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centrosome amplification

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https://www.readbyqxmd.com/read/28186092/epstein-barr-virus-particles-induce-centrosome-amplification-and-chromosomal-instability
#1
Anatoliy Shumilov, Ming-Han Tsai, Yvonne T Schlosser, Anne-Sophie Kratz, Katharina Bernhardt, Susanne Fink, Tuba Mizani, Xiaochen Lin, Anna Jauch, Josef Mautner, Annette Kopp-Schneider, Regina Feederle, Ingrid Hoffmann, Henri-Jacques Delecluse
Infections with Epstein-Barr virus (EBV) are associated with cancer development, and EBV lytic replication (the process that generates virus progeny) is a strong risk factor for some cancer types. Here we report that EBV infection of B-lymphocytes (in vitro and in a mouse model) leads to an increased rate of centrosome amplification, associated with chromosomal instability. This effect can be reproduced with virus-like particles devoid of EBV DNA, but not with defective virus-like particles that cannot infect host cells...
February 10, 2017: Nature Communications
https://www.readbyqxmd.com/read/28171744/centrosome-amplification-and-cancer-a-question-of-sufficiency
#2
Jordan W Raff, Renata Basto
Centrosome amplification is a common feature of many types of cancer, but whether it is a cause or consequence is hotly debated. In this issue of Developmental Cell, Levine et al. (2017) provide strong evidence that centrosome amplification is sufficient to initiate tumorigenesis in a mouse model.
February 6, 2017: Developmental Cell
https://www.readbyqxmd.com/read/28148738/cell-scientist-to-watch-andrew-holland
#3
(no author information available yet)
Andrew received his first degree in natural sciences from the University of Cambridge and a Masters degree from the University of Manchester, followed by a PhD with Stephen Taylor in Manchester. He then moved to California in 2007 with an EMBO long-term fellowship for his postdoctoral research with Don Cleveland at the Ludwig Institute for Cancer Research. In 2013, Andrew started his own lab as an Assistant Professor in the Department of Molecular Biology and Genetics at the Johns Hopkins University School of Medicine, having been named a Kimmel Scholar and a Pew-Stewart Scholar in 2014...
February 1, 2017: Journal of Cell Science
https://www.readbyqxmd.com/read/28132847/centrosome-amplification-is-sufficient-to-promote-spontaneous-tumorigenesis-in-mammals
#4
Michelle S Levine, Bjorn Bakker, Bram Boeckx, Julia Moyett, James Lu, Benjamin Vitre, Diana C Spierings, Peter M Lansdorp, Don W Cleveland, Diether Lambrechts, Floris Foijer, Andrew J Holland
Centrosome amplification is a common feature of human tumors, but whether this is a cause or a consequence of cancer remains unclear. Here, we test the consequence of centrosome amplification by creating mice in which centrosome number can be chronically increased in the absence of additional genetic defects. We show that increasing centrosome number elevated tumor initiation in a mouse model of intestinal neoplasia. Most importantly, we demonstrate that supernumerary centrosomes are sufficient to drive aneuploidy and the development of spontaneous tumors in multiple tissues...
February 6, 2017: Developmental Cell
https://www.readbyqxmd.com/read/28104305/cp39-cp75-and-cp91-are-major-structural-components-of-the-dictyostelium-centrosome-s-core-structure
#5
Irene Meyer, Tatjana Peter, Petros Batsios, Oliver Kuhnert, Anne Krüger-Genge, Carl Camurça, Ralph Gräf
The acentriolar Dictyostelium centrosome is a nucleus-associated body consisting of a core structure with three plaque-like layers, which are surrounded by a microtubule-nucleating corona. The core duplicates once per cell cycle at the G2/M transition, whereby its central layer disappears and the two outer layers form the mitotic spindle poles. Through proteomic analysis of isolated centrosomes, we have identified CP39 and CP75, two essential components of the core structure. Both proteins can be assigned to the central core layer as their centrosomal presence is correlated to the disappearance and reappearance of the central core layer in the course of centrosome duplication...
