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  • 1
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    Keywords: CELLS ; EXPRESSION ; Germany ; MODEL ; GENE ; GENE-EXPRESSION ; GENES ; RNA ; SACCHAROMYCES-CEREVISIAE ; DNA ; MECHANISM ; mechanisms ; CELL-CYCLE ; CHROMATIN ; chromatin remodeling ; gene expression ; DNA methylation ; REGION ; HISTONE DEACETYLASE ; ESTABLISHMENT ; HETEROCHROMATIN FORMATION ; METHYLATION ; FACTOR UBF ; STATES ; review ; RE ; XENOPUS-LAEVIS ; INHERITANCE ; histone modification ; POLYMERASE-I TRANSCRIPTION ; LOCUS ; CHROMATIN-STRUCTURE ; NOR ; NoRC ; NUCLEOLAR DOMINANCE ; EPIGENETICS ; histone and DNA modification ; MAMMALIAN CHROMOSOMES ; NUCLEOLAR ORGANIZER REGIONS
    Abstract: Over the past decade emerging evidence has indicated that epigenctic factors control and regulate nuclear processes. The genes encoding ribosomal RNA (rRNA) represent an ideal model to study how epigenetics and chromatin can modulate gene expression. The reason for this is that in each cell, the rRNA genes exist in two distinct types of chromatin structure: an 'open' one corresponding to transcriptionally active genes and a 'closed' one representing the silent genes. Recent studies indicate that an epigenetic network mediates the transcriptional state of rDNA. Interplay of DNA methylation, histone modification and chromatin-remodeling activities establishes silencing at the rDNA locus in higher eukaryotes as well as at the underdominant genes in hybrid cells. The aim of this review is to summarize current knowledge about the active and silent states of rRNA genes and of nucleolar organizing regions and to analyze the mechanisms involved in the establishment and inheritance of rDNA silencing
    Type of Publication: Journal article published
    PubMed ID: 16041568
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  • 2
    Keywords: CANCER ; EXPRESSION ; GROWTH-FACTOR ; proliferation ; carcinoma ; CELL ; CELL-PROLIFERATION ; Germany ; SYSTEM ; DISEASE ; GENE ; GENE-EXPRESSION ; BIOLOGY ; DISCOVERY ; MUTATION ; COLORECTAL-CANCER ; MUTATIONS ; ADHESION ; CELL-ADHESION ; CARCINOMAS ; L1 ; NEURITE OUTGROWTH ; CELL-ADHESION MOLECULE ; HUMAN TUMOR-CELLS ; TISSUE-SPECIFIC EXPRESSION ; chemoresistance ; DISORDERS ; review ; LIFE ; L1 KNOCKOUT MICE ; MOLECULE L1 ; development ; cell migration ; MOTILITY ; EXPANSION ; PARAPLEGIA ; SPECTRUM DISORDERS ; CELL BIOLOGY ; CELL ADHESION MOLECULE ; CONTRIBUTE ; HIRSCHSPRUNGS-DISEASE ; L1 syndrome ; Neurological disorders ; X-LINKED HYDROCEPHALUS
    Abstract: Research over the last 25 years on the cell adhesion molecule L1 has revealed its pivotal role in nervous system function. Mutations of the human L1CAM gene have been shown to cause neurodevelopmental disorders such as X-linked hydrocephalus, spastic paraplegia and mental retardation. Impaired L1 function has been also implicated in the aetiology of fetal alcohol spectrum disorders, defective enteric nervous system development and malformations of the renal system. Importantly, aberrant expression of L1 has emerged as a critical factor in the development of human carcinomas, where it enhances cell proliferation, motility and chemoresistance. This discovery promoted collaborative work between tumour biologists and neurobiologists, which has led to a substantial expansion of the basic knowledge about L1 function and regulation. Here we provide an overview of the pathological conditions caused by L1 malfunction. We further discuss how the available data on gene regulation, molecular interactions and posttranslational processing of L1 may contribute to a better understanding of associated neurological and cancerous diseases
    Type of Publication: Journal article published
    PubMed ID: 20237819
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  • 3
    Keywords: APOPTOSIS ; PATHWAYS ; DEATH ; MESSENGER-RNA ; IDENTIFICATION ; chemotherapy ; PROGRESS ; Anti-cancer ; ENDOPLASMIC-RETICULUM-STRESS ; ACTIVATING TRANSCRIPTION FACTOR-3 ; Bio-weapon ; Depurination ; RICIN ; RIP ; Riproximin ; UPR ; Volkensin ; XIMENIA-AMERICANA
    Abstract: Cytotoxic ribosome-inactivating proteins (RIPs) of type II such as ricin were investigated as anti-cancer agents, but also pose a threat as biological weapons. The molecular mechanism leading to their toxic effects is, however, not yet clear. The current paradigm, which states that the irreversible depurination of 28S rRNA results in a general translational arrest eventually leading to cell death, has been questioned. Using micro-array, qRT-PCR and Western blot, we identified the unfolded protein response (UPR), a cellular mechanism activated in response to endoplasmic reticulum stress, that is induced in HCT116 and MDA-MB-231 cells exposed to the plant type II RIPs ricin, riproximin and volkensin. Apoptosis was induced by concentrations at which translation of UPR-related genes still occurred, despite concomitant ribosomal depurination. We conclude that UPR induction represents a model that better describes the cellular effects of RIP exposure at concentrations at which selected proteins are translated despite ribosomal depurination.
