Base de dados : MEDLINE
Pesquisa : G04.165.750 [Categoria DeCS]
Referências encontradas : 44 [refinar]
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[PMID]:29198709
[Au] Autor:Ruan B; Zhang B; Chen A; Yuan L; Liang J; Wang M; Zhang Z; Fan J; Yu X; Zhang X; Niu Z; Zheng Y; Gu S; Liu X; Du H; Wang J; Hu X; Gao L; Chen Z; Huang H; Wang X; Sun Q
[Ad] Endereço:School of Biology and Biological Engineering, South China University of Technology, Guangzhou 510000, PR China; Laboratory of Cell Engineering, Institute of Biotechnology, 20 Dongda Street, Beijing 100071, PR China.
[Ti] Título:Cholesterol inhibits entotic cell-in-cell formation and actomyosin contraction.
[So] Source:Biochem Biophys Res Commun;495(1):1440-1446, 2018 01 01.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cell-in-cell structure is prevalent in human cancer, and associated with several specific pathophysiological phenomena. Although cell membrane adhesion molecules were found critical for cell-in-cell formation, the roles of other membrane components, such as lipids, remain to be explored. In this study, we attempted to investigate the effects of cholesterol and phospholipids on the formation of cell-in-cell structures by utilizing liposome as a vector. We found that Lipofectamine-2000, the reagent commonly used for routine transfection, could significantly reduce entotic cell-in-cell formation in a cell-specific manner, which is correlated with suppressed actomyosin contraction as indicated by reduced ß-actin expression and myosin light chain phosphorylation. The influence on cell-in-cell formation was likely dictated by specific liposome components as some liposomes affected cell-in-cell formation while some others didn't. Screening on a limited number of lipids, the major components of liposome, identified phosphatidylethanolamine (PE), stearamide (SA), lysophosphatidic acid (LPA) and cholesterol (CHOL) as the inhibitors of cell-in-cell formation. Importantly, cholesterol treatment significantly inhibited myosin light chain phosphorylation, which resembles the effect of Lipofectamine-2000, suggesting cholesterol might be partially responsible for liposomes' effects on cell-in-cell formation. Together, our findings supporting a role of membrane lipids and cholesterol in cell-in-cell formation probably via regulating actomyosin contraction.
[Mh] Termos MeSH primário: Actomiosina/metabolismo
Membrana Celular/metabolismo
Colesterol/administração & dosagem
Entose/fisiologia
Lipídeos/administração & dosagem
Lipídeos de Membrana/metabolismo
[Mh] Termos MeSH secundário: Actomiosina/efeitos dos fármacos
Entose/efeitos dos fármacos
Seres Humanos
Células MCF-7
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Lipids); 0 (Lipofectamine); 0 (Membrane Lipids); 9013-26-7 (Actomyosin); 97C5T2UQ7J (Cholesterol)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180105
[Lr] Data última revisão:
180105
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171205
[St] Status:MEDLINE


  2 / 44 MEDLINE  
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[PMID]:28774893
[Au] Autor:Hinojosa LS; Holst M; Baarlink C; Grosse R
[Ad] Endereço:Institute of Pharmacology, Biochemisch-Pharmakologisches Centrum Marburg, University of Marburg, Marburg, Germany.
[Ti] Título:MRTF transcription and Ezrin-dependent plasma membrane blebbing are required for entotic invasion.
[So] Source:J Cell Biol;216(10):3087-3095, 2017 Oct 02.
[Is] ISSN:1540-8140
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Entosis is a nonapoptotic form of cell death initiated by actomyosin-dependent homotypic cell-in-cell invasion that can be observed in malignant exudates during tumor progression. We previously demonstrated formin-mediated actin dynamics at the rear of the invading cell as well as nonapoptotic plasma membrane (PM) blebbing in this cellular motile process. Although the contractile actin cortex involved in bleb-driven motility is well characterized, a role for transcriptional regulation in this process has not been studied. Here, we explore the impact of the actin-controlled MRTF-SRF (myocardin-related transcription factor-serum response factor) pathway for sustained PM blebbing and entotic invasion. We find that cortical blebbing is tightly coupled to MRTF nuclear shuttling to promote the SRF transcriptional activity required for entosis. Furthermore, PM blebbing triggered SRF-mediated up-regulation of the metastasis-associated ERM protein Ezrin. Notably, Ezrin is sufficient and important to sustain bleb dynamics for cell-in-cell invasion when SRF is suppressed. Our results highlight the critical role of the actin-regulated MRTF transcriptional pathway for bleb-associated invasive motility, such as during entosis.
[Mh] Termos MeSH primário: Estruturas da Membrana Celular/metabolismo
Proteínas do Citoesqueleto/biossíntese
Entose/fisiologia
Transativadores/metabolismo
Transcrição Genética/fisiologia
Regulação para Cima/fisiologia
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Estruturas da Membrana Celular/genética
Proteínas do Citoesqueleto/genética
Seres Humanos
Fator de Resposta Sérica/genética
Fator de Resposta Sérica/metabolismo
Transativadores/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytoskeletal Proteins); 0 (MKL1 protein, human); 0 (SRF protein, human); 0 (Serum Response Factor); 0 (Trans-Activators); 0 (ezrin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171006
[Lr] Data última revisão:
171006
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170805
[St] Status:MEDLINE
[do] DOI:10.1083/jcb.201702010


