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Pesquisa : D12.776.157.530.200.374.750.500 [Categoria DeCS]
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[PMID]:28784848
[Au] Autor:Jensen H; Potempa M; Gotthardt D; Lanier LL
[Ad] Endereço:Department of Microbiology and Immunology, University of California, San Francisco, San Francisco, CA 94143; and.
[Ti] Título:Cutting Edge: IL-2-Induced Expression of the Amino Acid Transporters SLC1A5 and CD98 Is a Prerequisite for NKG2D-Mediated Activation of Human NK Cells.
[So] Source:J Immunol;199(6):1967-1972, 2017 Sep 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Priming of human NK cells with IL-2 is necessary to render them functionally competent upon NKG2D engagement. We examined the underlying mechanisms that control NKG2D responsiveness in NK cells and found that IL-2 upregulates expression of the amino acid transporters SLC1A5 and CD98. Using specific inhibitors to block SLC1A5 and CD98 function, we found that production of IFN-γ and degranulation by CD56 and CD56 NK cells following NKG2D stimulation were dependent on both transporters. IL-2 priming increased the activity of mTORC1, and inhibition of mTORC1 abrogated the ability of the IL-2-primed NK cells to produce IFN-γ in response to NKG2D-mediated stimulation. This study identifies a series of IL-2-induced cellular changes that regulates the NKG2D responsiveness in human NK cells.
[Mh] Termos MeSH primário: Sistema ASC de Transporte de Aminoácidos/metabolismo
Proteína-1 Reguladora de Fusão/metabolismo
Células Matadoras Naturais/fisiologia
Antígenos de Histocompatibilidade Menor/metabolismo
[Mh] Termos MeSH secundário: Sistema ASC de Transporte de Aminoácidos/genética
Antígeno CD56/metabolismo
Células Cultivadas
Citotoxicidade Imunológica
Seres Humanos
Interferon gama/metabolismo
Interleucina-2/imunologia
Interleucina-2/metabolismo
Ativação Linfocitária
Alvo Mecanístico do Complexo 1 de Rapamicina
Antígenos de Histocompatibilidade Menor/genética
Complexos Multiproteicos/antagonistas & inibidores
Subfamília K de Receptores Semelhantes a Lectina de Células NK/metabolismo
Serina-Treonina Quinases TOR/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amino Acid Transport System ASC); 0 (CD56 Antigen); 0 (Fusion Regulatory Protein-1); 0 (Interleukin-2); 0 (KLRK1 protein, human); 0 (Minor Histocompatibility Antigens); 0 (Multiprotein Complexes); 0 (NK Cell Lectin-Like Receptor Subfamily K); 0 (SLC1A5 protein, human); 82115-62-6 (Interferon-gamma); EC 2.7.1.1 (TOR Serine-Threonine Kinases); EC 2.7.11.1 (Mechanistic Target of Rapamycin Complex 1)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170809
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700497


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[PMID]:28414312
[Au] Autor:Porpiglia E; Samusik N; Van Ho AT; Cosgrove BD; Mai T; Davis KL; Jager A; Nolan GP; Bendall SC; Fantl WJ; Blau HM
[Ad] Endereço:Blau Laboratory, Stanford University School of Medicine, Stanford, California 94305, USA.
[Ti] Título:High-resolution myogenic lineage mapping by single-cell mass cytometry.
[So] Source:Nat Cell Biol;19(5):558-567, 2017 May.
[Is] ISSN:1476-4679
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Muscle regeneration is a dynamic process during which cell state and identity change over time. A major roadblock has been a lack of tools to resolve a myogenic progression in vivo. Here we capitalize on a transformative technology, single-cell mass cytometry (CyTOF), to identify in vivo skeletal muscle stem cell and previously unrecognized progenitor populations that precede differentiation. We discovered two cell surface markers, CD9 and CD104, whose combined expression enabled in vivo identification and prospective isolation of stem and progenitor cells. Data analysis using the X-shift algorithm paired with single-cell force-directed layout visualization defined a molecular signature of the activated stem cell state (CD44 /CD98 /MyoD ) and delineated a myogenic trajectory during recovery from acute muscle injury. Our studies uncover the dynamics of skeletal muscle regeneration in vivo and pave the way for the elucidation of the regulatory networks that underlie cell-state transitions in muscle diseases and ageing.