    Type of Publication: Journal article published
    PubMed ID: 20844919
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  • 4
    Keywords: GENE ; TUMORS ; FREQUENCY ; FUSION ; TUMOR-SUPPRESSOR GENE ; LOW-GRADE ASTROCYTOMAS ; BRAF ; MAPK ; astrocytoma ; senescence ; NEUROFIBROMATOSIS TYPE-1 ; low grade glioma ; PROGENITOR-CELL ; TARGETED THERAPY ; neural progenitors ; BRAF FUSION GENE ; VONRECKLINGHAUSEN NEUROFIBROMATOSIS ; ERK SIGNALING PATHWAY ; LGG ; MALIGNANT ASTROCYTOMA ; OPTIC-GLIOMA FORMATION ; Pilocytic
    Abstract: Pilocytic astrocytoma (PA) is the most common tumor of the pediatric central nervous system (CNS). A body of research over recent years has demonstrated a key role for mitogen-activated protein kinase (MAPK) pathway signaling in the development and behavior of PAs. Several mechanisms lead to activation of this pathway in PA, mostly in a mutually exclusive manner, with constitutive BRAF kinase activation subsequent to gene fusion being the most frequent. The high specificity of this fusion to PA when compared with other CNS tumors has diagnostic utility. In addition, the frequency of alteration of this key pathway provides an opportunity for molecularly targeted therapy in this tumor. Here, we review the current knowledge on mechanisms of MAPK activation in PA and some of the downstream consequences of this activation, which are now starting to be elucidated both in vitro and in vivo, as well as clinical considerations and possible future directions.
    Type of Publication: Journal article published
    PubMed ID: 22159586
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  • 5
    Keywords: ENDOTHELIAL GROWTH-FACTOR ; HEMATOPOIETIC STEM-CELLS ; SURFACTANT PROTEIN-A ; DEFICIENT MICE ; PULMONARY SURFACTANT ; HYPOXIA-INDUCIBLE FACTORS ; CORNEAL NEOVASCULARIZATION ; VEGF-A ; FACTOR 2-ALPHA PLAYS ; ANGIOCRINE FACTORS
    Abstract: Blood vessels have been described a long time ago as passive circuits providing sufficient blood supply to ensure proper distribution of oxygen and nutrition. Blood vessels are mainly formed during embryonic development and in the early postnatal period. In the adult, blood vessels are quiescent, but can be activated and subsequently induced under pathophysiological conditions, such as ischemia and tumor growth. Surprisingly, recent data have suggested an active function for blood vessels, named angiocrine signaling, releasing trophogens which regulate organ development and organ regeneration including in the pancreas, lung, tumor cells, liver and bone. Lung development is driven by hypoxia as well as an intense endothelial-epithelial interaction, and important mechanisms contributing to these processes have recently been identified. This review aims to summarize recent developments and concepts about embryonic pulmonary vascular development and lung regeneration. We discuss hypoxia-inducible factor HIF-2alpha and vascular endothelial growth factor VEGF as important mediators in lung development and focus on endothelial-epithelial interactions and angiocrine signaling mechanisms.
    Type of Publication: Journal article published
    PubMed ID: 25894695
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  • 6
    Keywords: COLORECTAL-CANCER ; HUMAN GENOME ; DNA-DAMAGE ; COPY NUMBER CHANGES ; MULTIPLE-MYELOMA ; RENAL-CELL CARCINOMA ; PREFERENTIAL INTEGRATION ; VIRAL INTEGRATION ; HUMAN-CHROMOSOME 7 ; REPLICATION DYNAMICS
    Abstract: The cytogenetic hypothesis that common fragile sites (cFSs) are hotspots of cancer breakpoints is increasingly supported by recent data from whole-genome profiles of different cancers. cFSs are components of the normal chromosome structure that are particularly prone to breakage under conditions of replication stress. In recent years, cFSs have become of increasing interest in cancer research, as they not only appear to be frequent targets of genomic alterations in progressive tumors, but also already in precancerous lesions. Despite growing evidence of their importance in disease development, most cFSs have not been investigated at the molecular level and most cFS genes have not been identified. In this review, we summarize the current data on molecularly characterized cFSs, their genetic and epigenetic characteristics, and put emphasis on less-studied cFS genes as potential contributors to cancer development.
