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[PMID]:28465354
[Au] Autor:Farabegoli F; Govoni M; Spisni E; Papi A
[Ad] Endereço:Department of Pharmacology and Biotechnology (FaBiT), University of Bologna, Bologna, Italy fulvia.farabegoli@unibo.it.
[Ti] Título:EGFR inhibition by (-)-epigallocatechin-3-gallate and IIF treatments reduces breast cancer cell invasion.
[So] Source:Biosci Rep;37(3), 2017 Jun 30.
[Is] ISSN:1573-4935
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Epidermal growth factor receptor (EGFR) expression is an important marker in breast carcinoma pathology and is considered a pivotal molecule for cancer cell proliferation, invasion and metastasis. We investigated the effects of epigallocatechin-3-gallate (EGCG), the most active green tea catechin, in combination with 6-OH-11-O-hydroxyphenanthrene (IIF), a synthetic retinoid X receptor-γ (RXRγ) agonist, on three breast carcinoma cell lines: MCF-7, MCF-7TAM and MDA-MB-231. EGFR and AKT activation and molecular markers of cell motility and migration (CD44, extracellular matrix metalloproteinase (MMP) inducer (EMMPRIN), MMP-2, MMP-9 and tissue inhibitor of metalloproteinases (TIMPs)) were studied after EGCG and IIF treatments. The EGCG + IIF treatment was the most active in down-regulating EGFR phosphorylation at Tyr in all the investigated cell lines; p473AKT was also down-regulated in MCF-TAM cells. EGCG + IIF was also the most active treatment in reducing the expression of markers of invasion and migration in all the three cell lines: CD44, EMMPRIN, MMP-2 and -9 expression decreased, whereas TIMPs were up-regulated. Zymography and scratch assay also confirmed the reduced invasion tendency. We considered that EGCG and IIF treatments could alter the molecular network based on EGFR, CD44 and EMMPRIN expression interdependence and reduced the migration tendency in MCF-7, MCF-7TAM and MDA-MB-231 cells. These events only occurred in association with AKT inactivation in MCF-7TAM cells. In conclusion, the combination of EGCG and IIF significantly attenuated the invasive behaviour of breast carcinoma cells.
[Mh] Termos MeSH primário: Neoplasias da Mama/tratamento farmacológico
Catequina/análogos & derivados
Movimento Celular/efeitos dos fármacos
Invasividade Neoplásica/patologia
Fenantrenos/farmacologia
Receptor do Fator de Crescimento Epidérmico/antagonistas & inibidores
[Mh] Termos MeSH secundário: Basigina/metabolismo
Neoplasias da Mama/metabolismo
Neoplasias da Mama/patologia
Catequina/farmacologia
Linhagem Celular Tumoral
Regulação para Baixo/efeitos dos fármacos
Feminino
Seres Humanos
Células MCF-7
Metaloproteinase 2 da Matriz/metabolismo
Metaloproteinase 9 da Matriz/metabolismo
Fosforilação/efeitos dos fármacos
Inibidores de Proteínas Quinases/farmacologia
Proteínas Proto-Oncogênicas c-akt/metabolismo
Transdução de Sinais/efeitos dos fármacos
Inibidor Tecidual de Metaloproteinase-1/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (6-OH-11-O-hydroxyphenanthrene); 0 (Phenanthrenes); 0 (Protein Kinase Inhibitors); 0 (Tissue Inhibitor of Metalloproteinase-1); 136894-56-9 (Basigin); 8R1V1STN48 (Catechin); BQM438CTEL (epigallocatechin gallate); EC 2.7.10.1 (EGFR protein, human); EC 2.7.10.1 (Receptor, Epidermal Growth Factor); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 3.4.24.24 (Matrix Metalloproteinase 2); EC 3.4.24.35 (Matrix Metalloproteinase 9)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE


  2 / 1245 MEDLINE  
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[PMID]:29202620
[Au] Autor:Tramm T; Kyndi M; Sørensen FB; Overgaard J; Alsner J
[Ad] Endereço:a Department of Pathology , Aarhus University Hospital , Aarhus , Denmark.
[Ti] Título:Influence of intra-tumoral heterogeneity on the evaluation of BCL2, E-cadherin, EGFR, EMMPRIN, and Ki-67 expression in tissue microarrays from breast cancer.
[So] Source:Acta Oncol;57(1):102-106, 2018 Jan.