[Mh] Termos MeSH primário: Linhagem da Célula
Separação Celular/métodos
Citometria de Fluxo/métodos
Desenvolvimento Muscular
Músculo Esquelético/metabolismo
Mioblastos Esqueléticos/metabolismo
Regeneração
Análise de Célula Única/métodos
Células-Tronco/metabolismo
[Mh] Termos MeSH secundário: Animais
Biomarcadores/metabolismo
Proliferação Celular
Células Cultivadas
Venenos Elapídicos/toxicidade
Proteína-1 Reguladora de Fusão/metabolismo
Genes Reporter
Genótipo
Ensaios de Triagem em Larga Escala
Receptores de Hialuronatos/metabolismo
Integrina beta4/metabolismo
Proteínas Luminescentes/genética
Proteínas Luminescentes/metabolismo
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Desenvolvimento Muscular/efeitos dos fármacos
Músculo Esquelético/efeitos dos fármacos
Músculo Esquelético/lesões
Músculo Esquelético/patologia
Proteína MyoD/metabolismo
Mioblastos Esqueléticos/efeitos dos fármacos
Mioblastos Esqueléticos/patologia
Fator de Transcrição PAX7/deficiência
Fator de Transcrição PAX7/genética
Fenótipo
Regeneração/efeitos dos fármacos
Células-Tronco/efeitos dos fármacos
Células-Tronco/patologia
Tetraspanina-29/metabolismo
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Cd44 protein, mouse); 0 (Cd9 protein, mouse); 0 (Elapid Venoms); 0 (Fusion Regulatory Protein-1); 0 (Hyaluronan Receptors); 0 (Integrin beta4); 0 (Luminescent Proteins); 0 (MyoD Protein); 0 (MyoD1 myogenic differentiation protein); 0 (PAX7 Transcription Factor); 0 (Pax7 protein, mouse); 0 (Tetraspanin-29); 37223-96-4 (notexin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170418
[St] Status:MEDLINE
[do] DOI:10.1038/ncb3507


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[PMID]:28356536
[Au] Autor:Maeda F; Arii J; Hirohata Y; Maruzuru Y; Koyanagi N; Kato A; Kawaguchi Y
[Ad] Endereço:Division of Molecular Virology, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
[Ti] Título:Herpes Simplex Virus 1 UL34 Protein Regulates the Global Architecture of the Endoplasmic Reticulum in Infected Cells.
[So] Source:J Virol;91(12), 2017 Jun 15.
[Is] ISSN:1098-5514
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Upon herpes simplex virus 1 (HSV-1) infection, the CD98 heavy chain (CD98hc) is redistributed around the nuclear membrane (NM), where it promotes viral de-envelopment during the nuclear egress of nucleocapsids. In this study, we attempted to identify the factor(s) involved in CD98hc accumulation and demonstrated the following: (i) the null mutation of HSV-1 UL34 caused specific dispersion throughout the cytoplasm of CD98hc and the HSV-1 de-envelopment regulators, glycoproteins B and H (gB and gH); (ii) as observed with CD98hc, gB, and gH, wild-type HSV-1 infection caused redistribution of the endoplasmic reticulum (ER) markers calnexin and ERp57 around the NM, whereas the UL34-null mutation caused cytoplasmic dispersion of these markers; (iii) the ER markers colocalized efficiently with CD98hc, gB, and gH in the presence and absence of UL34 in HSV-1-infected cells; (iv) at the ultrastructural level, wild-type HSV-1 infection caused ER compression around the NM, whereas the UL34-null mutation caused cytoplasmic dispersion of the ER; and (v) the UL34-null mutation significantly decreased the colocalization efficiency of lamin protein markers of the NM with CD98hc and gB. Collectively, these results indicate that HSV-1 infection causes redistribution of the ER around the NM, with resulting accumulation of ER-associated CD98hc, gB, and gH around the NM and that UL34 is required for ER redistribution, as well as for efficient recruitment to the NM of the ER-associated de-envelopment factors. Our study suggests that HSV-1 induces remodeling of the global ER architecture for recruitment of regulators mediating viral nuclear egress to the NM. The ER is an important cellular organelle that exists as a complex network extending throughout the cytoplasm. Although viruses often remodel the ER to facilitate viral replication, information on the effects of herpesvirus infections on ER morphological integrity is limited. Here, we showed that HSV-1 infection led to compression of the global ER architecture around the NM, resulting in accumulation of ER-associated regulators associated with nuclear egress of HSV-1 nucleocapsids. We also identified HSV-1 UL34 as a viral factor that mediated ER remodeling. Furthermore, we demonstrated that UL34 was required for efficient targeting of these regulators to the NM. To our knowledge, this is the first report showing that a herpesvirus remodels ER global architecture. Our study also provides insight into the mechanism by which the regulators for HSV-1 nuclear egress are recruited to the NM, where this viral event occurs.
