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centrosome amplification

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https://www.readbyqxmd.com/read/29138111/recent-advances-in-melanoma-research-via-omics-platforms
#1
REVIEW
Carmen Rodríguez-Cerdeira, Alberto Molares-Vila, Miguel Carnero-Gregorio, Alberte Corbalán-Rivas
Melanoma has a high mortality rate and metastatic melanoma is highly resistant to conventional therapies. "Omics" fields such as proteomics and microRNA and exosome studies have provided new knowledge to complement the information generated by genomic studies. This work aimed to review the current status of biomarker discovery for melanoma through multi-"omics" platforms. A few sets of novel microRNAs and proteins are described, some of them with important implications in suppressing melanoma at different stages...
November 11, 2017: Journal of Proteomics
https://www.readbyqxmd.com/read/29133484/loss-of-e-cadherin-provides-tolerance-to-centrosome-amplification-in-epithelial-cancer-cells
#2
Alexander D Rhys, Pedro Monteiro, Christopher Smith, Malti Vaghela, Teresa Arnandis, Takuya Kato, Birgit Leitinger, Erik Sahai, Andrew McAinsh, Guillaume Charras, Susana A Godinho
Centrosome amplification is a common feature of human tumors. To survive, cancer cells cluster extra centrosomes during mitosis, avoiding the detrimental effects of multipolar divisions. However, it is unclear whether clustering requires adaptation or is inherent to all cells. Here, we show that cells have varied abilities to cluster extra centrosomes. Epithelial cells are innately inefficient at clustering even in the presence of HSET/KIFC1, which is essential but not sufficient to promote clustering. The presence of E-cadherin decreases cortical contractility during mitosis through a signaling cascade leading to multipolar divisions, and its knockout promotes clustering and survival of cells with multiple centrosomes...
November 13, 2017: Journal of Cell Biology
https://www.readbyqxmd.com/read/29100415/the-e2f-activators-control-multiple-mitotic-regulators-and-maintain-genomic-integrity-through-sgo1-and-bubr1
#3
Miyoung Lee, Yainyrette Rivera-Rivera, Carlos S Moreno, Harold I Saavedra
The E2F1, E2F2, and E2F3a transcriptional activators control proliferation. However, how the E2F activators regulate mitosis to maintain genomic integrity is unclear. Centrosome amplification (CA) and unregulated spindle assembly checkpoint (SAC) are major generators of aneuploidy and chromosome instability (CIN) in cancer. Previously, we showed that overexpression of single E2F activators induced CA and CIN in mammary epithelial cells, and here we show that combined overexpression of E2F activators did not enhance CA...
September 29, 2017: Oncotarget
https://www.readbyqxmd.com/read/28777490/a-novel-genetic-syndrome-with-stard9-mutation-and-abnormal-spindle-morphology
#4
Nobuhiko Okamoto, Yuki Tsuchiya, Fuyuki Miya, Tatsuhiko Tsunoda, Kumiko Yamashita, Keith A Boroevich, Mitsuhiro Kato, Shinji Saitoh, Mami Yamasaki, Yonehiro Kanemura, Kenjiro Kosaki, Daiju Kitagawa
Intellectual disability (ID) is one of neurodevelopmental disorders characterized by serious defects in both intelligence and adaptive behavior. Although it has been suggested that genetic aberrations associated with the process of cell division underlie ID, the cytological evidence for mitotic defects in actual patient's cells is rarely reported. Here, we report a novel mutation in the STARD9 (also known as KIF16A) gene found in a patient with severe ID, characteristic features, epilepsy, acquired microcephaly, and blindness...
August 4, 2017: American Journal of Medical Genetics. Part A
https://www.readbyqxmd.com/read/28763871/-the-function-of-aurora-a-and-its-role-in-the-development-of-liver-cancer
#5
M Li, Z G Ren
Aurora A plays a key role in cellular mitosis. It is located in the centrosome and spindle, and is mainly involved in the processes of centrosome maturation and separation, bipolar spindle assembly, and the regulation of mitotic progression. Recent studies have suggested that Aurora A is involved in tumorigenesis and tumor development through multiple mechanisms. Overexpression of Aurora A could cause abnormal centrosome amplification, aneuploidy formation, and G2/M checkpoint defects, which result in chromosome instability and imbalance between cell division and apoptosis, and eventually leads to abnormal cell proliferation...
June 20, 2017: Zhonghua Gan Zang Bing za Zhi, Zhonghua Ganzangbing Zazhi, Chinese Journal of Hepatology
https://www.readbyqxmd.com/read/28739695/synergistic-effects-of-arsenite-on-radiosensitization-of-glioblastoma-cells
#6
Yasuharu Ninomiya, Dong Yu, Emiko Sekine-Suzuki, Tetsuo Nakajima
BACKGROUND/AIM: Glioblastoma is a frequent type of brain tumor and is radioresistant. Arsenite, which crosses the blood-brain barrier, shows synergistic effects with radiation in vitro and in vivo. The mechanism remains unclear. MATERIALS AND METHODS: As synergistic radiosensitization has been reported in p53-deficient cancer cells, radiosensitization was evaluated using the glioblastoma cell line, U87MG-E6, which harbors inactivated p53, in comparison with the cell line, HCT116 p53 (-/-)...