  3 / 44 MEDLINE  
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[PMID]:27445312
[Au] Autor:Russell MR; Lerner TR; Burden JJ; Nkwe DO; Pelchen-Matthews A; Domart MC; Durgan J; Weston A; Jones ML; Peddie CJ; Carzaniga R; Florey O; Marsh M; Gutierrez MG; Collinson LM
[Ad] Endereço:Electron Microscopy Science Technology Platform, The Francis Crick Institute, 1 Midland Road, London NW1 1AT, UK.
[Ti] Título:3D correlative light and electron microscopy of cultured cells using serial blockface scanning electron microscopy.
[So] Source:J Cell Sci;130(1):278-291, 2017 Jan 01.
[Is] ISSN:1477-9137
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The processes of life take place in multiple dimensions, but imaging these processes in even three dimensions is challenging. Here, we describe a workflow for 3D correlative light and electron microscopy (CLEM) of cell monolayers using fluorescence microscopy to identify and follow biological events, combined with serial blockface scanning electron microscopy to analyse the underlying ultrastructure. The workflow encompasses all steps from cell culture to sample processing, imaging strategy, and 3D image processing and analysis. We demonstrate successful application of the workflow to three studies, each aiming to better understand complex and dynamic biological processes, including bacterial and viral infections of cultured cells and formation of entotic cell-in-cell structures commonly observed in tumours. Our workflow revealed new insight into the replicative niche of Mycobacterium tuberculosis in primary human lymphatic endothelial cells, HIV-1 in human monocyte-derived macrophages, and the composition of the entotic vacuole. The broad application of this 3D CLEM technique will make it a useful addition to the correlative imaging toolbox for biomedical research.
[Mh] Termos MeSH primário: Células Endoteliais/ultraestrutura
Imagem Tridimensional
Macrófagos/ultraestrutura
Microscopia Eletrônica de Varredura/métodos
[Mh] Termos MeSH secundário: Sobrevivência Celular
Células Cultivadas
Células Endoteliais/microbiologia
Entose
HIV/ultraestrutura
Seres Humanos
Espaço Intracelular/microbiologia
Macrófagos/virologia
Monócitos/citologia
Mycobacterium tuberculosis/crescimento & desenvolvimento
Mycobacterium tuberculosis/ultraestrutura
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160723
[St] Status:MEDLINE
[do] DOI:10.1242/jcs.188433