[Mh] Termos MeSH primário: Retículo Endoplasmático/ultraestrutura
Retículo Endoplasmático/virologia
Herpesvirus Humano 1/genética
Herpesvirus Humano 1/fisiologia
Proteínas Virais/metabolismo
[Mh] Termos MeSH secundário: Transporte Ativo do Núcleo Celular
Animais
Calnexina/metabolismo
Cercopithecus aethiops
Retículo Endoplasmático/metabolismo
Retículo Endoplasmático/patologia
Proteína-1 Reguladora de Fusão/metabolismo
Herpesvirus Humano 1/química
Seres Humanos
Mutação
Membrana Nuclear/fisiologia
Membrana Nuclear/virologia
Nucleocapsídeo/metabolismo
Ligação Proteica
Células Vero
Proteínas Virais/genética
Montagem de Vírus
Liberação de Vírus
Replicação Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fusion Regulatory Protein-1); 0 (UL34 protein, Human herpesvirus 1); 0 (Viral Proteins); 139873-08-8 (Calnexin)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171126
[Lr] Data última revisão:
171126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170331
[St] Status:MEDLINE


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[PMID]:28179310
[Au] Autor:Satoh T; Kaira K; Takahashi K; Takahashi N; Kanai Y; Asao T; Horiguchi J; Oyama T
[Ad] Endereço:Department of Thoracic and Visceral Organ Surgery, Gunma University Graduate School of Medicine, Gunma, Japan.
[Ti] Título:Prognostic Significance of the Expression of CD98 (4F2hc) in Gastric Cancer.
[So] Source:Anticancer Res;37(2):631-636, 2017 02.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: CD98 expression is high in various human neoplasms. However, the relationship of CD98 expression with the clinicopathological factors of gastric cancer (GC) remains unclear. This study examined CD98 expression and its clinicopathological impact on GC. PATIENTS AND METHODS: Three hundred and thirty-one patients with surgically resected GC were evaluated. Tumor sections were stained and analyzed using immunohistochemistry to assess CD98 expression. RESULTS: CD98 was positively expressed in 19% (66/331) of our patient cohort. Increased CD98 expression was significantly associated with advanced GC stage, lymph node metastasis, non-signet histology, lymphatic permeation, and vascular invasion. Positive CD98 expression was also a significant prediction marker for unfavorable prognosis postoperatively. However, CD98 was not identified as GC's independent prognostic predictor. CONCLUSION: CD98 could be a novel prediction marker for worse prognosis in GC-affected patients. Our data suggests that increased CD98 expression plays an essential role in tumor aggressiveness and metastasis.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/biossíntese
Proteína-1 Reguladora de Fusão/biossíntese
Avaliação de Resultados (Cuidados de Saúde)/métodos
Neoplasias Gástricas/metabolismo
[Mh] Termos MeSH secundário: Idoso
Feminino
Seres Humanos
Imuno-Histoquímica
Estimativa de Kaplan-Meier
Metástase Linfática
Masculino
Meia-Idade
Análise Multivariada
Estadiamento de Neoplasias
Avaliação de Resultados (Cuidados de Saúde)/estatística & dados numéricos
Prognóstico
Estudos Retrospectivos
Neoplasias Gástricas/patologia
Neoplasias Gástricas/cirurgia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (Fusion Regulatory Protein-1)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170210
[St] Status:MEDLINE


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[PMID]:27924161
[Au] Autor:Xiao B; Zhang Z; Viennois E; Kang Y; Zhang M; Han MK; Chen J; Merlin D
[Ad] Endereço:Institute for Clean Energy and Advanced Materials, Faculty of Materials and Energy, Southwest University, Chongqing, 400715, P. R. China.; Institute for Biomedical Sciences, Center for Diagnostics and Therapeutics, Georgia State University, Atlanta, 30302, USA.
