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  • Cell Research
    Online Publication Current Issue Top 10 VOLUME 24 ISSUE 11 11 2014 1280 1281 Entosis a key player in cancer cell competition FREE Guido Kroemer 1 2 3 4 and Jean Luc Perfettini 5 6 7 8 1 Equipe 11 labellisée par la Ligue Nationale contre le Cancer Centre de Recherche des Cordeliers INSERM U1138 F 75006 Paris France 2 Université Paris Descartes Sorbonne Paris Cité F 75005 Paris France 3 Metabolomics and Cell Biology Platforms Gustave Roussy F 94805 Villejuif France 4 Pôle de Biologie Hôpital Européen Georges Pompidou AP HP F 75015 Paris France 5 Cell death and Aging team Gustave Roussy F 94805 Villejuif France 6 Laboratory of Molecular Radiotherapy INSERM U1030 Gustave Roussy F 94805 Villejuif France 7 Gustave Roussy F 94805 Villejuif France 8 Université Paris Sud Paris 11 F 94805 Villejuif France Correspondence Guido Kroemer E mail kroemer orange fr Cell in cell structures also referred to as entosis are frequently found in human malignancies although their prognostic impact remains to be defined Two articles recently published in Cell Research report the stimulation of entosis by one prominent oncogene Kras as well as by one class of tumor suppressors namely epithelial cadherins E and

    Original URL path: http://www.cell-research.com/arts.asp?id=2009 (2016-02-14)
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  • Cell Research
    Per Johnsson 1 and Kevin V Morris 2 3 1 Department of Oncology and Pathology Karolinska Institutet SE 171 77 Stockholm Sweden 2 Biotechnology and Biomedical Sciences The University of New South Wales NSW 2052 Sydney Australia 3 Department of Molecular and Experimental Medicine The Scripps Research Institute La Jolla CA 92037 USA Correspondence Kevin V Morris E mail kmorris unsw edu au New findings bring to light a previously

    Original URL path: http://www.cell-research.com/arts.asp?id=2011 (2016-02-14)
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  • Cell Research
    2014 1286 1287 Detecting different Pyrin senses modified GTPases FREE Marcel R de Zoete 1 2 and Richard A Flavell 1 2 1 Department of Immunobiology Yale University School of Medicine New Haven CT 06520 USA 2 Howard Hughes Medical Institute Yale University New Haven CT 06520 USA Correspondence Richard A Flavell E mail richard flavell yale edu Pathogenic bacteria secrete effector proteins that target host cell Rho GTPases to

    Original URL path: http://www.cell-research.com/arts.asp?id=2012 (2016-02-14)
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  • Cell Research
    Brigham and Women s Hospital and Harvard Medical School Boston MA 02115 USA 4 Department of Oncology Beijing Shijitan Hospital of Capital Medical University 10 TIEYI Road Beijing 100038 China 5 Department of Anatomy and Structural Biology and Gruss Lipper Biophotonics Center Albert Einstein College of Medicine of Yeshiva University Bronx NY USA 6 BCMB Allied Program Weill Cornell Medical College 1300 York Avenue New York NY 10065 USA Correspondence Michael Overholtzer Tel 1 212 639 6536 Fax 1 212 794 4342 E mail overhom1 mskcc org Qiang Sun Tel 86 10 66948820 E mail sunqiang1975 126 com Cell engulfment typically targets dead or dying cells for clearance from metazoan tissues However recent evidence demonstrates that live cells can also be targeted and that engulfment can cause cell death Entosis is one mechanism proposed to mediate the engulfment and killing of live tumor cells by their neighbors an activity often referred to as cell cannibalism Here we report that the expression of exogenous epithelial cadherin proteins E or P cadherin in human breast tumor cells lacking endogenous expression of epithelial cadherins induces entosis and inhibits transformed growth Entosis induced by cadherin expression is associated with the polarized distribution of Rho

    Original URL path: http://www.cell-research.com/arts.asp?id=2019 (2016-02-14)
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  • Cell Research
    Johns Hopkins University School of Medicine Baltimore MD 21205 USA 4 Signalling Programme The Babraham Institute Cambridge CB22 3AT UK 5 Department of Cell Biology School of Medicine Fukuoka University Fukuoka 814 0180 Japan 6 Department of Pathology Research Institute International Medical Center of Japan Tokyo 163 8655 Japan 7 BCMB Allied Program Weill Cornell Medical College 1300 York Avenue New York NY 10065 USA Correspondence Michael Overholtzer Tel 1 212 639 6536 Fax 1 212 794 4342 E mail overhom1 mskcc org Qiang Sun Tel 86 10 66948820 E mail sunqiang1975 126 com Human carcinomas are comprised of complex mixtures of tumor cells that are known to compete indirectly for nutrients and growth factors Whether tumor cells could also compete directly for example by elimination of rivals is not known Here we show that human cells can directly compete by a mechanism of engulfment called entosis By entosis cells are engulfed or cannibalized while alive and subsequently undergo cell death We find that the identity of engulfing winner and engulfed loser cells is dictated by mechanical deformability controlled by RhoA and actomyosin where tumor cells with high deformability preferentially engulf and outcompete neighboring cells with low deformability in heterogeneous

