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Pesquisa : D12.776.220.145 [Categoria DeCS]
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  1 / 905 MEDLINE  
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[PMID]:29337056
[Au] Autor:Iderzorig T; Kellen J; Osude C; Singh S; Woodman JA; Garcia C; Puri N
[Ad] Endereço:Department of Biomedical Sciences, University of Illinois College of Medicine at Rockford, Illinois, USA.
[Ti] Título:Comparison of EMT mediated tyrosine kinase inhibitor resistance in NSCLC.
[So] Source:Biochem Biophys Res Commun;496(2):770-777, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In the United States, lung cancer is the second most common cancer in men and women. In 2017, 222,500 new cases and 155,870 deaths from lung cancer are estimated to have occurred. A tyrosine kinase receptor, epidermal growth factor receptor (EGFR), is over expressed or mutated in non-small cell lung cancer (NSCLC) resulting in increased cell proliferation and survival. Tyrosine kinase inhibitors (TKIs) are currently being used as therapy for NSCLC patients, however, they have limited efficacy in NSCLC patients due to acquisition of resistance. This study investigates the role of epithelial-mesenchymal transition (EMT) in the development of resistance against TKIs in NSCLC. Currently, the role of p120-catenin, Kaiso factor and PRMT-1 in reversal of EMT in T790M mutated and TKI-resistant NSCLC cells is a new line of study. In this investigation we found upregulation of cytoplasmic p120-catenin, which was co-localized with Kaiso factor. In the nucleus, binding of p120-catenin to Kaiso factor initiates transcription by activating EMT-transcription factors such as Snail, Slug, Twist, and ZEB1. PRMT-1 was also found to be upregulated, which induces methylation of Twist and repression of E-cadherin activity, thus promoting EMT. We confirmed that TKI-resistant cells have mesenchymal cell type characteristics based on their cell morphology and gene or protein expression of EMT related proteins. EMT proteins, Vimentin and N-cadherin, displayed increased expression, whereas E-cadherin expression was downregulated. Finally, we found that the knockdown of p120-catenin and PRMT-1 by siRNA or use of a PRMT-1 inhibitor Furamidine increased Erlotinib sensitivity and could reverse EMT to overcome TKI resistance.
[Mh] Termos MeSH primário: Carcinoma Pulmonar de Células não Pequenas/tratamento farmacológico
Resistência a Medicamentos Antineoplásicos
Transição Epitelial-Mesenquimal/efeitos dos fármacos
Cloridrato de Erlotinib/farmacologia
Neoplasias Pulmonares/tratamento farmacológico
Inibidores de Proteínas Quinases/farmacologia
Proteínas Tirosina Quinases/antagonistas & inibidores
[Mh] Termos MeSH secundário: Antineoplásicos/farmacologia
Carcinoma Pulmonar de Células não Pequenas/metabolismo
Cateninas/metabolismo
Linhagem Celular Tumoral
Feminino
Seres Humanos
Neoplasias Pulmonares/metabolismo
Masculino
Proteínas Tirosina Quinases/metabolismo
Receptor do Fator de Crescimento Epidérmico/antagonistas & inibidores
Receptor do Fator de Crescimento Epidérmico/metabolismo
Fatores de Transcrição/metabolismo
Vimentina/metabolismo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Catenins); 0 (Protein Kinase Inhibitors); 0 (Transcription Factors); 0 (Vimentin); 0 (ZNF-kaiso protein, human); DA87705X9K (Erlotinib Hydrochloride); EC 2.7.10.1 (EGFR protein, human); EC 2.7.10.1 (Protein-Tyrosine Kinases); EC 2.7.10.1 (Receptor, Epidermal Growth Factor)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180216
[Lr] Data última revisão:
180216
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180117
[St] Status:MEDLINE


  2 / 905 MEDLINE  
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[PMID]:29216867
[Au] Autor:Pham TND; Perez White BE; Zhao H; Mortazavi F; Tonetti DA
[Ad] Endereço:Department of Biopharmaceutical Sciences, University of Illinois at Chicago, 833 South Wood Street M/C 865, Chicago, IL, 60612, USA.
[Ti] Título:Protein kinase C α enhances migration of breast cancer cells through FOXC2-mediated repression of p120-catenin.
[So] Source:BMC Cancer;17(1):832, 2017 12 07.