[Is] ISSN:1651-226X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: The influence of intra-tumoral heterogeneity on the evaluation of immunohistochemical (IHC) biomarker expression may affect the analytical validity of new biomarkers substantially and hence compromise the clinical utility. The aim of this study was to examine the influence of intra-tumoral heterogeneity as well as inter-observer variability on the evaluation of various IHC markers with potential prognostic impact in breast cancer (BCL2, E-cadherin, EGFR, EMMPRIN and Ki-67). MATERIAL AND METHODS: From each of 27 breast cancer patients, two tumor-containing paraffin blocks were chosen. Intra-tumoral heterogeneity was evaluated (1) within a single tumor-containing paraffin block ('intra-block agreement') by comparing information from a central, a peripheral tissue microarray (TMA) core and a whole slide section (WS), (2) between two different tumor-containing blocks from the same primary tumor ('inter-block agreement') by comparing information from TMA cores (central/peripheral) and WS. IHC markers on WS and TMA cores were evaluated by two observers independently, and agreements were estimated by Kappa statistics. RESULTS: For BCL2, E-cadherin and EGFR, an almost perfect intra- and inter-block agreement was found. EMMPRIN and Ki-67 showed a more heterogeneous expression with moderate to substantial intra-block agreements. For both stainings, there was a moderate inter-block agreement that improved slightly for EMMPRIN, when using WS instead of TMA cores. Inter-observer agreements were found to be almost perfect for BCL2, E-cadherin and EGFR (WS: κ > 0.82, TMAs: κ > 0.90), substantial for EMMPRIN (κ > 0.63), but only fair to moderate for Ki-67 (WS: κ = 0.54, TMAs: κ = 0.33). CONCLUSIONS: BCL2, E-cadherin and EGFR were found to be homogeneously expressed, whereas EMMPRIN and Ki-67 showed a more pronounced degree of intra-tumoral heterogeneity. The results emphasize the importance of securing the analytical validity of new biomarkers by examining the intra-tumoral heterogeneity of immunohistochemical stainings applied to TMA cores individually in each type of cancer.
[Mh] Termos MeSH primário: Neoplasias da Mama/metabolismo
[Mh] Termos MeSH secundário: Basigina/metabolismo
Biomarcadores Tumorais/metabolismo
Caderinas/metabolismo
Carcinoma Ductal de Mama/metabolismo
Carcinoma Lobular/metabolismo
Feminino
Seres Humanos
Imuno-Histoquímica
Antígeno Ki-67/metabolismo
Proteínas Proto-Oncogênicas c-bcl-2/metabolismo
Receptor do Fator de Crescimento Epidérmico/metabolismo
Análise Serial de Tecidos
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (BCL2 protein, human); 0 (BSG protein, human); 0 (Biomarkers, Tumor); 0 (CDH1 protein, human); 0 (Cadherins); 0 (Ki-67 Antigen); 0 (Proto-Oncogene Proteins c-bcl-2); 136894-56-9 (Basigin); EC 2.7.10.1 (EGFR protein, human); EC 2.7.10.1 (Receptor, Epidermal Growth Factor)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180201
[Lr] Data última revisão:
180201
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171206
[St] Status:MEDLINE
[do] DOI:10.1080/0284186X.2017.1404128


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[PMID]:29253870
[Au] Autor:Sasidhar MV; Chevooru SK; Eickelberg O; Hartung HP; Neuhaus O
[Ad] Endereço:Department of Neurology, Heinrich Heine University, Düsseldorf, Germany.
[Ti] Título:Downregulation of monocytic differentiation via modulation of CD147 by 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors.
[So] Source:PLoS One;12(12):e0189701, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:CD147 is an activation induced glycoprotein that promotes the secretion and activation of matrix metalloproteinases (MMPs) and is upregulated during the differentiation of macrophages. Interestingly, some of the molecular functions of CD147 rely on its glycosylation status: the highly glycosylated forms of CD147 induce MMPs whereas the lowly glycosylated forms inhibit MMP activation. Statins are hydroxy-methylglutaryl coenzyme A reductase inhibitors that block the synthesis of mevalonate, thereby inhibiting all mevalonate-dependent pathways, including isoprenylation, N-glycosylation and cholesterol synthesis. In this study, we investigated the role of statins in the inhibition of macrophage differentiation and the associated process of MMP secretion through modulation of CD147. We observed that differentiation of the human monocytic cell line THP-1 to a macrophage phenotype led to upregulation of CD147 and CD14 and that this effect was inhibited by statins. At the molecular level, statins altered CD147 expression, structure and function by inhibiting isoprenylation and N-glycosylation. In addition, statins induced a shift of CD147 from its highly glycosylated form to its lowly glycosylated form. This shift in N-glycosylation status was accompanied by a decrease in the production and functional activity of MMP-2 and MMP-9. In conclusion, these findings describe a novel molecular mechanism of immune regulation by statins, making them interesting candidates for autoimmune disease therapy.
