scholarly journals Role of CD1A and HSP60 in the antitumoral response of oesophageal cancer

2011 ◽  
pp. 225-232
Author(s):  
Simona Corrao ◽  
Giampiero La Rocca ◽  
Rita Anzalone ◽  
Lorenzo Marasà ◽  
Felicia Farina ◽  
...  
Keyword(s):  
Oesophageal Cancer ◽  
Molecular Mechanisms ◽  
Tumor Antigens ◽  
Normal Epithelium ◽  
Improve Treatment ◽  
Molecular Events ◽  
New Strategies ◽  
Stimulation Of

Oesophageal cancer (OC) is one of the most common and severe forms of tumor. A wider knowledge of molecular mechanisms which lead to a normal epithelium becoming a neoplasm may reveal new strategies to improve treatment and outcome of this disease. In this review, we report recent findings concerning molecular events which take place during carcinogenesis of the oesophagus. In particular, we focus on the role of two molecules, CD1a and Hsp60, which are overexpressed in oesophageal and many other types of tumor. Both molecules may present tumor antigens and promote in situ the stimulation of an antitumoral immune activity. We suggest there is a synergistic action between these molecules. Further knowledge about their intracellular pathways and extracellular roles may help develop new antitumoral tools for OC.

scholarly journals Rare variants in axonogenesis genes connect three families with sound–color synesthesia

2018 ◽  
Vol 115 (12) ◽  
pp. 3168-3173 ◽  
Author(s):  
Amanda K. Tilot ◽  
Katerina S. Kucera ◽  
Arianna Vino ◽  
Julian E. Asher ◽  
Simon Baron-Cohen ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Rare Variants ◽  
Autism Spectrum ◽  
Sensory Experiences ◽  
Limited Success ◽  
Whole Exome ◽  
Rare Genetic Variants ◽  
Sound Color ◽  
Stimulation Of

Synesthesia is a rare nonpathological phenomenon where stimulation of one sense automatically provokes a secondary perception in another. Hypothesized to result from differences in cortical wiring during development, synesthetes show atypical structural and functional neural connectivity, but the underlying molecular mechanisms are unknown. The trait also appears to be more common among people with autism spectrum disorder and savant abilities. Previous linkage studies searching for shared loci of large effect size across multiple families have had limited success. To address the critical lack of candidate genes, we applied whole-exome sequencing to three families with sound–color (auditory–visual) synesthesia affecting multiple relatives across three or more generations. We identified rare genetic variants that fully cosegregate with synesthesia in each family, uncovering 37 genes of interest. Consistent with reports indicating genetic heterogeneity, no variants were shared across families. Gene ontology analyses highlighted six genes—COL4A1, ITGA2, MYO10, ROBO3, SLC9A6, and SLIT2—associated with axonogenesis and expressed during early childhood when synesthetic associations are formed. These results are consistent with neuroimaging-based hypotheses about the role of hyperconnectivity in the etiology of synesthesia and offer a potential entry point into the neurobiology that organizes our sensory experiences.

scholarly journals Molecular Events Involved in Influenza A Virus-Induced Cell Death

2022 ◽  
Vol 12 ◽  
Author(s):  
Rui Gui ◽  
Quanjiao Chen
Keyword(s):  
Cell Death ◽  
Influenza A Virus ◽  
Influenza A ◽  
Regulatory Networks ◽  
Molecular Mechanisms ◽  
Tissue Destruction ◽  
Inflammatory Reactions ◽  
Molecular Events ◽  
Host Death

Viral infection usually leads to cell death. Moderate cell death is a protective innate immune response. By contrast, excessive, uncontrolled cell death causes tissue destruction, cytokine storm, or even host death. Thus, the struggle between the host and virus determines whether the host survives. Influenza A virus (IAV) infection in humans can lead to unbridled hyper-inflammatory reactions and cause serious illnesses and even death. A full understanding of the molecular mechanisms and regulatory networks through which IAVs induce cell death could facilitate the development of more effective antiviral treatments. In this review, we discuss current progress in research on cell death induced by IAV infection and evaluate the role of cell death in IAV replication and disease prognosis.

scholarly journals Transcriptome-Wide Analyses Provide Insights into Development of the Hedychium Coronarium Flower, Revealing Potential Roles of PTL