[Is] ISSN:1471-2407
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Despite recent advances in the diagnosis and treatment of breast cancer, metastasis remains the main cause of death. Since migration of tumor cells is considered a prerequisite for tumor cell invasion and metastasis, a pressing goal in tumor biology has been to elucidate factors regulating their migratory activity. Protein kinase C alpha (PKCα) is a serine-threonine protein kinase implicated in cancer metastasis and associated with poor prognosis in breast cancer patients. In this study, we set out to define the signaling axis mediated by PKCα to promote breast cancer cell migration. METHODS: Oncomine™ overexpression analysis was used to probe for PRKCA (PKCα) and FOXC2 expression in mRNA datasets. The heat map of PRKCA, FOXC2, and CTNND1 were obtained from the UC Santa Cruz platform. Survival data were obtained by PROGgene and available at http://www.compbio.iupui.edu/proggene . Markers for EMT and adherens junction were assessed by Western blotting and quantitative polymerase chain reaction. Effects of PKCα and FOXC2 on migration and invasion were assessed in vitro by transwell migration and invasion assays respectively. Cellular localization of E-cadherin and p120-catenin was determined by immunofluorescent staining. Promoter activity of p120-catenin was determined by dual luciferase assay using a previously validated p120-catenin reporter construct. Interaction between FOXC2 and p120-catenin promoter was verified by chromatin immunoprecipitation assay. RESULTS: We determined that PKCα expression is necessary to maintain the migratory and invasive phenotype of both endocrine resistant and triple negative breast cancer cell lines. FOXC2 acts as a transcriptional repressor downstream of PKCα, and represses p120-catenin expression. Consequently, loss of p120-catenin leads to destabilization of E-cadherin at the adherens junction. Inhibition of either PKCα or FOXC2 is sufficient to rescue p120-catenin expression and trigger relocalization of p120-catenin and E-cadherin to the cell membrane, resulting in reduced tumor cell migration and invasion. CONCLUSIONS: Taken together, these results suggest that breast cancer metastasis may partially be controlled through PKCα/FOXC2-dependent repression of p120-catenin and highlight the potential for PKCα signal transduction networks to be targeted for the treatment of endocrine resistant and triple negative breast cancer.
[Mh] Termos MeSH primário: Neoplasias da Mama/metabolismo
Cateninas/metabolismo
Movimento Celular/genética
Fatores de Transcrição Forkhead/metabolismo
Proteína Quinase C-alfa/metabolismo
[Mh] Termos MeSH secundário: Neoplasias da Mama/genética
Cateninas/genética
Linhagem Celular Tumoral
Imunoprecipitação da Cromatina
Feminino
Fatores de Transcrição Forkhead/análise
Fatores de Transcrição Forkhead/genética
Perfilação da Expressão Gênica
Seres Humanos
Invasividade Neoplásica/genética
Proteína Quinase C-alfa/análise
Proteína Quinase C-alfa/genética
Transdução de Sinais/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Catenins); 0 (Forkhead Transcription Factors); 0 (delta catenin); 0 (mesenchyme fork head 1 protein); EC 2.7.11.13 (PRKCA protein, human); EC 2.7.11.13 (Protein Kinase C-alpha)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180217
[Lr] Data última revisão:
180217
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171209
[St] Status:MEDLINE
[do] DOI:10.1186/s12885-017-3827-y


  3 / 905 MEDLINE  
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[PMID]:28465325
[Au] Autor:Leblanc C; Langlois MJ; Coulombe G; Vaillancourt-Lavigueur V; Jones C; Carrier JC; Boudreau F; Rivard N
[Ad] Endereço:Département d'Anatomie et de Biologie Cellulaire, Faculté de Médecine et des Sciences de la Santé, Université de Sherbrooke, Sherbrooke, Quebec, Canada.
[Ti] Título:Epithelial Src homology region 2 domain-containing phosphatase-1 restrains intestinal growth, secretory cell differentiation, and tumorigenesis.
[So] Source:FASEB J;31(8):3512-3526, 2017 08.