  4 / 44 MEDLINE  
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[PMID]:27163289
[Au] Autor:Gilloteaux J; Ruffo C; Jamison JM; Summers JL
[Ad] Endereço:a Department of Anatomical Sciences , St. George's University International School of Medicine, K. B. Taylor Global Scholar's Program at Northumbria University , Newcastle upon Tyne , UK.
[Ti] Título:Modes of internalizations of human prostate carcinoma (DU145) cells in vitro and in murine xenotransplants.
[So] Source:Ultrastruct Pathol;40(5):231-9, 2016 Sep-Oct.
[Is] ISSN:1521-0758
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Ultrastructural data compiled from DU145 human prostate carcinoma cells growing in vivo and, more often in vitro or after treatment by pro-oxidant reactants, can induce and encompass several processes of cell internalization or entosis. These events were observed after tumor cells were essentially undergoing autoschizic injuries and other cell deaths without externalization of phosphatidylserine. Based on other previous observations made on DU145 cells, one hypothesizes that, as a means of survival, tumor cells find sources of nutrients through phagocytosis of apparently intact, injured cells, corpses, and cell debris by cannibalism. These peculiar activities occurred sporadically, in a small population of cells and could be dictated by their widely adapted energetic metabolism, now impaired, either due to the location of the cells in the growing tumors or in vitro as a result of this pro-oxidant anticancer treatment causing damage and abolishing their adapted metabolism.
[Mh] Termos MeSH primário: Entose/fisiologia
Neoplasias da Próstata/patologia
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Xenoenxertos
Seres Humanos
Masculino
Camundongos
Microscopia Eletrônica de Transmissão
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170330
[Lr] Data última revisão:
170330
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160511
[St] Status:MEDLINE
[do] DOI:10.1080/01913123.2016.1174908


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[PMID]:27048820
[Au] Autor:Krishna S; Overholtzer M
[Ad] Endereço:Cell Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY, 10065, USA.
[Ti] Título:Mechanisms and consequences of entosis.
[So] Source:Cell Mol Life Sci;73(11-12):2379-86, 2016 06.
[Is] ISSN:1420-9071
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Multiple mechanisms have emerged where the engulfment of whole live cells, leading to the formation of what are called 'cell-in-cell' structures, induces cell death. Entosis is one such mechanism that drives cell-in-cell formation during carcinogenesis and development. Curiously, entotic cells participate actively in their own engulfment, by invading into their hosts, and are then killed non-cell-autonomously. Here we review the mechanisms of entosis and entotic cell death and the consequences of entosis on cell populations.
[Mh] Termos MeSH primário: Apoptose/fisiologia
Carcinogênese/patologia
Entose/fisiologia
Fagocitose/fisiologia
[Mh] Termos MeSH secundário: Autofagia/fisiologia
Seres Humanos
Neoplasias/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; REVIEW
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170912
[Lr] Data última revisão:
170912
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160407
[St] Status:MEDLINE
[do] DOI:10.1007/s00018-016-2207-0


  6 / 44 MEDLINE  
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[PMID]:26671576
[Au] Autor:Balvan J; Gumulec J; Raudenska M; Krizova A; Stepka P; Babula P; Kizek R; Adam V; Masarik M
[Ad] Endereço:Department of Pathological Physiology, Faculty of Medicine, Masaryk University / Kamenice 5, CZ-625 00, Brno, Czech Republic.
[Ti] Título:Oxidative Stress Resistance in Metastatic Prostate Cancer: Renewal by Self-Eating.
[So] Source:PLoS One;10(12):e0145016, 2015.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Resistant cancer phenotype is a key obstacle in the successful therapy of prostate cancer. The primary aim of our study was to explore resistance mechanisms in the advanced type of prostate cancer cells (PC-3) and to clarify the role of autophagy in these processes. We performed time-lapse experiment (48 hours) with ROS generating plumbagin by using multimodal holographic microscope. Furthermore, we also performed the flow-cytometric analysis and the qRT-PCR gene expression analysis at 12 selected time points. TEM and confocal microscopy were used to verify the results. We found out that autophagy (namely mitophagy) is an important resistance mechanism. The major ROS producing mitochondria were coated by an autophagic membrane derived from endoplasmic reticulum and degraded. According to our results, increasing ROS resistance may be also accompanied by increased average cell size and polyploidization, which seems to be key resistance mechanism when connected with an escape from senescence. Many different types of cell-cell interactions were recorded including entosis, vesicular transfer, eating of dead or dying cells, and engulfment and cannibalism of living cells. Entosis was disclosed as a possible mechanism of polyploidization and enabled the long-term survival of cancer cells. Significantly reduced cell motility was found after the plumbagin treatment. We also found an extensive induction of pluripotency genes expression (NANOG, SOX2, and POU5F1) at the time-point of 20 hours. We suppose, that overexpression of pluripotency genes in the portion of prostate tumour cell population exposed to ROS leads to higher developmental plasticity and capability to faster respond to changes in the extracellular environment that could ultimately lead to an alteration of cell fate.
[Mh] Termos MeSH primário: Autorrenovação Celular
Estresse Oxidativo
Neoplasias da Próstata/patologia
[Mh] Termos MeSH secundário: Autofagia/efeitos dos fármacos
Comunicação Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Autorrenovação Celular/efeitos dos fármacos
Tamanho Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Retículo Endoplasmático/efeitos dos fármacos
Retículo Endoplasmático/metabolismo
Entose/efeitos dos fármacos
Citometria de Fluxo
Perfilação da Expressão Gênica
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Concentração Inibidora 50
Masculino
Degradação Mitocondrial/efeitos dos fármacos
Naftoquinonas/farmacologia
Metástase Neoplásica
Estresse Oxidativo/efeitos dos fármacos
Análise de Componente Principal
Neoplasias da Próstata/genética
Espécies Reativas de Oxigênio/metabolismo
Imagem com Lapso de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Naphthoquinones); 0 (Reactive Oxygen Species); YAS4TBQ4OQ (plumbagin)
[Em] Mês de entrada:1606
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151217
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0145016