2020 ◽  
Author(s):  
Tong Zhao ◽  
Alma Piñeyro-Nelson ◽  
Qianxia Yu ◽  
Xiaoying Hu ◽  
Huanfang Liu ◽  
...  
Keyword(s):  
In Situ Hybridization ◽  
Flower Development ◽  
Molecular Mechanisms ◽  
Expression Patterns ◽  
Floral Organ ◽  
Mrna In Situ Hybridization ◽  
Hedychium Coronarium ◽  
Organ Identity

Abstract Background:The flower of Hedychium coronarium possesses highly specialized floral organs: a synsepalous calyx, petaloid staminodes and a labellum. The formation of these organs is controlled by two gene categories: floral organ identity genes and organ boundary genes, which may function individually or jointly during flower development. Although the floral organogenesis of H. coronarium has been studied at the morphological level, the underlying molecular mechanisms involved in its floral development still remain poorly understood. In addition, previous works analyzing the role of MADS-box genes in controlling floral organ specification in some Zingiberaceae did not address the molecular mechanisms involved in the formation of particular organ morphologies that emerge later in flower development, such as the synsepalous calyx formed through intercalary growth of adjacent sepals. Results:Here, we used comparative transcriptomics combined with Real-time quantitative PCR and mRNA in situ hybridization to investigate gene expression patterns of ABC-class genes in H. coronarium flowers, as well as the homolog of the organ boundary gene PETAL LOSS (HcPTL). qRT-PCR detection showed that HcAP3 and HcAG were expressed in both the petaloid staminode and the fertile stamen. mRNA in situ hybridization showed that HcPTL was expressed in developing meristems, including cincinnus primordia, floral primordia, common primordia and almost all new initiating floral organ primordia.Conclusions:Our studies found that stamen/petal identity or stamen fertility in H. coronarium was not necessarily correlated with the differential expression of HcAP3 and HcAG. We also found a novel spatio-temporal expression pattern for HcPTL mRNA, suggesting it may have evolved a lineage-specific role in the morphogenesis of the Hedychium flower. Our study provides a new transcriptome reference and a functional hypothesis regarding the role of a boundary gene in organ fusion that should be further addressed through phylogenetic analyzes of this gene, as well as functional studies.

scholarly journals Regulation of ST6GAL1 sialyltransferase expression in cancer cells

Glycobiology ◽  
2020 ◽  
Author(s):  
Kaitlyn A Dorsett ◽  
Michael P Marciel ◽  
Jihye Hwang ◽  
Katherine E Ankenbauer ◽  
Nikita Bhalerao ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Translational Regulation ◽  
Molecular Mechanisms ◽  
Current Knowledge ◽  
Sialic Acids ◽  
Invasion Resistance ◽  
Cell Behaviors ◽  
Molecular Events ◽  
Wide Range

Abstract The ST6GAL1 sialyltransferase, which adds α2–6 linked sialic acids to N-glycosylated proteins, is overexpressed in a wide range of human malignancies. Recent studies have established the importance of ST6GAL1 in promoting tumor cell behaviors such as invasion, resistance to cell stress, and chemoresistance. Furthermore, ST6GAL1 activity has been implicated in imparting cancer stem cell characteristics. However, despite the burgeoning interest in the role of ST6GAL1 in the phenotypic features of tumor cells, insufficient attention has been paid to the molecular mechanisms responsible for ST6GAL1 upregulation during neoplastic transformation. Evidence suggests that these mechanisms are multifactorial, encompassing genetic, epigenetic, transcriptional, and post-translational regulation. The purpose of this review is to summarize current knowledge regarding the molecular events that drive enriched ST6GAL1 expression in cancer cells.

scholarly journals Treatment of Metastatic Disease through Natural Killer Cell Modulation by Infected Cell Vaccines

Viruses ◽  
2019 ◽  
Vol 11 (5) ◽  
pp. 434
Author(s):  
Seyedeh Raheleh Niavarani ◽  
Christine Lawson ◽  
Lee-Hwa Tai
Keyword(s):  
Infected Cell ◽  
Natural Killer ◽  
Tumor Antigens ◽  
Critical Role ◽  
Killer Cell ◽  
Oncolytic Viruses ◽  
Cell Vaccine ◽  
Tumor Killing