[Is] ISSN:1530-6860
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Shp-1 (Src homology region 2 domain-containing protein tyrosine phosphatase-1) is a phosphatase that is highly expressed in hematopoietic and epithelial cells. Whereas its function is largely characterized in hematopoietic cells, its role in epithelial cells, such as intestinal epithelial cells (IECs), is not well known. Here, we generated mice with an IEC-specific knockout of (Src homology region 2 domain-containing phosphatase-1; ). We showed that the loss of epithelial leads to an intestinalomegaly that is associated with an increase in epithelial cell proliferation and size. Histologic analysis demonstrates significant perturbation of the crypt-villus architecture with an apparent increase in the number of goblet and Paneth cells and increased expression of their respective markers { (mucin 2), α , and [SRY (sex determining region Y)-box 9]}. Expansion of intermediate cells-common progenitors of goblet and Paneth cell lineages-is also observed in mice. Although sustained activation of Wnt/ß-catenin and PI3K/Akt/mammalian target of rapamycin signaling is observed, mice fail to develop any intestinal tumors after 15 mo; however, the loss of in IECs markedly enhances tumor load mice. These findings show a novel role for Shp-1 in the regulation of IEC growth and secretory lineage allocation, possibly modulation of PI3K/Akt-dependent signaling pathways. Finally, Shp-1 does not function as a classic tumor suppressor gene in the intestinal epithelium.-Leblanc, C., Langlois, M.-J., Coulombe, G., Vaillancourt-Lavigueur, V., Jones, C., Carrier, J. C., Boudreau, F., Rivard, N. Epithelial Src homology region 2 domain-containing phosphatase-1 restrains intestinal growth, secretory cell differentiation, and tumorigenesis.
[Mh] Termos MeSH primário: Neoplasias do Colo/metabolismo
Regulação da Expressão Gênica/fisiologia
Intestinos/crescimento & desenvolvimento
Proteína Tirosina Fosfatase não Receptora Tipo 6/metabolismo
[Mh] Termos MeSH secundário: Animais
Cateninas/genética
Cateninas/metabolismo
Células Epiteliais/fisiologia
Seres Humanos
Intestinos/citologia
Intestinos/metabolismo
Camundongos
Camundongos Knockout
Camundongos Transgênicos
Fosfatidilinositol 3-Quinases/genética
Fosfatidilinositol 3-Quinases/metabolismo
Proteína Tirosina Fosfatase não Receptora Tipo 6/genética
Proteínas Proto-Oncogênicas c-akt
Proteínas Wnt/genética
Proteínas Wnt/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Catenins); 0 (Wnt Proteins); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 3.1.3.48 (PTPN6 protein, human); EC 3.1.3.48 (Protein Tyrosine Phosphatase, Non-Receptor Type 6); EC 3.1.3.48 (Ptpn6 protein, mouse)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:180206
[Lr] Data última revisão:
180206
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1096/fj.201601378R


  4 / 905 MEDLINE  
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[PMID]:28692740
[Au] Autor:Maddala R; Rao PV
[Ad] Endereço:Department of Ophthalmology, Duke University School of Medicine, Durham, North Carolina, United States.
[Ti] Título:Switching of α-Catenin From Epithelial to Neuronal Type During Lens Epithelial Cell Differentiation.
[So] Source:Invest Ophthalmol Vis Sci;58(9):3445-3455, 2017 Jul 01.
[Is] ISSN:1552-5783
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Purpose: Ocular lens fiber cell elongation, differentiation, and compaction are associated with extensive reorganization of cell adhesive interactions and cytoskeleton; however, our knowledge of proteins critical to these events is still evolving. This study characterizes the distribution pattern of neuronal-specific α-catenin (αN-catenin) and its interaction with the N-cadherin-associated adherens junctions (AJs) and their stability in the mouse lens fibers. Methods: Expression and distribution of αN-catenin in developing mouse and adult human lenses was determined by RT-PCR, immunoblot, and immunofluorescence analyses. Characterization of αN-catenin and N-cadherin interacting proteins and colocalization analyses were performed using immunoprecipitation, mass spectrometry, and confocal imaging. Effects of periaxin deficiency on the stability of lens fiber cell AJs were evaluated using perixin-null mice. Results: αN-catenin exhibits discrete distribution to lens fibers in both mouse and human lenses, undergoing a robust up-regulation during fiber cell differentiation and maturation. Epithelial-specific α-catenin (αE-catenin), in contrast, distributes primarily to the lens epithelium. αN-catenin and N-cadherin reciprocally coimmunoprecipitate and colocalize along with ß-catenin, actin, spectrin, vinculin, Armadillo repeat protein deleted in velo-cardio-facial syndrome homolog, periaxin, and ankyrin-B in lens fibers. Fiber cells from periaxin-null mouse lenses revealed disrupted N-cadherin/αN-catenin-based AJs. Conclusions: These results suggest that the discrete shift in α-catenin expression from αE-catenin to αN-catenin subtype that occurs during lens epithelial cell differentiation may play a key role in fiber cell cytoarchitecture by regulating the assembly and stability of N-cadherin-based AJs. This study also provides evidence for the importance of the fiber cell-specific cytoskeletal interacting periaxin, in the stability of N-cadherin/αN-catenin-based AJs in lens fibers.