[Ti] Título:Combination Therapy for Ulcerative Colitis: Orally Targeted Nanoparticles Prevent Mucosal Damage and Relieve Inflammation.
[So] Source:Theranostics;6(12):2250-2266, 2016.
[Is] ISSN:1838-7640
[Cp] País de publicação:Australia
[La] Idioma:eng
[Ab] Resumo:Combination therapy is an emerging strategy that is under intensive preclinical investigation for the treatment of various diseases. CD98 is highly overexpressed on the surfaces of epithelial cells and macrophages in the colon tissue with ulcerative colitis (UC), which is usually associated with mucosal damage and inflammation. We previously proved that CD98 siRNA (siCD98)-induced down-regulation of CD98 in colitis tissue decreased the severity of UC to a certain extent. In an effort to further improve the therapeutic efficacy, we aim to simultaneously deliver siCD98 in combination with a potent anti-inflammatory agent, curcumin (CUR), using hyaluronic acid (HA)-functionalized polymeric nanoparticles (NPs). The resultant spherical HA-siCD98/CUR-NPs are featured by a desirable particle size (∼246 nm) and slightly negative zeta potential (∼-14 mV). The NPs functionalized with HA are able to guide the co-delivery of drugs to the targeted cells related to UC therapy (colonic epithelial cells and macrophages). Compared to either siCD98- or CUR-based monotherapy, co-delivery of siCD98 and CUR by HA-functionalized NPs can exert combinational effects against UC by protecting the mucosal layer and alleviating inflammation both and . This study shows the promising capability of the co-delivered siCD98 and CUR for boosting the conventional monotherapy via this novel nanotherapeutic agent, which offers a structurally simple platform for orally administered delivery of drugs to target cells in UC therapy.
[Mh] Termos MeSH primário: Anti-Inflamatórios/administração & dosagem
Produtos Biológicos/administração & dosagem
Colite Ulcerativa/tratamento farmacológico
Curcumina/administração & dosagem
Mucosa Intestinal/fisiologia
Nanopartículas/administração & dosagem
RNA Interferente Pequeno/administração & dosagem
[Mh] Termos MeSH secundário: Administração Oral
Animais
Linhagem Celular
Colo/fisiologia
Portadores de Fármacos/administração & dosagem
Quimioterapia Combinada
Células Epiteliais/efeitos dos fármacos
Proteína-1 Reguladora de Fusão/antagonistas & inibidores
Ácido Hialurônico/metabolismo
Inflamação/prevenção & controle
Ácido Láctico/administração & dosagem
Macrófagos/efeitos dos fármacos
Masculino
Camundongos
Terapia de Alvo Molecular
Ácido Poliglicólico/administração & dosagem
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Biological Products); 0 (Drug Carriers); 0 (Fusion Regulatory Protein-1); 0 (RNA, Small Interfering); 0 (polylactic acid-polyglycolic acid copolymer); 26009-03-0 (Polyglycolic Acid); 33X04XA5AT (Lactic Acid); 9004-61-9 (Hyaluronic Acid); IT942ZTH98 (Curcumin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161208
[St] Status:MEDLINE


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[PMID]:27908736
[Au] Autor:Bajaj J; Konuma T; Lytle NK; Kwon HY; Ablack JN; Cantor JM; Rizzieri D; Chuah C; Oehler VG; Broome EH; Ball ED; van der Horst EH; Ginsberg MH; Reya T
[Ad] Endereço:Department of Pharmacology, University of California San Diego School of Medicine, La Jolla, CA 92093, USA; Sanford Consortium for Regenerative Medicine, La Jolla, CA 92037, USA; Moores Cancer Center, University of California San Diego School of Medicine, La Jolla, CA 92093, USA; Department of Medic
[Ti] Título:CD98-Mediated Adhesive Signaling Enables the Establishment and Propagation of Acute Myelogenous Leukemia.