August 2017: Anticancer Research
https://www.readbyqxmd.com/read/28720575/hsp72-and-nek6-cooperate-to-cluster-amplified-centrosomes-in-cancer-cells
#7
Josephina Sampson, Laura O'Regan, Martin J S Dyer, Richard Bayliss, Andrew M Fry
Cancer cells frequently possess extra amplified centrosomes clustered into two poles whose pseudo-bipolar spindles exhibit reduced fidelity of chromosome segregation and promote genetic instability. Inhibition of centrosome clustering triggers multipolar spindle formation and mitotic catastrophe, offering an attractive therapeutic approach to selectively kill cells with amplified centrosomes. However, mechanisms of centrosome clustering remain poorly understood. Here, we identify a new pathway that acts through NIMA-related kinase 6 (Nek6) and Hsp72 to promote centrosome clustering...
September 15, 2017: Cancer Research
https://www.readbyqxmd.com/read/28600782/dividing-with-extra-centrosomes-a-double-edged-sword-for-cancer-cells
#8
REVIEW
Alexander D Rhys, Susana A Godinho
The presence of supernumerary centrosomes is a hallmark of human tumours. Recent work in animal models suggests that extra centrosomes are not just bystanders in cancer but can accelerate tumourigenesis in the absence of the tumour suppressor p53. Centrosome amplification could indeed actively participate in tumour progression through the induction of chromosome instability, disruption of tissue architecture and promoting cell invasion. Paradoxically, however, centrosome amplification is rather poorly tolerated in normal cells and there are several hurdles cells need to overcome in order to efficiently proliferate in the presence of extra centrosomes...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/28515047/centrosome-amplification-a-suspect-in-breast-cancer-and-racial-disparities
#9
Angela Ogden, Padmashree C G Rida, Ritu Aneja
The multifaceted involvement of centrosome amplification (CA) in tumorigenesis is coming into focus following years of meticulous experimentation, which have elucidated the powerful abilities of CA to promote cellular invasion, disrupt stem cell division, drive chromosomal instability (CIN), and perturb tissue architecture, activities that can accelerate tumor progression. Integration of the extant in vitro, in vivo, and clinical data suggests that in some tissues CA may be a tumor-initiating event, in others a consequential "hit" in multistep tumorigenesis, and in still others non-tumorigenic...
May 17, 2017: Endocrine-related Cancer
https://www.readbyqxmd.com/read/28454331/centrosome-amplification-in-chondrosarcomas-a-primary-cell-culture-and-cryopreserved-tumor-sample-study
#10
Carla Aparecida Pinheiro, Iberê Cauduro Soares, Valter Penna, Jeremy Squire, Rui Manuel Vieira Reis, Sandra Regina Morini da Silva, Isabela de Carvalho, Marjori Leiva Camparoto, Maicon Fernando Zanon da Silva, Adhemar Longatto Longatto Filho
The genetics background underlying the aggressiveness of chondrosarcoma (CS) is poorly understood. One possible cause of malignant transformation is chromosomal instability, which involves an error in mitotic segregation due to numerical and/or functional abnormalities of centrosomes. The present study aimed to evaluate centrosome amplification in cryopreserved samples of tumor tissue from patients with CS. An analysis was performed on 3 primary cultures of tumors from patients who underwent surgery between January 2012 and December 2012 at the Department of Orthopedics at the Barretos Cancer Hospital (Barretos, Brazil)...
March 2017: Oncology Letters
https://www.readbyqxmd.com/read/28415605/kifc1-is-essential-for-acrosome-formation-and-nuclear-shaping-during-spermiogenesis-in-the-lobster-procambarus-clarkii
#11
Dan-Dan Ma, Lian Bi, Wan-Xi Yang
In order to study the function of kinesin-14 motor protein KIFC1 during spermatogenesis of Procambarus clarkii, the full length of kifc1 was cloned from testes cDNA using Rapid-Amplification of cDNA Ends (RACE). The deduced KIFC1 protein sequence showed the highest similarity between Procambarus clarkii and Eriocheir senensis (similarity rate as 64%). According to the results of in situ hybridization (ISH), the kifc1 mRNA was gathered in the acrosome location above nucleus in the mid- and late-stage spermatids...
May 30, 2017: Oncotarget
https://www.readbyqxmd.com/read/28402684/a-nonsense-alms1-mutation-underlies-alstr%C3%A3-m-syndrome-in-an-extended-mennonite-kindred-settled-in-north-mexico
#12
Marisa Cruz-Aguilar, Carlos Galaviz-Hernández, José Hiebert-Froese, Martha Sosa-Macías, Juan Carlos Zenteno
AIM: Alström syndrome (AS) is a rare autosomal recessive multisystem disease caused by biallelic mutations in ALMS1, a gene encoding a widely expressed centrosomal/basal body protein. Although more than 200 pathogenic mutations in ALMS1 have been identified to date in AS patients from various ethnic populations, there are very few reports of ALMS1 founder mutations in isolated populations. Our aim was to describe the molecular characterization of a cohort of AS patients from an extended inbred Mennonite kindred settled in Mexico...