[Mh] Termos MeSH primário: Cateninas/metabolismo
Diferenciação Celular/fisiologia
Células Epiteliais/metabolismo
Cristalino/metabolismo
[Mh] Termos MeSH secundário: Animais
Seres Humanos
Immunoblotting
Cristalino/embriologia
Espectrometria de Massas
Proteínas de Membrana/deficiência
Camundongos
Reação em Cadeia da Polimerase Via Transcriptase Reversa
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Catenins); 0 (Membrane Proteins); 0 (periaxin)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171003
[Lr] Data última revisão:
171003
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170711
[St] Status:MEDLINE
[do] DOI:10.1167/iovs.17-21539


  5 / 905 MEDLINE  
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[PMID]:28682550
[Au] Autor:Zhong C; Mei Z; Yong X
[Ad] Endereço:Dept. of Stomatology, Xiamen Medical College, Xiamen 361008, China.
[Ti] Título:[Cadherin switching induced by P120-catenin can promote the migration and invasion of oral squamous cell cancer cells].
[So] Source:Hua Xi Kou Qiang Yi Xue Za Zhi;35(2):183-186, 2017 Apr 01.
[Is] ISSN:1000-1182
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:OBJECTIVE: The main goal is to investigate the role of P120-catenin (P120ctn) in cadherin switching, as well as migration and invasion, of oral squamous cell cancer (OSCC) cells. METHODS: The plasmid pGFP-V-RS-P120ctn shRNA was used to transfect TSCCA cells and significantly reduce the expression of P120ctn in these cells. Real-time fluorescent quantitative polymerase chain reaction and Western blot were conducted to determine the mRNA and protein expression levels of P120ctn, E-cadherin (E-cad), and N-cadherin (N-cad). By contrast, the Transwell cell invasion and cell migration assay was used to determine the invasion and migration capacities before and after the transfection. RESULTS: After the plasmid pGFP-V-RS-P120ctn shRNA was transfected into the TSCCA cells, we found that as the P120ctn expression significantly decreased, E-cad mRNA and protein expression decreased significantly. Moreover, N-cad mRNA and protein expression increased significantly (P<0.05). Lastly, the cell migration and invasion capacities were augmented significantly (P<0.05). CONCLUSIONS: In OSCC cells, P120ctn may be involved in cadherin switching and promote metastasis and invasion.
[Mh] Termos MeSH primário: Caderinas
Carcinoma de Células Escamosas
Cateninas
Neoplasias Bucais
Invasividade Neoplásica
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Movimento Celular
Seres Humanos
Metástase Neoplásica
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CDH1 protein, human); 0 (Cadherins); 0 (Catenins); 0 (delta catenin)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170807
[Lr] Data última revisão:
170807
[Sb] Subgrupo de revista:D; IM
[Da] Data de entrada para processamento:170707
[St] Status:MEDLINE
[do] DOI:10.7518/hxkq.2017.02.014


  6 / 905 MEDLINE  
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[PMID]:28486541
[Au] Autor:Zhao Y; Wu K; Nguyen C; Smbatyan G; Melendez E; Higuchi Y; Chen Y; Kahn M
[Ad] Endereço:Department of Medicine, Keck School of Medicine of University of Southern California, Los Angeles, California, United States of America.
[Ti] Título:Small molecule p300/catenin antagonist enhances hematopoietic recovery after radiation.