[So] Source:Cancer Cell;30(5):792-805, 2016 Nov 14.
[Is] ISSN:1878-3686
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Acute myelogenous leukemia (AML) is an aggressive disease associated with drug resistance and relapse. To improve therapeutic strategies, it is critical to better understand the mechanisms that underlie AML progression. Here we show that the integrin binding glycoprotein CD98 plays a central role in AML. CD98 promotes AML propagation and lethality by driving engagement of leukemia cells with their microenvironment and maintaining leukemic stem cells. Further, delivery of a humanized anti-CD98 antibody blocks growth of patient-derived AML, highlighting the importance of this pathway in human disease. These findings indicate that microenvironmental interactions are key regulators of AML and that disrupting these signals with targeted inhibitors such as CD98 antibodies may be a valuable therapeutic approach for adults and children with this disease.
[Mh] Termos MeSH primário: Anticorpos/administração & dosagem
Proteína-1 Reguladora de Fusão/genética
Leucemia Mieloide Aguda/tratamento farmacológico
Células-Tronco Neoplásicas/patologia
[Mh] Termos MeSH secundário: Animais
Anticorpos/farmacologia
Adesão Celular
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Proteína-1 Reguladora de Fusão/antagonistas & inibidores
Técnicas de Inativação de Genes
Seres Humanos
Leucemia Mieloide Aguda/genética
Leucemia Mieloide Aguda/patologia
Camundongos
Transplante de Neoplasias
[Pt] Tipo de publicação:JOURNAL ARTICLE; COMMENT
[Nm] Nome de substância:
0 (Antibodies); 0 (Fusion Regulatory Protein-1)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161203
[St] Status:MEDLINE


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[PMID]:27840151
[Au] Autor:Ip H; Sethi T
[Ad] Endereço:Guy's and St Thomas' NHS Foundation Trust, United Kingdom. Electronic address: hughip@gmail.com.
[Ti] Título:CD98 signals controlling tumorigenesis.
[So] Source:Int J Biochem Cell Biol;81(Pt A):148-150, 2016 Dec.
[Is] ISSN:1878-5875
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:CD98 is implicated in a large number of cancers. CD98 regulates amino acid transport and integrin signaling, which are key drivers in tumor progression. The light chain in the CD98 heterodimer functions as an amino acid exchanger. Alongside the light chain, the heavy chain forms a heterocomplex at the plasma membrane to mediate signaling pathways. In this article, we review various approaches to blocking CD98 activity, which may lead to novel opportunities in cancer therapeutics.
[Mh] Termos MeSH primário: Carcinogênese
Proteína-1 Reguladora de Fusão/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Animais
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Fusion Regulatory Protein-1)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161115
[St] Status:MEDLINE


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[PMID]:27834933
[Au] Autor:Wu B; Zhou Y; Wang Y; Yang XM; Liu ZY; Li JH; Feng F; Chen ZN; Jiang JL
[Ad] Endereço:National Translational Science Center for Molecular Medicine, Cell Engineering Research Centre and Department of Cell Biology, State Key Laboratory of Cancer Biology, Fourth Military Medical University, Xi'an 710032, China. soldier2158wubo@163.com.
[Ti] Título:Dominant Suppression of ß1 Integrin by Ectopic CD98-ICD Inhibits Hepatocellular Carcinoma Progression.