  7 / 44 MEDLINE  
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[PMID]:26615438
[Au] Autor:Garanina AS; Khashba LA; Onishchenko GE
[Ad] Endereço:Lomonosov Moscow State University, Biological Faculty, Moscow, 119991, Russia. anastasiacit@gmail.com.
[Ti] Título:Stages of Cell Cannibalism--Entosis--in Normal Human Keratinocyte Culture.
[So] Source:Biochemistry (Mosc);80(11):1469-77, 2015 Nov.
[Is] ISSN:1608-3040
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Entosis is a type of cell cannibalism during which one cell penetrates into another cell and usually dies inside it. Researchers mainly pay attention to initial and final stages of entosis. Besides, tumor cells in suspension are the primary object of studies. In the present study, we investigated morphological changes of both cells-participants of entosis during this process. The substrate-dependent culture of human normal keratinocytes HaCaT was chosen for the work. A combination of light microscopy and scanning electron microscopy was used to prove that one cell was completely surrounded by the plasma membrane of another cell. We investigated such "cell-in-cell" structures and described the structural and functional changes of both cells during entosis. The outer cell nucleus localization and shape were changed. Gradual degradation of the inner cell nucleus and of the junctions between the inner and the outer cells was revealed. Moreover, repeated redistribution of the outer cell membrane organelles (Golgi apparatus, lysosomes, mitochondria, and autophagosomes), rearrangement of its cytoskeleton, and change in the lysosomal, autophagosomal, and mitochondrial state in both entotic cells were observed during entosis. On the basis of these data, we divided entosis into five stages that make it possible to systematize description of this type of cell death.
[Mh] Termos MeSH primário: Entose/fisiologia
Queratinócitos/citologia
[Mh] Termos MeSH secundário: Autofagia
Linhagem Celular
Núcleo Celular/metabolismo
Citoesqueleto/metabolismo
Complexo de Golgi/metabolismo
Seres Humanos
Queratinócitos/metabolismo
Lisossomos/metabolismo
Microscopia Eletrônica de Varredura
Microtúbulos/metabolismo
Mitocôndrias/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Mês de entrada:1609
[Cu] Atualização por classe:151130
[Lr] Data última revisão:
151130
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151130
[St] Status:MEDLINE
[do] DOI:10.1134/S0006297915110085


  8 / 44 MEDLINE  
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[PMID]:26511711
[Au] Autor:Florey O; Kim SE; Overholtzer M
[Ti] Título:Entosis: Cell-in-Cell Formation that Kills Through Entotic Cell Death.
[So] Source:Curr Mol Med;15(9):861-6, 2015.
[Is] ISSN:1875-5666
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Entosis is a cell-in-cell formation mechanism that targets viable cells for uptake in epithelial cell cultures and human tumors. Entotic cells control their own engulfment, by invading into their hosts in a Rho-GTPase and actomyosin-dependent manner. Although entotic cells are internalized while alive, most eventually undergo a non-apoptotic form of cell death, called entotic cell death, that is executed non-cell-autonomously by autophagy proteins and lysosomes. Here we review the current understanding of entosis and entotic cell death and discuss the potential roles of this process in cancer.
[Mh] Termos MeSH primário: Morte Celular/fisiologia
Entose/fisiologia
[Mh] Termos MeSH secundário: Animais
Apoptose
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; REVIEW
[Em] Mês de entrada:1610
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151030
[St] Status:MEDLINE