January 12, 2017: European Journal of Cell Biology
https://www.readbyqxmd.com/read/28100636/centriole-splitting-caused-by-loss-of-the-centrosomal-linker-protein-c-nap1-reduces-centriolar-satellite-density-and-impedes-centrosome-amplification
#6
Anne-Marie Flanagan, Elena Stavenschi, Shivakumar Basavaraju, David Gaboriau, David A Hoey, Ciaran G Morrison
Duplication of the centrosomes is a tightly regulated process. Abnormal centrosome numbers can impair cell division and cause changes in how cells migrate. Duplicated centrosomes are held together by a proteinaceous linker made up of rootletin filaments anchored to the centrioles by C-NAP1. This linker is removed in a NEK2A kinase-dependent manner as mitosis begins. To explore C-NAP1 activities in regulating centrosome activities, we used genome editing to ablate it. C-NAP1 null cells were viable and had an increased frequency of premature centriole separation, accompanied by reduced density of the centriolar satellites, with re-expression of C-NAP1 rescuing both these phenotypes...
January 18, 2017: Molecular Biology of the Cell
https://www.readbyqxmd.com/read/28063737/discovery-of-centrosomal-protein-70-as-an-important-player-in-the-development-and-progression-of-breast-cancer
#7
Xingjuan Shi, Dengwen Li, Yujue Wang, Shiyu Liu, Juan Qin, Jun Wang, Jie Ran, Yu Zhang, Qinghai Huang, Xiangdong Liu, Jun Zhou, Min Liu
Centrosome abnormalities have been implicated in the development and progression of breast cancer. However, the molecular players involved in the above processes remain largely uncharacterized. Herein, we identify centrosomal protein 70 (Cep70) as an important factor that mediates breast cancer growth and metastasis. Cep70 is up-regulated in breast cancer tissues and cell lines, and its expression is closely correlated with several clinicopathologic variables associated with breast cancer progression. Mechanistic studies reveal that the up-regulation of Cep70 in breast cancer occurs at the mRNA level and is independent of gene amplification...
March 2017: American Journal of Pathology
https://www.readbyqxmd.com/read/28008224/centrosome-a-promising-anti-cancer-target
#8
REVIEW
Yainyrette Rivera-Rivera, Harold I Saavedra
The centrosome, an organelle discovered >100 years ago, is the main microtubule-organizing center in mammalian organisms. The centrosome is composed of a pair of centrioles surrounded by the pericentriolar material (PMC) and plays a major role in the regulation of cell cycle transitions (G1-S, G2-M, and metaphase-anaphase), ensuring the normality of cell division. Hundreds of proteins found in the centrosome exert a variety of roles, including microtubule dynamics, nucleation, and kinetochore-microtubule attachments that allow correct chromosome alignment and segregation...
2016: Biologics: Targets & Therapy
https://www.readbyqxmd.com/read/27998958/bisphenol-a-and-its-analogues-disrupt-centrosome-cycle-and-microtubule-dynamics-in-prostate-cancer
#9
Shuk-Mei Ho, Rahul Rao, Sarah To, Emma Schoch, Pheruza Tarapore
Humans are increasingly exposed to structural analogues of bisphenol A (BPA), as BPA is being replaced by these compounds in BPA-free consumer products. We have previously shown that chronic and developmental exposure to BPA is associated with increased prostate cancer (PCa) risk in human and animal models. Here, we examine whether exposure of PCa cells (LNCaP, C4-2) to low-dose BPA and its structural analogues (BPS, BPF, BPAF, TBBPA, DMBPA and TMBPA) affects centrosome amplification (CA), a hallmark of cancer initiation and progression...
February 2017: Endocrine-related Cancer
https://www.readbyqxmd.com/read/27926524/selective-hdac-inhibition-by-acy-241-enhances-the-activity-of-paclitaxel-in-solid-tumor-models
#10
Pengyu Huang, Ingrid Almeciga-Pinto, Matthew Jarpe, John H van Duzer, Ralph Mazitschek, Min Yang, Simon S Jones, Steven N Quayle
ACY-241 is a novel, orally available and selective histone deacetylase (HDAC) 6 inhibitor in Phase 1b clinical development in multiple myeloma (NCT 02400242). Like the structurally related drug ACY-1215 (ricolinostat), ACY-241 has the potential for a substantially reduced side effect profile versus current nonselective HDAC inhibitor drug candidates due to reduced potency against Class I HDACs while retaining the potential for anticancer effectiveness. We now show that combination treatment of xenograft models with paclitaxel and either ricolinostat or ACY-241 significantly suppresses solid tumor growth...