[So] Source:Int J Mol Sci;17(11), 2016 Nov 10.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Hepatocellular carcinoma (HCC) is currently the third most common cause of cancer-related death in the Asia-Pacific region. Our previous work showed that knockdown of CD98 significantly inhibits malignant HCC cell phenotypes in vitro and in vivo. The level of CD98 in the membrane is tightly regulated to mediate complex processes associated with cell-cell communication and intracellular signaling. In addition, the intracellular domain of CD98 (CD98-ICD) seems to be of vital importance for recycling CD98 to the membrane after it is endocytosed. The intracellular and transmembrane domains of CD98 associate with ß-integrins (primarily ß1 but also ß3), and this association is essential for CD98 mediation of integrin-like signaling and complements dominant suppression of ß1-integrin. We speculated that isolated CD98-ICD would similarly suppress ß1-integrin activation and inhibit the malignant behaviors of cancer cells. In particular, the exact role of CD98-ICD has not been studied independently in HCC. In this study, we found that ectopic expression of CD98-ICD inhibited the malignant phenotypes of HCC cells, and the mechanism possibly involves ß1-integrin suppression. Moreover, the expression levels of CD98, ß1-integrin-A (the activated form of ß1-integrin) and Ki-67 were significantly increased in HCC tissues relative to those of normal liver tissues. Therefore, our preliminary study indicates that ectopic CD98-ICD has an inhibitory role in the malignant development of HCC, and shows that CD98-ICD acts as a dominant negative mutant of CD98 that attenuates ß1-integrin activation. CD98-ICD may emerge as a promising candidate for antitumor treatment.
[Mh] Termos MeSH primário: Carcinoma Hepatocelular/metabolismo
Proteína-1 Reguladora de Fusão/metabolismo
Integrina beta1/metabolismo
Neoplasias Hepáticas/metabolismo
[Mh] Termos MeSH secundário: Animais
Sítios de Ligação/genética
Western Blotting
Carcinoma Hepatocelular/genética
Carcinoma Hepatocelular/patologia
Linhagem Celular Tumoral
Progressão da Doença
Citometria de Fluxo
Proteína-1 Reguladora de Fusão/genética
Seres Humanos
Imuno-Histoquímica
Antígeno Ki-67/metabolismo
Neoplasias Hepáticas/genética
Neoplasias Hepáticas/patologia
Camundongos Endogâmicos BALB C
Camundongos Nus
Microscopia Confocal
Transfecção
Transplante Heterólogo
Carga Tumoral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fusion Regulatory Protein-1); 0 (Integrin beta1); 0 (Ki-67 Antigen)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161112
[St] Status:MEDLINE


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[PMID]:27678353
[Au] Autor:Si XY; Merlin D; Xiao B
[Ad] Endereço:Xiao-Ying Si, Bo Xiao, Institute for Clean Energy and Advanced Materials, Faculty of Materials and Energy, Southwest University, Chongqing 400715, China.
[Ti] Título:Recent advances in orally administered cell-specific nanotherapeutics for inflammatory bowel disease.
[So] Source:World J Gastroenterol;22(34):7718-26, 2016 Sep 14.
[Is] ISSN:2219-2840
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Inflammatory bowel disease (IBD) is a chronic relapsing disease in gastrointestinal tract. Conventional medications lack the efficacy to offer complete remission in IBD therapy, and usually associate with serious side effects. Recent studies indicated that nanoparticle-based nanotherapeutics may offer precise and safe alternative to conventional medications via enhanced targeting, sustained drug release, and decreased adverse effects. Here, we reviewed orally cell-specific nanotherapeutics developed in recent years. In addition, the various obstacles for oral drug delivery are also reviewed in this manuscript. Orally administrated cell-specific nanotherapeutics is expected to become a novel therapeutic approach for IBD treatment.
[Mh] Termos MeSH primário: Administração Oral
Doenças Inflamatórias Intestinais/terapia
Nanopartículas/química
Preparações Farmacêuticas/administração & dosagem
[Mh] Termos MeSH secundário: Animais
Núcleo Celular/metabolismo
Portadores de Fármacos/química
Endossomos/metabolismo
Epitélio/metabolismo
Proteína-1 Reguladora de Fusão/química
Galactose/química
Trato Gastrointestinal/efeitos dos fármacos
Seres Humanos
Ácido Hialurônico/química
Hidrogéis/química
Concentração de Íons de Hidrogênio
Manose/química
Permeabilidade
Espécies Reativas de Oxigênio/metabolismo
Receptores da Transferrina/química
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Drug Carriers); 0 (Fusion Regulatory Protein-1); 0 (Hydrogels); 0 (Pharmaceutical Preparations); 0 (Reactive Oxygen Species); 0 (Receptors, Transferrin); 9004-61-9 (Hyaluronic Acid); PHA4727WTP (Mannose); X2RN3Q8DNE (Galactose)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160929
[St] Status:MEDLINE
[do] DOI:10.3748/wjg.v22.i34.7718


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[PMID]:27465934
[Au] Autor:Ohshima Y; Kaira K; Yamaguchi A; Oriuchi N; Tominaga H; Nagamori S; Kanai Y; Yokobori T; Miyazaki T; Asao T; Tsushima Y; Kuwano H; Ishioka NS
[Ad] Endereço:Department of Radiation-Applied Biology Research, Quantum Beam Science Research Directorate, National Institutes for Quantum and Radiological Science and Technology, Takasaki, Japan. b16gradmmptimp@yahoo.co.jp.