[Mh] Termos MeSH primário: Basigina/metabolismo
Inibidores de Hidroximetilglutaril-CoA Redutases/química
Receptores de Lipopolissacarídeos/metabolismo
Monócitos/efeitos dos fármacos
[Mh] Termos MeSH secundário: Doenças Autoimunes
Biotinilação
Diferenciação Celular
Membrana Celular/metabolismo
Glicosilação
Seres Humanos
Sistema Imunitário
Macrófagos/citologia
Macrófagos/efeitos dos fármacos
Metaloproteinase 2 da Matriz/metabolismo
Metaloproteinase 9 da Matriz/metabolismo
Monócitos/citologia
Permeabilidade
Fenótipo
Prenilação
Células THP-1
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (BSG protein, human); 0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors); 0 (Lipopolysaccharide Receptors); 136894-56-9 (Basigin); EC 3.4.24.24 (MMP2 protein, human); EC 3.4.24.24 (Matrix Metalloproteinase 2); EC 3.4.24.35 (MMP9 protein, human); EC 3.4.24.35 (Matrix Metalloproteinase 9)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180108
[Lr] Data última revisão:
180108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171219
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189701


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[PMID]:29034777
[Au] Autor:Wang S; Liu C; Liu X; He Y; Shen D; Luo Q; Dong Y; Dong H; Pang Z
[Ad] Endereço:Department of General Surgery, The Second Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
[Ti] Título:Effects of matrix metalloproteinase inhibitor doxycycline and CD147 antagonist peptide-9 on gallbladder carcinoma cell lines.
[So] Source:Tumour Biol;39(10):1010428317718192, 2017 Oct.
[Is] ISSN:1423-0380
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Gallbladder carcinoma is the most common and aggressive malignancy of the biliary tree and highly expresses CD147, which is closely related to disease prognosis in a variety of human cancers. Doxycycline exhibited anti-tumor properties in many cancer cells. CD147 antagonist peptide-9 is a polypeptide and can specifically bind to CD147. The effect of these two drugs on gallbladder cancer cells has not been studied. The aim of this study is to investigate the effect of doxycycline and antagonist peptide-9 on gallbladder carcinoma cells and the possible mechanism of inhibition on cancer cell of doxycycline. To investigate the effects of doxycycline and antagonist peptide-9 on gallbladder carcinoma cells (GBC-SD and SGC-996), cell proliferation, CD147 expression, and early-stage apoptosis rate were measured after treated with doxycycline. Matrix metalloproteinase-2 and matrix metalloproteinase-9 activities were measured after treated with different concentrations of doxycycline, antagonist peptide-9, and their combination. The results demonstrated that doxycycline inhibited cell proliferation, reduced CD147 expression level, and induced an early-stage apoptosis response in GBC-SD and SGC-996 cells. The matrix metalloproteinase-2 and matrix metalloproteinase-9 activities were inhibited by antagonist peptide-9 and doxycycline, and the inhibitory effects were enhanced by combined drugs in gallbladder carcinoma cell lines. Taken together, doxycycline showed inhibitory effects on gallbladder carcinoma cell lines and reduced the expression of CD147, and this may be the mechanism by which doxycycline inhibits cancer cells. This study provides new information and tries to implement the design of adjuvant therapy method for gallbladder carcinoma.
[Mh] Termos MeSH primário: Basigina/metabolismo
Doxiciclina/farmacologia
Neoplasias da Vesícula Biliar/tratamento farmacológico
Inibidores de Metaloproteinases de Matriz/farmacologia
Peptídeos/farmacologia
[Mh] Termos MeSH secundário: Apoptose/efeitos dos fármacos
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Neoplasias da Vesícula Biliar/metabolismo
Seres Humanos
Metaloproteinase 2 da Matriz/metabolismo
Metaloproteinase 9 da Matriz/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Matrix Metalloproteinase Inhibitors); 0 (Peptides); 136894-56-9 (Basigin); EC 3.4.24.24 (Matrix Metalloproteinase 2); EC 3.4.24.35 (Matrix Metalloproteinase 9); N12000U13O (Doxycycline)
[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:171017
[St] Status:MEDLINE
[do] DOI:10.1177/1010428317718192


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[PMID]:28832687
[Au] Autor:Chen J; Peng C; Lei L; Zhang J; Zeng W; Chen X
[Ad] Endereço:Department of Dermatology, Xiangya Hospital, Central South University. Changsha, Hunan, P.R. China.