[So] Source:PLoS One;12(5):e0177245, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:There is currently no FDA approved therapeutic agent for ARS mitigation post radiation exposure. Here we report that the small molecule YH250, which specifically antagonizes p300/catenin interaction, stimulates hematopoiesis in lethally or sublethally irradiated mice. A single administration of YH250 24 hours post irradiation can significantly stimulate HSC proliferation, improve survival and accelerate peripheral blood count recovery. Our studies suggest that promotion of the expansion of the remaining HSC population via stimulation of symmetric non-differentiative proliferation is at least part of the mechanism of action.
[Mh] Termos MeSH primário: Cateninas/antagonistas & inibidores
Hematopoese/efeitos dos fármacos
Compostos Heterocíclicos com 2 Anéis/farmacologia
Compostos Heterocíclicos com 2 Anéis/uso terapêutico
Lesões por Radiação/tratamento farmacológico
Fatores de Transcrição de p300-CBP/antagonistas & inibidores
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Camundongos
Camundongos Transgênicos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Catenins); 0 (Heterocyclic Compounds, 2-Ring); 0 (YH250 compound); EC 2.3.1.48 (p300-CBP Transcription Factors)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170510
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0177245


  7 / 905 MEDLINE  
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[PMID]:28393211
[Au] Autor:Shimizu D; Inokawa Y; Sonohara F; Inaoka K; Nomoto S
[Ad] Endereço:Department of Surgery, Aichi Gakuin University School of Dentistry, Chikusa-ku, Nagoya 464-8651, Japan.
[Ti] Título:Search for useful biomarkers in hepatocellular carcinoma, tumor factors and background liver factors (Review).
[So] Source:Oncol Rep;37(5):2527-2542, 2017 May.
[Is] ISSN:1791-2431
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:Hepatocarcinogenesis is a complex and multistep process that involves the accumulation of genetic and epigenetic alterations in regulatory genes. To understand the development of hepatocellular carcinoma (HCC), current research has utilized improved array technologies. The identification of cancer-related molecules could lead to the development of novel molecular targets for treatment and biomarkers for predicting prognosis. However, prognostic prediction is insufficient when considering only tumor factors, since hepatocarcinogenesis is also greatly influenced by the status of the background liver. Clinical background liver factors, such as the presence of chronic active hepatitis or cirrhosis, are well known as risk factors for developing HCC. In contrast, genetic or epigenetic background liver factors remain unknown, albeit those are important to understand the developing process of HCC. Investigating background liver factors could contribute to the development of carcinogenic markers of HCC and to the prevention of the development of HCC. In the present study, we review the currently identified tumor factors and background liver factors from a molecular biological viewpoint and also introduce our combination array analysis.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/metabolismo
Carcinoma Hepatocelular/genética
Regulação Neoplásica da Expressão Gênica
Neoplasias Hepáticas/genética
[Mh] Termos MeSH secundário: Biomarcadores Tumorais/análise
Biomarcadores Tumorais/genética
Carcinoma Hepatocelular/metabolismo
Carcinoma Hepatocelular/patologia
Cateninas/genética
Cateninas/metabolismo
Epigênese Genética
Galectina 1/genética
Galectina 1/metabolismo
Seres Humanos
Janus Quinase 2/genética
Janus Quinase 2/metabolismo
Neoplasias Hepáticas/metabolismo
Neoplasias Hepáticas/patologia
Metaloendopeptidases/metabolismo
MicroRNAs
Oncogenes
Análise Serial de Proteínas
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (Catenins); 0 (Galectin 1); 0 (MicroRNAs); 0 (delta catenin); EC 2.7.10.2 (JAK2 protein, human); EC 2.7.10.2 (Janus Kinase 2); EC 3.4.24.- (Metalloendopeptidases); EC 3.4.24.15 (thimet oligopeptidase)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170622
[Lr] Data última revisão:
170622
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170411
[St] Status:MEDLINE
[do] DOI:10.3892/or.2017.5541


  8 / 905 MEDLINE  
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[PMID]:28338646
[Au] Autor:Backert S; Tegtmeyer N
[Ad] Endereço:Division of Microbiology, Department of Biology, Friedrich Alexander University Erlangen-Nuremberg, Staudtstr. 5, D-91058 Erlangen, Germany. steffen.backert@fau.de.
[Ti] Título:Type IV Secretion and Signal Transduction of Helicobacter pylori CagA through Interactions with Host Cell Receptors.