January 10, 2017: Oncotarget
https://www.readbyqxmd.com/read/27924065/the-more-the-messier-centrosome-amplification-as-a-novel-biomarker-for-personalized-treatment-of-colorectal-cancers
#11
REVIEW
Monica M Mahathre, Padmashree Cg Rida, Ritu Aneja
Colon cancer is currently the third most common cancer and second most fatal cancer in the United States, resulting in approximately 600,000 deaths annually. Though colorectal cancer death rates are decreasing by about 3% every year, disease outcomes could be substantially improved with more research into the drivers of colon carcinogenesis, the determinants of aggressiveness in colorectal cancer and the identification of biomarkers that could enable choice of more optimal treatments. Colon carcinogenesis is notably a slow process that can take decades...
November 2016: Journal of Biomedical Research
https://www.readbyqxmd.com/read/27911707/the-plk4-stil-sas-6-module-at-the-core-of-centriole-duplication
#12
REVIEW
Christian Arquint, Erich A Nigg
Centrioles are microtubule-based core components of centrosomes and cilia. They are duplicated exactly once during S-phase progression. Central to formation of each new (daughter) centriole is the formation of a nine-fold symmetrical cartwheel structure onto which microtubule triplets are deposited. In recent years, a module comprising the protein kinase polo-like kinase 4 (PLK4) and the two proteins STIL and SAS-6 have been shown to stay at the core of centriole duplication. Depletion of any one of these three proteins blocks centriole duplication and, conversely, overexpression causes centriole amplification...
October 15, 2016: Biochemical Society Transactions
https://www.readbyqxmd.com/read/27872092/plk4-promotes-cancer-invasion-and-metastasis-through-arp2-3-complex-regulation-of-the-actin-cytoskeleton
#13
Karineh Kazazian, Christopher Go, Hannah Wu, Olga Brashavitskaya, Roland Xu, James W Dennis, Anne-Claude Gingras, Carol J Swallow
The polo family serine threonine kinase Plk4 has been proposed as a therapeutic target in advanced cancers based on increased expression in primary human cancers, facilitation of tumor growth in murine xenograft models, and centrosomal amplification induced by its overexpression. However, both the causal link between these phenomena and the feasibility of selective Plk4 inhibition remain unclear. Here we characterize Plk4-dependent cancer cell migration and invasion as well as local invasion and metastasis of cancer xenografts...
January 15, 2017: Cancer Research
https://www.readbyqxmd.com/read/27796307/kat2a-kat2b-targeted-acetylome-reveals-a-role-for-plk4-acetylation-in-preventing-centrosome-amplification
#14
Marjorie Fournier, Meritxell Orpinell, Cédric Grauffel, Elisabeth Scheer, Jean-Marie Garnier, Tao Ye, Virginie Chavant, Mathilde Joint, Fumiko Esashi, Annick Dejaegere, Pierre Gönczy, László Tora
Lysine acetylation is a widespread post-translational modification regulating various biological processes. To characterize cellular functions of the human lysine acetyltransferases KAT2A (GCN5) and KAT2B (PCAF), we determined their acetylome by shotgun proteomics. One of the newly identified KAT2A/2B substrate is polo-like kinase 4 (PLK4), a key regulator of centrosome duplication. We demonstrate that KAT2A/2B acetylate the PLK4 kinase domain on residues K45 and K46. Molecular dynamics modelling suggests that K45/K46 acetylation impairs kinase activity by shifting the kinase to an inactive conformation...
October 31, 2016: Nature Communications
https://www.readbyqxmd.com/read/27693136/centrosome-amplification-increases-single-cell-branching-in-post-mitotic-cells
#15
Delia Ricolo, Myrto Deligiannaki, Jordi Casanova, Sofia J Araújo
Centrosome amplification is a hallmark of cancer, although we are still far from understanding how this process affects tumorigenesis [1, 2]. Besides the contribution of supernumerary centrosomes to mitotic defects, their biological effects in the post-mitotic cell are not well known. Here, we exploit the effects of centrosome amplification in post-mitotic cells during single-cell branching. We show that Drosophila tracheal cells with extra centrosomes branch more than wild-type cells. We found that mutations in Rca1 and CycA affect subcellular branching, causing tracheal tip cells to form more than one subcellular lumen...