    Original URL path: http://www.cell-research.com/arts.asp?id=2020 (2016-02-14)
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  • Cell Research
    2 Ge Gao 2 Zhichao Zhang 3 Xiaoling Yang 3 Xiru Wu 3 Yuehua Zhang 3 and Liping Wei 1 2 1 National Institute of Biological Sciences Beijing 102206 China 2 Center for Bioinformatics State Key Laboratory of Protein and Plant Gene Research School of Life Sciences Peking University Beijing 100871 China 3 Peking University First Hospital Peking University Beijing 100034 China 4 Peking Tsinghua Center for Life Sciences Beijing 100871 China 5 Academy for Advanced Interdisciplinary Studies Peking University Beijing 100871 China 6 Graduate School of Peking Union Medical College Beijing 100730 China Correspondence Liping Wei E mail weilp mail cbi pku edu cn Yuehua Zhang E mail zhangyhd hotmail com Postzygotic single nucleotide mutations pSNMs have been studied in cancer and a few other overgrowth human disorders at whole genome scale and found to play critical roles However in clinically unremarkable individuals pSNMs have never been identified at whole genome scale largely due to technical difficulties and lack of matched control tissue samples and thus the genome wide characteristics of pSNMs remain unknown We developed a new Bayesian based mosaic genotyper and a series of effective error filters using which we were able to identify 17 SNM sites from 80 whole genome sequencing of peripheral blood DNAs from three clinically unremarkable adults The pSNMs were thoroughly validated using pyrosequencing Sanger sequencing of individual cloned fragments and multiplex ligation dependent probe amplification The mutant allele fraction ranged from 5 31 We found that Cright arrowT and Cright arrowA were the predominant types of postzygotic mutations similar to the somatic mutation profile in tumor tissues Simulation data showed that the overall mutation rate was an order of magnitude lower than that in cancer We detected varied allele fractions of the pSNMs among multiple samples obtained from the same individuals including

    Original URL path: http://www.cell-research.com/arts.asp?id=2013 (2016-02-14)
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  • Cell Research
    organs by deubiquitinating Cep70 and inactivating HDAC6 Yunfan Yang Jie Ran Min Liu Dengwen Li Yuanyuan Li Xingjuan Shi Dan Meng Junmin Pan Guangshuo Ou Ritu Aneja Shao Cong Sun and Jun Zhou Cilia are hair like organelles extending from the cell surface with important sensory and motility functions Ciliary defects can result in a wide range of human diseases known as ciliopathies However the molecular mechanisms controlling ciliogenesis remain poorly defined Here we show that cylindromatosis CYLD a tumor suppressor protein harboring deubiquitinase activity plays a critical role in the assembly of both primary and motile cilia in multiple organs CYLD knockout mice exhibit polydactyly and various ciliary defects such as failure in basal body anchorage and disorganization of basal bodies and axenomes The ciliary function of CYLD is partially attributed to its deconjugation of the polyubiquitin chain from centrosomal protein of 70 kDa Cep70 a requirement for Cep70 to interact with γ tubulin and localize at the centrosome In addition CYLD mediated inhibition of histone deacetylase 6 HDAC6 which promotes tubulin acetylation constitutes another mechanism for the ciliary function of CYLD Small molecule inhibitors of HDAC6 could partially rescue the ciliary defects in CYLD knockout mice These findings

    Original URL path: http://www.cell-research.com/arts.asp?id=2021 (2016-02-14)
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  • Cell Research
    Hsieh 1 3 4 1 Human Oncology Pathogenesis Program Memorial Sloan Kettering Cancer Center New York NY 10065 USA 2 Department of Pathology Memorial Sloan Kettering Cancer Center New York NY 10065 USA 3 Department of Medicine Memorial Sloan Kettering Cancer Center New York NY 10065 USA 4 Department of Medicine Weill Cornell Medical College New York NY 10021 USA 5 Department of Internal Medicine Washington University St Louis MO 63110 USA Correspondence James J Hsieh E mail hsiehj mskcc org Taspase1 a highly conserved threonine protease cleaves nuclear transcriptional regulators mixed lineage leukemia MLL MLL1 MLL2 TFIIA and ALF to orchestrate a wide variety of biological processes In vitro studies thus far demonstrated that Taspase1 plays important roles in the proliferation of various cancer cell lines including HER2 positive breast cancer cells To investigate the role of Taspase1 in breast tumorigenesis in vivo we deleted Taspase1 from mouse mammary glands by generating MMTV neu MMTV cre Tasp1F mice We demonstrate that initiation of MMTV neu but not MMTV wnt driven breast cancer is blocked in the absence of Taspase1 Importantly Taspase1 loss alone neither impacts normal development nor pregnancy physiology of the mammary gland In mammary glands Taspase1 deficiency abrogates MMTV neu induced cyclins E and A expression thereby preventing tumorigenesis The mechanisms were explored in HER2 positive breast cancer cell line BT474 and HER2 transformed MCF10A cells and validated using knockdown resistant Taspase1 As Taspase1 was shown to cleave MLL which forms complexes with E2F transcription factors to regulate Cyclins E A and B expression in mouse embryonic fibroblasts MEFs we investigated whether the cleavage of MLL by Taspase1 constitutes an essential in vivo axis for HER2 neu induced mammary tumorigenesis To this end we generated MMTV neu MLLnc nc transgenic mice that carry homozygous non cleavable MLL

    Original URL path: http://www.cell-research.com/arts.asp?id=2015 (2016-02-14)
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