[Ti] Título:Nuclear envelope-distributed CD147 interacts with and inhibits the transcriptional function of RING1 and promotes melanoma cell motility.
[So] Source:PLoS One;12(8):e0183689, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Melanoma accounts for nearly 80% of all deaths associated with skin cancer.CD147 plays a very important role in melanoma progression and the expression level may correlate with tumor malignancy. RING1 can bind DNA and act as a transcriptional repressor, play an important role in the aggressive phenotype in melanoma. The interactions between CD147 and RING1 were identified with a yeast two-hybrid and RING1 interacted with CD147 through the transmembrane domain. RING1 inhibits CD147's capability promoting melanoma cell migration. In conclusion, the study identified novel interactions between CD147 and RING1, recovered CD147 nuclear envelope distribution in melanoma cells, and suggested a new mechanism underlying how cytoplasmic CD147 promotes melanoma development.
[Mh] Termos MeSH primário: Basigina/imunologia
Movimento Celular/imunologia
Melanoma/patologia
Membrana Nuclear/imunologia
Complexo Repressor Polycomb 1/fisiologia
Transcrição Genética/fisiologia
[Mh] Termos MeSH secundário: Basigina/genética
Técnicas de Silenciamento de Genes
Seres Humanos
Melanoma/metabolismo
Complexo Repressor Polycomb 1/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
136894-56-9 (Basigin); EC 2.3.2.27 (Polycomb Repressive Complex 1); EC 2.3.2.27 (RING1 protein, human)
[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:170824
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0183689


  6 / 1245 MEDLINE  
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[PMID]:28729360
[Au] Autor:Dawar FU; Xiong Y; Khattak MNK; Li J; Lin L; Mei J
[Ad] Endereço:College of Fisheries, Huazhong Agricultural University, Wuhan, Hubei, China.
[Ti] Título:Potential role of cyclophilin A in regulating cytokine secretion.
[So] Source:J Leukoc Biol;102(4):989-992, 2017 Oct.
[Is] ISSN:1938-3673
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cyclophilin A (CypA), a peptidylprolyl - isomerase, is a ubiquitous and multifunctional protein. In addition to its role as a host-cell receptor for cyclosporine A, CypA has diverse functions in inflammatory conditions and diseases. CypA secreted in response to inflammatory stimuli binds to the cell surface via its receptor CD147 and induces secretion of various inflammatory cytokines. However, silencing and inhibition of either CypA or CD147 inhibits inflammatory cytokine expression and inflammation. This report reviews the literature related to the mechanism of CypA-dependent cytokine secretion and discusses this factor as a possible therapeutic target in inflammatory diseases.
[Mh] Termos MeSH primário: Basigina/imunologia
Ciclofilina A/imunologia
Citocinas/imunologia
[Mh] Termos MeSH secundário: Animais
Seres Humanos
Inflamação/imunologia
Inflamação/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (BSG protein, human); 0 (Cytokines); 136894-56-9 (Basigin); EC 5.2.1.- (Cyclophilin A)
[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:170722
[St] Status:MEDLINE
[do] DOI:10.1189/jlb.3RU0317-090RR


  7 / 1245 MEDLINE  
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[PMID]:28716558
[Au] Autor:Kanemitsu M; Tsupykov O; Potter G; Boitard M; Salmon P; Zgraggen E; Gascon E; Skibo G; Dayer AG; Kiss JZ
[Ad] Endereço:Department of Basic Neurosciences, University Medical Center, University of Geneva Medical School, Geneva, Switzerland.
[Ti] Título:EMMPRIN overexpression in SVZ neural progenitor cells increases their migration towards ischemic cortex.
[So] Source:Exp Neurol;297:14-24, 2017 Nov.
[Is] ISSN:1090-2430
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Stimulation of endogenous neurogenesis and recruitment of neural progenitors from the subventricular zone (SVZ) neurogenic site may represent a useful strategy to improve regeneration in the ischemic cortex. Here, we tested whether transgenic overexpression of extracellular matrix metalloproteinase inducer (EMMPRIN), the regulator of matrix metalloproteinases (MMPs) expression, in endogenous neural progenitor cells (NPCs) in the subventricular zone (SVZ) could increase migration towards ischemic injury. For this purpose, we applied a lentivector-mediated gene transfer system. We found that EMMPRIN-transduced progenitors exhibited enhanced MMP-2 activity in vitro and showed improved motility in 3D collagen gel as well as in cortical slices. Using a rat model of neonatal ischemia, we showed that EMMPRIN overexpressing SVZ cells invade the injured cortical tissue more efficiently than controls. Our results suggest that EMMPRIN overexpression could be suitable approach to improve capacities of endogenous or transplanted progenitors to invade the injured cortex.