September 17, 2016: Current Biology: CB
https://www.readbyqxmd.com/read/27634760/pharmacological-inhibition-of-centrosome-clustering-by-slingshot-mediated-cofilin-activation-and-actin-cortex-destabilization
#16
Gleb Konotop, Elena Bausch, Tomoaki Nagai, Andrey Turchinovich, Natalia Becker, Axel Benner, Michael Boutros, Kensaku Mizuno, Alwin Krämer, Marc Steffen Raab
Centrosome amplification is a hallmark of virtually all types of cancers, including solid tumors and hematologic malignancies. Cancer cells with extra centrosomes use centrosome clustering (CC) to allow for successful division. Because normal cells do not rely on this mechanism, CC is regarded as a promising target to selectively eradicate cells harboring supernumerary centrosomes. To identify novel inhibitors of CC, we developed a cell-based high-throughput screen that reports differential drug cytotoxicity for isogenic cell populations with different centrosome contents...
September 13, 2016: Cancer Research
https://www.readbyqxmd.com/read/27621083/the-centrosomal-deubiquitylase-usp21-regulates-gli1-transcriptional-activity-and-stability
#17
Claire Heride, Daniel J Rigden, Erithelgi Bertsoulaki, Danilo Cucchi, Enrico De Smaele, Michael J Clague, Sylvie Urbé
USP21 is a centrosome-associated deubiquitylase (DUB) that has been implicated in the formation of primary cilia - crucial organelles for the regulation of the Hedgehog (Hh) signaling pathway in vertebrates. Here, we identify KCTD6 - a cullin-3 E3-ligase substrate adapter that has been previously linked to Hh signaling - as well as Gli1, the key transcription factor responsible for Hh signal amplification, as new interacting partners of USP21. We identify a cryptic structured protein interaction domain in KCTD6, which is predicted to have a similar fold to Smr domains...
November 1, 2016: Journal of Cell Science
https://www.readbyqxmd.com/read/27592797/an-interaction-between-arsenic-induced-epigenetic-modification-and-inflammatory-promotion-in-a-skin-equivalent-during-arsenic-carcinogenesis
#18
Wei-Ting Liao, Jian-He Lu, Chih-Hung Lee, Cheng-Che E Lan, Jan-Gowth Chang, Chee-Yin Chai, Hsin-Su Yu
Animal studies have shown that chemical carcinogenesis consists of a three-stage process: initiation, promotion, and progression. However, because of the lack of a suitable tissue model, the molecular mechanisms of cell-cell interactions involved in those processes remain unclear. We have established a human intraepidermal carcinoma skin equivalent with organotypic culture-consisting of keratinocytes, fibroblasts, and peripheral blood mononuclear cells - induced by arsenic treatment. This SE shows the pathognomonic characteristics of arsenic-induced Bowen's disease, including acanthosis, dysplasia, and dyskeratosis...
January 2017: Journal of Investigative Dermatology
https://www.readbyqxmd.com/read/27544453/t0070907-inhibits-repair-of-radiation-induced-dna-damage-by-targeting-rad51
#19
Zhengzhe An, Jae-Ran Yu, Woo-Yoon Park
T0070907 (T007), a PPARγ inhibitor, can reduce α and β tubulin proteins in some cancer cell lines. Thus, T007 has been suggested as an antimicrotubule drug. We previously reported that T007 increased radiosensitivity by inducing mitotic catastrophe in cervical cancer cells. In this study, we investigated the underlying mechanisms of the T007-mediated increase in radiosensitivity. T007 pre-treatment attenuated RAD51 protein levels and ionising radiation (IR)-induced nuclear foci formation, resulting in more frequent centrosome amplification and multipolar mitotic spindle formation in cervical cancer cells...
December 2016: Toxicology in Vitro: An International Journal Published in Association with BIBRA
https://www.readbyqxmd.com/read/27443516/ccne1-amplification-and-centrosome-number-abnormality-in-serous-tubal-intraepithelial-carcinoma-further-evidence-supporting-its-role-as-a-precursor-of-ovarian-high-grade-serous-carcinoma
#20
Elisabetta Kuhn, Tian-Li Wang, Kai Doberstein, Asli Bahadirli-Talbott, Ayse Ayhan, Ann Smith Sehdev, Ronny Drapkin, Robert J Kurman, Ie-Ming Shih
Aberration in chromosomal structure characterizes almost all cancers and has profound biological significance in tumor development. It can be facilitated by various mechanisms including overexpression of cyclin E1 and centrosome amplification. As ovarian high-grade serous carcinoma has pronounced chromosomal instability, in this study we sought to determine whether increased copy number of CCNE1 which encodes cyclin E1 and centrosome amplification (>2 copies) occurs in its putative precursor, serous tubal intraepithelial carcinoma...
October 2016: Modern Pathology: An Official Journal of the United States and Canadian Academy of Pathology, Inc
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