Oncolytic viruses (OVs) are a form of immunotherapy that release tumor antigens in the context of highly immunogenic viral signals following tumor-targeted infection and destruction. Emerging preclinical and clinical evidence suggests that this in situ vaccine effect is critical for successful viro-immunotherapy. In this review, we discuss the application of OV as an infected cell vaccine (ICV) as one method of enhancing the potency and breadth of anti-tumoral immunity. We focus on understanding and manipulating the critical role of natural killer (NK) cells and their interactions with other immune cells to promote a clinical outcome. With a synergistic tumor killing and immune activating mechanism, ICVs represent a valuable new addition to the cancer fighting toolbox with the potential to treat malignant disease.

scholarly journals HCV and Lymphoproliferation

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Anna Linda Zignego ◽  
Carlo Giannini ◽  
Laura Gragnani
Keyword(s):  
Molecular Mechanisms ◽  
Public Health Problem ◽  
Viral Proteins ◽  
Mixed Cryoglobulinemia ◽  
Lymphoproliferative Disorders ◽  
Hcv Infection ◽  
Ideal Model ◽  
The Past ◽  
Stimulation Of

Hepatitis C virus (HCV) infection is a serious public health problem because of its worldwide diffusion and sequelae. It is not only a hepatotropic but also a lymphotropic agent and is responsible not only for liver injury—potentially evolving to cirrhosis and hepatocellular carcinoma—but also for a series of sometimes severely disabling extrahepatic diseases and, in particular, B-cell lymphoproliferative disorders. These latter range from benign, but prelymphomatous conditions, like mixed cryoglobulinemia, to frank lymphomas. Analogously withHelicobacter pylorirelated lymphomagenesis, the study of the effects of viral eradication confirmed the etiopathogenetic role of HCV and showed it is an ideal model for better understanding of the molecular mechanisms involved. Concerning these latter, several hypotheses have been proposed over the past two decades which are not mutually exclusive. These hypotheses have variously emphasized the important role played by sustained stimulation of the immune system by HCV, infection of the lymphatic cells, viral proteins, chromosomal aberrations, cytokines, or microRNA molecules. In this paper we describe the main hypotheses that have been proposed with the corresponding principal supporting data.

scholarly journals Oxidative stress and ageing of the post-ovulatory oocyte

Reproduction ◽  
2013 ◽  
Vol 146 (6) ◽  
pp. R217-R227 ◽  
Author(s):  
Tessa Lord ◽  
R John Aitken
Keyword(s):  
Oxidative Stress ◽  
Molecular Mechanisms ◽  
Embryo Quality ◽  
Fertilization Rates ◽  
Molecular Events ◽  
Post Implantation ◽  
Potential Use

With extended periods of time following ovulation, the metaphase II stage oocyte experiences deterioration in quality referred to as post-ovulatory oocyte ageing. Post-ovulatory ageing occurs both in vivo and in vitro and has been associated with reduced fertilization rates, poor embryo quality, post-implantation errors and abnormalities in the offspring. Although the physiological consequences of post-ovulatory oocyte ageing have largely been established, the molecular mechanisms controlling this process are not well defined. This review analyses the relationships between biochemical changes exhibited by the ageing oocyte and the symptoms associated with the ageing phenotype. We also discuss molecular events that are potentially involved in orchestrating post-ovulatory ageing with a particular focus on the role of oxidative stress. We propose that oxidative stress may act as the initiator for a cascade of events that create the aged oocyte phenotype. Specifically, oxidative stress has the capacity to cause a decline in levels of critical cell cycle factors such as maturation-promoting factor, impair calcium homoeostasis, induce mitochondrial dysfunction and directly damage multiple intracellular components of the oocyte such as lipids, proteins and DNA. Finally, this review addresses current strategies for delaying post-ovulatory oocyte ageing with a particular focus on the potential use of compounds such as caffeine or selected antioxidants in the development of more refined media for the preservation of oocyte integrity during IVF procedures.