June 2017: Genetic Testing and Molecular Biomarkers
https://www.readbyqxmd.com/read/28385950/the-daughter-centriole-controls-ciliogenesis-by-regulating-neurl-4-localization-at-the-centrosome
#13
Abdelhalim Loukil, Kati Tormanen, Christine Sütterlin
The two centrioles of the centrosome differ in age and function. Although the mother centriole mediates most centrosome-dependent processes, the role of the daughter remains poorly understood. A recent study has implicated the daughter centriole in centriole amplification in multiciliated cells, but its contribution to primary ciliogenesis is unclear. We found that manipulations that prevent daughter centriole formation or induce its separation from the mother abolish ciliogenesis. This defect was caused by stabilization of the negative ciliogenesis regulator CP110 and was corrected by CP110 depletion...
May 1, 2017: Journal of Cell Biology
https://www.readbyqxmd.com/read/28361952/usp9x-regulates-centrosome-duplication-and-promotes-breast-carcinogenesis
#14
Xin Li, Nan Song, Ling Liu, Xinhua Liu, Xiang Ding, Xin Song, Shangda Yang, Lin Shan, Xing Zhou, Dongxue Su, Yue Wang, Qi Zhang, Cheng Cao, Shuai Ma, Na Yu, Fuquan Yang, Yan Wang, Zhi Yao, Yongfeng Shang, Lei Shi
Defective centrosome duplication is implicated in microcephaly and primordial dwarfism as well as various ciliopathies and cancers. Yet, how the centrosome biogenesis is regulated remains poorly understood. Here we report that the X-linked deubiquitinase USP9X is physically associated with centriolar satellite protein CEP131, thereby stabilizing CEP131 through its deubiquitinase activity. We demonstrate that USP9X is an integral component of centrosome and is required for centrosome biogenesis. Loss-of-function of USP9X impairs centrosome duplication and gain-of-function of USP9X promotes centrosome amplification and chromosome instability...
March 31, 2017: Nature Communications
https://www.readbyqxmd.com/read/28325915/prognostic-value-of-ca20-a-score-based-on-centrosome-amplification-associated-genes-in-breast-tumors
#15
Angela Ogden, Padmashree C G Rida, Ritu Aneja
Centrosome amplification (CA) is a hallmark of cancer, observable in ≥75% of breast tumors. CA drives aggressive cellular phenotypes such as chromosomal instability (CIN) and invasiveness. Thus, assessment of CA may offer insights into the prognosis of breast cancer and identify patients who might benefit from centrosome declustering agents. However, it remains unclear whether CA is correlated with clinical outcomes after adjusting for confounding factors. To gain insights, we developed a signature, "CA20", comprising centrosome structural genes and genes whose dysregulation is implicated in inducing CA...
March 21, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28284839/depletion-of-tumor-suppressor-kank1-induces-centrosomal-amplification-via-hyperactivation-of-rhoa
#16
Jun-Ichiro Suzuki, Badal Chandra Roy, Takunori Ogaeri, Naoto Kakinuma, Ryoiti Kiyama
Chromosome instability, frequently found in cancer cells, is caused by a deficiency in cell division, including centrosomal amplification and cytokinesis failure, and can result in abnormal chromosome content or aneuploidy. The small GTPase pathways have been implicated as important processes in cell division. We found that knockdown of a tumor suppressor protein Kank1 increases the number of cells with a micronucleus or bi-/multi-nuclei, which was likely caused by centrosomal amplification. Kank1 interacts with Daam1, known to bind to and activate a small GTPase, RhoA, in actin assembly...
April 15, 2017: Experimental Cell Research
https://www.readbyqxmd.com/read/28277612/wdr62-overexpression-is-associated-with-a-poor-prognosis-in-patients-with-lung-adenocarcinoma
#17
Kazuya Shinmura, Hisami Kato, Yuichi Kawanishi, Hisaki Igarashi, Yusuke Inoue, Katsuhiro Yoshimura, Satoki Nakamura, Hidehiko Fujita, Kazuhito Funai, Masayuki Tanahashi, Hiroshi Niwa, Hiroshi Ogawa, Haruhiko Sugimura
Human WDR62, which is localized in the cytoplasm including the centrosome, is known to be responsible for primary microcephaly; however, the role of WDR62 abnormality in cancers remains largely unknown. In this study, we aimed to reveal the pathological role of WDR62 abnormality in lung adenocarcinoma (LAC). We first examined the WDR62 mRNA expression level of LAC (n = 64) using a QRT-PCR analysis and found that WDR62 mRNA transcripts were significantly overexpressed in LAC (P = 0.0432, Wilcoxon matched pairs test)...
August 2017: Molecular Carcinogenesis
https://www.readbyqxmd.com/read/28186092/epstein-barr-virus-particles-induce-centrosome-amplification-and-chromosomal-instability
#18
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
#19
COMMENT
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
#20
(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
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