[Ti] Título:Efficacy of system l amino acid transporter 1 inhibition as a therapeutic target in esophageal squamous cell carcinoma.
[So] Source:Cancer Sci;107(10):1499-1505, 2016 Oct.
[Is] ISSN:1349-7006
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:System l amino acid transporter 1 (LAT1) is highly expressed in various types of human cancer, and contributes to cancer growth and survival. Recently, we have shown that LAT1 expression is closely related to the growth and aggressiveness of esophageal cancer, and is an independent marker of poor prognosis. However, it remains unclear whether LAT1 inhibition could suppress esophageal cancer growth. In this study, we investigated the tumor-suppressive effects of the inhibition of LAT1. Both LAT1 and CD98, which covalently associates to LAT1 on the membrane, were expressed in human esophageal cancer cell lines KYSE30 and KYSE150. Quantitative PCR analysis showed that the expression of LAT1 was much higher than other subtypes of LAT. A selective inhibitor of LAT, 2-aminobicyclo-(2,2,1)-heptane-2-carboxylic acid (BCH), suppressed cellular uptake of l- C-leucine and cell proliferation in a dose-dependent manner. It also suppressed phosphorylation of mammalian target of rapamycin, 4E-BP1, and p70S6K protein, and induced cell cycle arrest at G phase. These results suggest that suppression of both mammalian target of rapamycin signaling and cell cycle progression is involved in BCH-induced growth inhibition. In tumor-bearing mice, daily treatment with BCH significantly delayed tumor growth and decreased glucose metabolism, indicating that LAT1 inhibition potentially suppresses esophageal cancer growth in vivo. Thus, our results suggest that LAT1 inhibition could be a promising molecular target for the esophageal cancer therapy.
[Mh] Termos MeSH primário: Sistema L de Transporte de Aminoácidos/antagonistas & inibidores
Antineoplásicos/farmacologia
Carcinoma de Células Escamosas/metabolismo
Neoplasias Esofágicas/metabolismo
[Mh] Termos MeSH secundário: Sistema L de Transporte de Aminoácidos/genética
Sistema L de Transporte de Aminoácidos/metabolismo
Aminoácidos/metabolismo
Animais
Antineoplásicos/administração & dosagem
Transporte Biológico/efeitos dos fármacos
Carcinoma de Células Escamosas/tratamento farmacológico
Carcinoma de Células Escamosas/genética
Carcinoma de Células Escamosas/patologia
Pontos de Checagem do Ciclo Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Modelos Animais de Doenças
Neoplasias Esofágicas/tratamento farmacológico
Neoplasias Esofágicas/genética
Neoplasias Esofágicas/patologia
Proteína-1 Reguladora de Fusão/genética
Proteína-1 Reguladora de Fusão/metabolismo
Perfilação da Expressão Gênica
Seres Humanos
Lactato Desidrogenases/metabolismo
Masculino
Camundongos
Terapia de Alvo Molecular
Transdução de Sinais/efeitos dos fármacos
Serina-Treonina Quinases TOR/metabolismo
Transcriptoma
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amino Acid Transport System L); 0 (Amino Acids); 0 (Antineoplastic Agents); 0 (Fusion Regulatory Protein-1); EC 1.1.- (Lactate Dehydrogenases); EC 2.7.1.1 (TOR Serine-Threonine Kinases)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160729
[St] Status:MEDLINE
[do] DOI:10.1111/cas.13021



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