    Type of Publication: Journal article published
    PubMed ID: 25231336
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  • 7
    Keywords: CELL ; MODEL ; MODELS ; intermediate filaments ; DNA-REPLICATION ; BUILDING-BLOCKS ; chromatin,coiled coils,filament assembly,lamina,lamina-associated proteins,laminopathy,nuclear membr ; DREIFUSS MUSCULAR-DYSTROPHY ; HUMAN-DISEASE ; lamin ; LEM DOMAIN ; MEMBRANE PROTEIN ; PARTIAL LIPODYSTROPHY ; PORE COMPLEXES ; RETINOBLASTOMA GENE-PRODUCT ; TRANSCRIPTIONAL REPRESSION
    Type of Publication: Journal article published
    PubMed ID: 14504651
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  • 8
    Abstract: Expression of the glycosylphosphatidylinositol-anchored membrane protein CD24 correlates with a poor prognosis for many human cancers, and in experimental tumors can promote metastasis. However, the mechanism by which CD24 contributes to tumor progression remains unclear. Here we report that in MTLy breast cancer cells CD24 interacts with and augments the kinase activity of c-src, a protein strongly implicated in promoting invasion and metastasis. This occurs within and is dependent upon intact lipid rafts. CD24-augmented c-src kinase activity increased formation of focal adhesion complexes, accelerated phosphorylation of FAK and paxillin and consequently enhanced integrin-mediated adhesion. Loss and gain of function approaches showed that c-src activity is necessary and sufficient to mediate the effects of CD24 on integrin-dependent adhesion and cell spreading, as well as on invasion. Together these results indicate that c-src is a CD24-activated mediator that promotes integrin-mediated adhesion and invasion, and suggest a mechanism by which CD24 might contribute to tumor progression through stimulating the activity of c-src or another member of the Src family.
    Type of Publication: Journal article published
    PubMed ID: 21710320
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  • 9
    Keywords: ACTIVATION ; CARCINOMA-CELLS ; LIPID RAFTS ; PROTEIN-TYROSINE KINASES ; focal adhesion kinase ; OVARIAN-CARCINOMA ; BREAST-CANCER CELLS ; GENE CD24 ; BIOLOGICAL ASPECTS ; SRC
    Abstract: CD24 is a glycosyl-phosphatidylinositol-anchored membrane protein that is frequently over-expressed in a variety of human carcinomas and is correlated with poor prognosis. In cancer cell lines, changes of CD24 expression can alter several cellular properties in vitro and tumor growth in vivo. However, little is known about how CD24 mediates these effects. Here we have analyzed the functional consequences of CD24 knock-down or over-expression in human cancer cell lines. Depletion of CD24 reduced cell proliferation and adhesion, enhanced apoptosis, and regulated the expression of various genes some of which were identified as STAT3 target genes. Loss of CD24 reduced STAT3 and FAK phosphorylation. Diminished STAT3 activity was confirmed by specific reporter assays. We found that reduced STAT3 activity after CD24 knock-down was accompanied by altered Src phosphorylation. Silencing of Src, similar to CD24, targeted the expression of prototype STAT3-regulated genes. Likewise, the over-expression of CD24 augmented Src-Y416 phosphorylation, the recruitment of Src into lipid rafts and the expression of STAT3-dependent target genes. An antibody to CD24 was effective in reducing tumor growth of A549 lung cancer and BxPC3 pancreatic cancer xenografts in mice. Antibody treatment affected the level of Src-phosphorylation in the tumor and altered the expression of STAT3 target genes. Our results provide evidence that CD24 regulates STAT3 and FAK activity and suggest an important role of Src in this process. Finally, the targeting of CD24 by antibodies could represent a novel route for tumor therapy.
    Type of Publication: Journal article published
    PubMed ID: 22760497
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  • 10
    Abstract: The link between inflammation and cancer is well established. Chronic inflammation promotes cancer initiation and progression. Various studies showed that the underlying mechanisms involve epigenetic alterations. These epigenetic alterations might culminate into an epigenetic switch that transforms premalignant cells into tumor cells or non-invasive into invasive tumor cells, thereby promoting metastasis. Epigenetic switches require an initiating event, which can be inflammation, whereas the resulting phenotype is inherited without the initiating signal. Epigenetic switches are induced and maintained by DNA methylation, histone modifications, polycomb group (PcG)/trithorax group (TrxG) proteins, and feedback loops consisting of transcription factors and microRNAs. Since epigenetic switches are reversible, they might represent an important basis for the design of novel anticancer therapeutics. This review summarizes published evidence of epigenetic switches in cancer development that are induced by inflammation.
    Type of Publication: Journal article published
    PubMed ID: 26394635
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