  9 / 44 MEDLINE  
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[PMID]:26511710
[Au] Autor:Wang Y; Wang XD
[Ti] Título:Entosis and Related Forms of Cell Death within Cells.
[So] Source:Curr Mol Med;15(9):805-9, 2015.
[Is] ISSN:1875-5666
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:By eliminating the unneeded or mutant cells, programmed cell death actively participates in a wide range of biological processes from embryonic development to homeostasis maintenance in adult. Continuing efforts have identified multiple cell death pathways, with apoptosis, necrosis and autophage the mostly studied. Recently a unique cell death pathway called "cell-in-cell death" has been defined. Unlike traditional cell death pathways, cell-in-cell death, characterized by cell death within another cell, is triggered by the invasion of one cell into its neighbor and executed by either lysosome-dependent degradation or caspase-dependent apoptosis. With remarkable progresses on cell-in-cell over past few years, multiple mechanisms, including entosis, cannibalism and emperitosis, are found to be responsible for cell-in-cell death. Some key questions, such as specific biochemical markers to distinguish precisely the properties of different cell-in-cell structures and the physiological and pathological relevance, remain to be addressed. In light of this situation and a surge of interests, leading scientists in this field intend to share with readers current research progresses on cell-in-cell structures from different model systems through this special edition on cell-in-cell. The mechanistic advances will be highlighted while the future researches be speculated.
[Mh] Termos MeSH primário: Entose/fisiologia
[Mh] Termos MeSH secundário: Animais
Apoptose/fisiologia
Autofagia/fisiologia
Morte Celular
Emperipolese/fisiologia
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Em] Mês de entrada:1610
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151030
[St] Status:MEDLINE


  10 / 44 MEDLINE  
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[PMID]:26511709
[Au] Autor:Lozupone F; Fais S
[Ti] Título:Cancer Cell Cannibalism: A Primeval Option to Survive.
[So] Source:Curr Mol Med;15(9):836-41, 2015.
[Is] ISSN:1875-5666
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Cancer cell cannibalism is currently defined as a phenomenon in which an ensemble of a larger cell containing a smaller one, often in a big cytoplasmic vacuole, is detected in either cultured tumor cells or a tumor sample. After almost one century of considering this phenomenon as a sort of neglected curiosity, some recent studies have first proposed tumor cell cannibalism as a sort of "aberrant phagocytosis", making malignant cells very similar to professional phagocytes. Later, further research has shown that, differently to macrophages, exclusively ingesting exogenous material, apoptotic bodies, or cell debris, tumor cells are able to engulf other cells, including lymphocytes and erythrocytes, either dead or alive, with the main purpose to feed on them. This phenomenon has been associated to the malignancy of tumors, mostly exclusive of metastatic cells, and often associated to poor prognosis. The cannibalistic behavior increased depending on the microenvironmental condition of tumor cells, such as low nutrient supply or low pH, suggesting its key survival option for malignant cancers. However, the evidence that malignant cells may cannibalize tumor-infiltrating lymphocytes that act as their killers, suggests that tumor cell cannibalism could be a very direct and efficient way to neutralize immune response, as well. Tumor cell cannibalism may represent a sign of regression to a simpler, ancestral or primeval life style, similar to that of unicellular microorganisms, such as amoebas, where the goal is to survive and propagate in an overcrowded and very hostile microenvironment. In fact, we discovered that metastatic melanoma cells share with amoebas a transmembrane protein TM9SF4, indeed related to the cannibal behavior of these cells. This review attempts to provide a comprehensive description of the current knowledge about the role of TM9SF4 in cancer, highlighting its role as a key player in the cannibal behavior of malignant cancer cells. Moreover, we discuss differences and similarities between tumor cannibalism, entosis, phagocytosis and emperipolesis.
[Mh] Termos MeSH primário: Citofagocitose
Neoplasias/patologia
[Mh] Termos MeSH secundário: Amoeba/metabolismo
Animais
Sobrevivência Celular
Emperipolese
Entose
Seres Humanos
Proteínas de Membrana/metabolismo
Neoplasias/imunologia
Neoplasias/metabolismo
Fagocitose
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (Membrane Proteins); 0 (TM9SF4 protein, human)
[Em] Mês de entrada:1610
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151030
[St] Status:MEDLINE



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