Molecular mechanisms of GABAB receptor activation: new insights from the mechanism of action of CGP7930, a positive allosteric modulator

2004 ◽  
Vol 32 (5) ◽  
pp. 871-872 ◽  
Author(s):  
V. Binet ◽  
C. Goudet ◽  
C. Brajon ◽  
L. Le Corre ◽  
F. Acher ◽  
...  
Keyword(s):  
G Protein ◽  
Mechanism Of Action ◽  
Molecular Mechanisms ◽  
Gabab Receptor ◽  
Receptor Activation ◽  
G Protein Coupled Receptors ◽  
Class Iii ◽  
G Protein Coupled ◽  
New Strategies

The GABAB (γ-aminobutyric acid-B) receptor is composed of two subunits, GABAB1 and GABAB2. Both subunits share structural homology with other class-III G-protein-coupled receptors. They contain two main domains, a heptahelical domain typical of all G-protein-coupled receptors and a large ECD (extracellular domain). It has not been demonstrated whether the association of these two subunits is always required for function. However, GABAB2 plays a major role in coupling with G-proteins, and GABAB1 has been shown to bind GABA. To date, only ligands interacting with GABAB1-ECD have been identified. In the present study, we explored the mechanism of action of CGP7930, a compound described as a positive allosteric regulator of the GABAB receptor. We have shown that it can weakly activate the wild-type GABAB receptor, but also the GABAB2 expressed alone, thus being the first described agonist of GABAB2. CGP7930 retains its weak agonist activity on a GABAB2 subunit deleted of its ECD. Thus the heptahelical domain of GABAB2 behaves similar to a rhodopsin-like receptor. These results open new strategies for studying the mechanism of activation of GABAB receptor and examine any possible role of GABAB2.

scholarly journals Role of calcium and calmodulin in ciliary stimulation induced by acetylcholine

2001 ◽  
Vol 280 (1) ◽  
pp. C100-C109 ◽  
Author(s):  
Orna Zagoory ◽  
Alex Braiman ◽  
Larisa Gheber ◽  
Zvi Priel
Keyword(s):  
Phospholipase C ◽  
Muscarinic Receptors ◽  
Elevated Level ◽  
Beat Frequency ◽  
Ciliary Beat Frequency ◽  
Combined Effect ◽  
Molecular Events ◽  
Intracellular Ca ◽  
Stimulation Of

The goal of this work was to elucidate the molecular events underlying stimulation of ciliary beat frequency (CBF) induced by acetylcholine (ACh) in frog esophagus epithelium. ACh induces a profound increase in CBF and in intracellular Ca2+ concentration ([Ca2+]i) through M1 and M3 muscarinic receptors. The [Ca2+]i slowly decays to the basal level, while CBF stabilizes at an elevated level. These results suggest that ACh triggers Ca2+-correlated and -uncorrelated modes of ciliary stimulation. ACh response is abolished by the phospholipase C (PLC) inhibitor U-73122 and by depletion of intracellular Ca2+ stores but is unaffected by reduction of extracellular Ca2+ concentration and by blockers of Ca2+influx. Therefore, ACh activates PLC and mobilizes Ca2+solely from intracellular stores. The calmodulin inhibitors W-7 and calmidazolium attenuate the ACh-induced increase in [Ca2+]i but completely abolish the elevation in CBF. Therefore, elevation of [Ca2+]i is necessary for CBF enhancement but does not lead directly to it. The combined effect of Ca2+ elevation and of additional factors, presumably mobilized by Ca2+-calmodulin, results in a robust CBF enhancement.

scholarly journals Molecular Mechanisms of Merkel Cell Polyomavirus Transformation and Replication

2020 ◽  
Vol 7 (1) ◽  
pp. 289-307 ◽  
Author(s):  
Wei Liu ◽  
Jianxin You
Keyword(s):  
Molecular Mechanisms ◽  
Human Tumor ◽  
Merkel Cell Polyomavirus ◽  
Merkel Cell ◽  
Virus Family ◽  
The Past ◽  
Molecular Events ◽  
Cellular Tropism ◽  
Novel Virus

Viral infection underlies a significant share of the global cancer burden. Merkel cell polyomavirus (MCPyV) is the newest member of the human oncogenic virus family. Its discovery over a decade ago marked the beginning of an exciting era in human tumor virology. Since then, significant evidence has emerged to support the etiologic role of MCPyV in Merkel cell carcinoma (MCC), an extremely lethal form of skin cancer. MCPyV infection is widespread in the general population. MCC diagnoses have tripled over the past 20 years, but effective treatments are currently lacking. In this review, we highlight recent discoveries that have shaped our understanding of MCPyV oncogenic mechanism and host cellular tropism, as well as the molecular events occurring in the viral infectious life cycle. These insights will guide future efforts in developing novel virus-targeted therapeutic strategies for treating the devastating human cancers associated with this new tumorigenic virus.

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