAs are expressed in periodontal cells in a cell-specific manner. They can function as microRNA sponges and can form circRNA–miRNA–mRNA networks during osteogenic differentiation for periodontal-tissue (or dental pulp)-derived progenitor cells.

scholarly journals Integrated Study of Transcriptome-wide m6A Methylome Reveals Novel Insights Into the Character and Function of m6A Methylation During Yak Adipocyte Differentiation

2021 ◽  
Vol 9 ◽  
Author(s):  
Yongfeng Zhang ◽  
Chunnian Liang ◽  
Xiaoyun Wu ◽  
Jie Pei ◽  
Xian Guo ◽  
...  
Keyword(s):  
Gene Expression ◽  
Molecular Mechanisms ◽  
Adipocyte Differentiation ◽  
Gene Expression Regulation ◽  
Positive Association ◽  
Cold Season ◽  
Vital Role ◽  
Functional Enrichment ◽  
Differentially Methylated Genes ◽  
And Function

Yak (Bos grunniens) is considered an iconic symbol of Tibet and high altitude, but they suffer from malnutrition during the cold season that challenges the metabolism of energy. Adipocytes perform a crucial role in maintaining the energy balance, and adipocyte differentiation is a complex process involving multiple changes in the expression of genes. N6-methyladenosine (m6A) plays a dynamic role in post-transcription gene expression regulation as the most widespread mRNA modification of the higher eukaryotes. However, currently there is no research existing on the m6A transcriptome-wide map of bovine animals and their potential biological functions in adipocyte differentiation. Therefore, we performed methylated RNA immunoprecipitation sequencing (MeRIP-seq) and RNA sequencing (RNA-seq) to determine the distinctions in m6A methylation and gene expression during yak adipocyte differentiation. In yak adipocyte and preadipocyte the content of m6A and m6A-associated enzymes was substantially different. In the two groups, a total of 14,710 m6A peaks and 13,388 m6A peaks were identified. For the most part, m6A peaks were enriched in stop codons, 3′-untranslated regions, and coding regions with consensus motifs of GGACU. The functional enrichment exploration displayed that differentially methylated genes participated in some of the pathways associated with adipogenic metabolism, and several candidate genes (KLF9, FOXO1, ZNF395, and UHRF1) were involved in these pathways. In addition to that, there was a positive association between m6A abundance and levels of gene expression, which displayed that m6A may play a vital role in modulating gene expression during yak adipocyte differentiation. Further, in the adipocyte group, several methylation gene protein expression levels were significantly higher than in preadipocytes. In short, it can be concluded that the current study provides a comprehensive explanation of the m6A features in the yak transcriptome, offering in-depth insights into m6A topology and associated molecular mechanisms underlying bovine adipocyte differentiation, which might be helpful for further understanding its mechanisms.

scholarly journals Two Worlds Colliding: The Interplay Between Natural Compounds and Non-Coding Transcripts in Cancer Therapy

2021 ◽  
Vol 12 ◽  
Author(s):  
Alexandru A. Sabo ◽  
Maria Dudau ◽  
George L. Constantin ◽  
Tudor C. Pop ◽  
Christoph-M. Geilfus ◽  
...  
Keyword(s):  
Gene Expression Regulation ◽  
Natural Compounds ◽  
Therapeutic Strategies ◽  
Chemotherapeutic Agents ◽  
Rna Molecules ◽  
Public Health Burden ◽  
Anti Cancer ◽  
Health Promoting ◽  
Non Coding Rnas ◽  
And Function

Cancer is a devastating disease and has recently become the leading cause of death in western countries, representing an immense public health burden. When it comes to cancer treatment, chemotherapy is one of the main pillars, especially for advanced stage tumors. Over the years, natural compounds have emerged as one of the most valuable resources for new chemotherapies. It is estimated that more than half of the currently used chemotherapeutic agents are derived from natural compounds. Usually, natural compounds are discovered empirically and an important limitation of introducing new anti-cancer natural products is lack of knowledge with regard to their mechanism of action. Recent data has proven that several natural compounds may function via modulating the expression and function of non-coding RNAs (ncRNAs). NcRNAs are a heterogenous class of RNA molecules which are usually not translated into proteins but have an important role in gene expression regulation and are involved in multiple tumorigenic processes, including response/resistance to pharmacotherapy. In this review, we will discuss how natural compounds function via ncRNAs while summarizing the available data regarding their effects on over 15 types of cancer. Moreover, we will critically analyze the current advances and limitations in understanding the way natural compounds exert these health-promoting effects by acting on ncRNAs. Finally, we will propose several hypotheses that may open new avenues and perspectives regarding the interaction between natural compounds and ncRNAs, which could lead to improved natural compound-based therapeutic strategies in cancer.