[So] Source:Toxins (Basel);9(4), 2017 Mar 24.
[Is] ISSN:2072-6651
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:is a highly successful human bacterium, which is exceptionally equipped to persistently inhabit the human stomach. Colonization by this pathogen is associated with gastric disorders ranging from chronic gastritis and peptic ulcers to cancer. Highly virulent strains express the well-established adhesins BabA/B, SabA, AlpA/B, OipA, and HopQ, and a type IV secretion system (T4SS) encoded by the pathogenicity island (PAI). The adhesins ascertain intimate bacterial contact to gastric epithelial cells, while the T4SS represents an extracellular pilus-like structure for the translocation of the effector protein CagA. Numerous T4SS components including CagI, CagL, CagY, and CagA have been shown to target the integrin-ß1 receptor followed by translocation of CagA across the host cell membrane. The interaction of CagA with membrane-anchored phosphatidylserine and CagA-containing outer membrane vesicles may also play a role in the delivery process. Translocated CagA undergoes tyrosine phosphorylation in C-terminal EPIYA-repeat motifs by oncogenic Src and Abl kinases. CagA then interacts with an array of host signaling proteins followed by their activation or inactivation in phosphorylation-dependent and phosphorylation-independent fashions. We now count about 25 host cell binding partners of intracellular CagA, which represent the highest quantity of all currently known virulence-associated effector proteins in the microbial world. Here we review the research progress in characterizing interactions of CagA with multiple host cell receptors in the gastric epithelium, including integrin-ß1, EGFR, c-Met, CD44, E-cadherin, and gp130. The contribution of these interactions to colonization, signal transduction, and gastric pathogenesis is discussed.
[Mh] Termos MeSH primário: Antígenos de Bactérias/metabolismo
Proteínas de Bactérias/metabolismo
Receptores de Superfície Celular/metabolismo
[Mh] Termos MeSH secundário: Animais
Caderinas/metabolismo
Cateninas/metabolismo
Membrana Celular/metabolismo
Endocitose
Seres Humanos
Fosfatidilserinas/metabolismo
Fosforilação
Proteínas Proto-Oncogênicas c-abl/metabolismo
Transdução de Sinais
beta-Defensinas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antigens, Bacterial); 0 (Bacterial Proteins); 0 (Cadherins); 0 (Catenins); 0 (Phosphatidylserines); 0 (Receptors, Cell Surface); 0 (beta-Defensins); 0 (beta-defensin 3, human); 0 (cagA protein, Helicobacter pylori); EC 2.7.10.2 (Proto-Oncogene Proteins c-abl)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171109
[Lr] Data última revisão:
171109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170325
[St] Status:MEDLINE


  9 / 905 MEDLINE  
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[PMID]:28295003
[Au] Autor:Brilliant YM; Brilliant AA; Sazonov SV
[Ad] Endereço:Institute for Medical Cell Technologies, Ministry of Health of the Sverdlovsk Region, Yekaterinburg, Russia; Ural State Medical University, Ministry of Health of Russia, Yekaterinburg, Russia.
[Ti] Título:[Epithelial cadherins and associated molecules in invasive lobular breast cancer].
[Ti] Título:Epitelial'nye kadgeriny i assotsiirovannye s nimi molekuly pri invazivnom dol'kovom rake molochnoi zhelezy..
[So] Source:Arkh Patol;79(1):12-18, 2017.
[Is] ISSN:0004-1955
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:AIM: to estimate the expression of cell adhesion molecules E- and P-cadherin, as well as that of cadherin-catenin complexes in invasive lobular breast cancer (BC) cells. MATERIAL AND METHODS: 250 cases of postoperative material from patients diagnosed with invasive lobular BC were studied. The expressions of cell adhesion molecules E-cadherin, P-cadherin, ß-catenin, p120 catenin, and vimentin were determined by immunohistochemical assay in all cases. The examined cases were divided into molecular biological subtypes, based on the evaluation of estrogen receptors (ER), progesterone receptors (PR), HER-2/neu, and Ki-67 proliferative index. RESULTS: The membrane expression of E-cadherin on the tumor cells was found to be preserved in 93%; the cytoplasmic expression of ß-catenin and p120-catenin appeared in 60 and 72% of cases, respectively. The expression of P-cadherin was detected in 82% of cases. The coexpression of E- and P-cadherin was noted in 90% of all the examined cases. There was a correlation between the expression of E- and P-cadherins (V=0.34; p<0.05). CONCLUSION: The BC cells showed the coexpression of E- and P-cadherins, as well as release of the molecules ß- and p120-catenins into the cytoplasm of tumor cells, which leads to the activation of intracellular mechanisms for changing the structure of the cytoskeleton and the level of proliferation. The above-mentioned mechanisms are accompanied by the activation of epithelial-mesenchymal transition. The intracellular mechanisms resulted in progressive cancer and its metastasis.