Regulation and function of JunB in cell proliferation

2008 ◽  
Vol 36 (5) ◽  
pp. 864-867 ◽  
Author(s):  
Marc Piechaczyk ◽  
Rosa Farràs
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Molecular Mechanisms ◽  
Kinase Inhibitor ◽  
Activator Protein 1 ◽  
Negative Effects ◽  
Cyclin Dependent Kinase Inhibitor ◽  
Dual Action ◽  
A Cell ◽  
And Function

JunB is a member of the AP-1 (activator protein-1) family of dimeric transcription factors. It exerts a dual action on the cell cycle. It is best known as a cell proliferation inhibitor, a senescence inducer and a tumour suppressor. As for the molecular mechanisms involved, they largely involve both positive actions on genes such as the p16INK4α cyclin-dependent kinase inhibitor and negative effects on genes such as cyclin D1 during the G1-phase of the cell cycle. However, JunB is also endowed with a cell-division-promoting activity, in particular via stimulation of cyclin A2 gene expression during S-phase. Strikingly, its role in G2 and M has received little attention so far despite its possible role in the preparation of mitosis. This review addresses the known and possible mechanisms whereby JunB is implicated in the control of the different phases of the cell cycle.

A Mucin-Specific Protease Enables Molecular and Functional Analysis of Human Cancer-Associated Mucins

2018 ◽  
Author(s):  
Stacy A. Malaker ◽  
Kayvon Pedram ◽  
Michael J. Ferracane ◽  
Elliot C. Woods ◽  
Jessica Kramer ◽  
...  
Keyword(s):  
Mass Spectrometry ◽  
Molecular Mechanisms ◽  
Cultured Cells ◽  
High Resolution Mass Spectrometry ◽  
Human Cancer ◽  
Glycosylation Sites ◽  
Bacterial Protease ◽  
Specific Protease ◽  
To Come ◽  
And Function

<div> <div> <div> <p>Mucins are a class of highly O-glycosylated proteins that are ubiquitously expressed on cellular surfaces and are important for human health, especially in the context of carcinomas. However, the molecular mechanisms by which aberrant mucin structures lead to tumor progression and immune evasion have been slow to come to light, in part because methods for selective mucin degradation are lacking. Here we employ high resolution mass spectrometry, polymer synthesis, and computational peptide docking to demonstrate that a bacterial protease, called StcE, cleaves mucin domains by recognizing a discrete peptide-, glycan-, and secondary structure- based motif. We exploited StcE’s unique properties to map glycosylation sites and structures of purified and recombinant human mucins by mass spectrometry. As well, we found that StcE will digest cancer-associated mucins from cultured cells and from ovarian cancer patient-derived ascites fluid. Finally, using StcE we discovered that Siglec-7, a glyco-immune checkpoint receptor, specifically binds sialomucins as biological ligands, whereas the related Siglec-9 receptor does not. Mucin-specific proteolysis, as exemplified by StcE, is therefore a powerful tool for the study of glycoprotein structure and function and for deorphanizing mucin-binding receptors. </p> </div> </div> </div>

Focal Adhesion Kinase in Ovarian Cancer: A Potential Therapeutic Target for Platinum and Taxane-Resistant Tumors

2019 ◽  
Vol 19 (3) ◽  
pp. 179-188 ◽  
Author(s):  
Arkene Levy ◽  
Khalid Alhazzani ◽  
Priya Dondapati ◽  
Ali Alaseem ◽  
Khadijah Cheema ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Focal Adhesion Kinase ◽  
Focal Adhesion ◽  
Tumor Stage ◽  
Current Status ◽  
Potential Therapeutic Target ◽  
Resistant Disease ◽  
Development Of Resistance ◽  
And Function ◽  
Mdr 1

Focal adhesion kinase (FAK) is a non-receptor tyrosine kinase, which is an essential player in regulating cell migration, invasion, adhesion, proliferation, and survival. Its overexpression and activation have been identified in sixty-eight percent of epithelial ovarian cancer patients and this is significantly associated with higher tumor stage, metastasis, and shorter overall survival of these patients. Most recently, a new role has emerged for FAK in promoting resistance to taxane and platinum-based therapy in ovarian and other cancers. The development of resistance is a complex network of molecular processes that make the identification of a targetable biomarker in platinum and taxane-resistant ovarian cancer a major challenge. FAK overexpression upregulates ALDH and XIAP activity in platinum-resistant and increases CD44, YB1, and MDR-1 activity in taxaneresistant tumors. FAK is therefore now emerging as a prognostically significant candidate in this regard, with mounting evidence from recent successes in preclinical and clinical trials using small molecule FAK inhibitors. This review will summarize the significance and function of FAK in ovarian cancer, and its emerging role in chemotherapeutic resistance. We will discuss the current status of FAK inhibitors in ovarian cancers, their therapeutic competencies and limitations, and further propose that the combination of FAK inhibitors with platinum and taxane-based therapies could be an efficacious approach in chemotherapeutic resistant disease.

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