[Mh] Termos MeSH primário: Caderinas/biossíntese
Cateninas/biossíntese
Neoplasias de Mama Triplo Negativas/genética
beta Catenina/biossíntese
[Mh] Termos MeSH secundário: Caderinas/genética
Cateninas/genética
Proliferação Celular/genética
Transição Epitelial-Mesenquimal/genética
Feminino
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Invasividade Neoplásica/genética
Prognóstico
Receptor ErbB-2/biossíntese
Neoplasias de Mama Triplo Negativas/classificação
Neoplasias de Mama Triplo Negativas/patologia
Vimentina/biossíntese
Vimentina/genética
beta Catenina/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CDH3 protein, human); 0 (Cadherins); 0 (Catenins); 0 (Vimentin); 0 (beta Catenin); 0 (delta catenin); EC 2.7.10.1 (ERBB2 protein, human); EC 2.7.10.1 (Receptor, ErbB-2)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170630
[Lr] Data última revisão:
170630
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170316
[St] Status:MEDLINE
[do] DOI:10.17116/patol201779112-18


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[PMID]:28276699
[Au] Autor:Duñach M; Del Valle-Pérez B; García de Herreros A
[Ad] Endereço:a Departament de Bioquímica i Biologia Molecular, CEB, Facultat de Medicina , Universitat Autònoma de Barcelona , Bellaterra , Spain.
[Ti] Título:p120-catenin in canonical Wnt signaling.
[So] Source:Crit Rev Biochem Mol Biol;52(3):327-339, 2017 Jun.
[Is] ISSN:1549-7798
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Canonical Wnt signaling controls ß-catenin protein stabilization, its translocation to the nucleus and the activation of ß-catenin/Tcf-4-dependent transcription. In this review, we revise and discuss the recent results describing actions of p120-catenin in different phases of this pathway. More specifically, we comment its involvement in four different steps: (i) the very early activation of CK1É›, essential for Dvl-2 binding to the Wnt receptor complex; (ii) the internalization of GSK3 and Axin into multivesicular bodies, necessary for a complete stabilization of ß-catenin; (iii) the activation of Rac1 small GTPase, required for ß-catenin translocation to the nucleus; and (iv) the release of the inhibitory action caused by Kaiso transcriptional repressor. We integrate these new results with the previously known action of other elements in this pathway, giving a particular relevance to the responses of the Wnt pathway not required for ß-catenin stabilization but for ß-catenin transcriptional activity. Moreover, we discuss the possible future implications, suggesting that the two cellular compartments where ß-catenin is localized, thus, the adherens junction complex and the Wnt signalosome, are more physically connected that previously thought.
[Mh] Termos MeSH primário: Cateninas/metabolismo
Receptores Wnt/metabolismo
Transcrição Genética/fisiologia
Via de Sinalização Wnt/fisiologia
[Mh] Termos MeSH secundário: Animais
Proteínas Desgrenhadas/metabolismo
Proteínas de Drosophila/metabolismo
Seres Humanos
Fatores de Transcrição/metabolismo
beta Catenina/metabolismo
Proteínas rac de Ligação ao GTP/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Catenins); 0 (DVL2 protein, human); 0 (Dishevelled Proteins); 0 (Drosophila Proteins); 0 (Rac1 protein, Drosophila); 0 (Receptors, Wnt); 0 (Transcription Factors); 0 (ZNF-kaiso protein, human); 0 (beta Catenin); 0 (delta catenin); EC 3.6.5.2 (rac GTP-Binding Proteins)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170621
[Lr] Data última revisão:
170621
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170310
[St] Status:MEDLINE
[do] DOI:10.1080/10409238.2017.1295920



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