[Mh] Termos MeSH primário: Basigina/biossíntese
Isquemia Encefálica/metabolismo
Movimento Celular/fisiologia
Córtex Cerebral/metabolismo
Ventrículos Laterais/metabolismo
Células-Tronco Neurais/metabolismo
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Basigina/genética
Isquemia Encefálica/patologia
Córtex Cerebral/patologia
Expressão Gênica
Ventrículos Laterais/patologia
Técnicas de Cultura de Órgãos
Ratos
Ratos Sprague-Dawley
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
136894-56-9 (Basigin)
[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:170719
[St] Status:MEDLINE


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[PMID]:28700599
[Au] Autor:Li H; Jiang C; Wu D; Shi S; Liao M; Wang J; Li Y; Xu Z
[Ad] Endereço:Reproductive Department, Xiangya Hospital, Central South University, Changsha, China.
[Ti] Título:The prognostic and clinicopathologic characteristics of CD147 and esophagus cancer: A meta-analysis.
[So] Source:PLoS One;12(7):e0180271, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: The prognostic significance of CD147 expression in esophageal cancer patients remains controversial. Using a meta-analysis, we investigated the prognostic and clinicopathologic characteristics of CD147 in esophageal cancer. METHODS: A comprehensive literature search of the PubMed (1966-2016), EMBASE (1980-2016), Cochrane Library (1996-2016), Web of Science (1945-2016), China National Knowledge Infrastructure (1982-2016), and Wanfang databases (1988-2016) was performed to identify studies of all esophageal cancer subtypes. Correlations between CD147 expression and survival outcomes and clinicopathological features were analyzed using meta-analysis methods. RESULTS: Seventeen studies were included. High CD147 expression reduced the 3-year survival rate (OR = 3.26, 95% CI = (1.53, 6.93), p = 0.02) and 5-year survival rate(OR = 4.35, 95% CI = (2.13, 8.90), p < 0.0001). High CD147 expression reduced overall survival in esophageal cancer (HR = 1.60, 95% CI = (1.19, 2.15), p = 0.02). Additionally, higher CD147 expression was detected in esophageal cancer tissues than noncancerous tissues (OR = 9.45, 95% CI = (5.39, 16.59), p < 0.00001), normal tissues (OR = 12.73, 95% CI = (3.49, 46.46), p = 0.0001), para-carcinoma tissues (OR = 12.80, 95% CI = (6.57, 24.92), p < 0.00001), and hyperplastic tissues (OR = 3.27, 95% CI = (1.47, 7.29), p = 0.004). CD147 expression was associated with TNM stage (OR = 3.66, 95% CI = (2.20, 6.09), p < 0.00001), tumor depth (OR = 7.97, 95% CI = (4.13, 15.38), p < 0.00001), and lymph node status (OR = 5.14, 95% CI = (2.03,13.01), p = 0.0005), but not with tumor differentiation, age, or sex. CONCLUSION: Our meta-analysis suggests that CD147 is an efficient prognostic factor in esophageal cancer. High CD147 expression in patients with esophageal cancer was associated with worse survival outcomes and common clinicopathological indicators of poor prognosis.
[Mh] Termos MeSH primário: Basigina/sangue
Biomarcadores Tumorais/sangue
Neoplasias Esofágicas/sangue
Neoplasias Esofágicas/patologia
[Mh] Termos MeSH secundário: Feminino
Seres Humanos
Masculino
Prognóstico
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 136894-56-9 (Basigin)
[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:170713
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0180271


  9 / 1245 MEDLINE  
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[PMID]:28684116
[Au] Autor:Qin H; Rasul A; Li X; Masood M; Yang G; Wang N; Wei W; He X; Watanabe N; Li J; Li X
[Ad] Endereço:The Key Laboratory of Molecular Epigenetic, Institute of Genetics and Cytology, Northeast Normal University, Changchun 130024, PR China.
[Ti] Título:CD147-induced cell proliferation is associated with Smad4 signal inhibition.
[So] Source:Exp Cell Res;358(2):279-289, 2017 Sep 15.
[Is] ISSN:1090-2422
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:CD147 is a multifunctional trans-membrane glycoprotein, which is highly expressed in many cancers. However, the mechanism by which CD147 modulates cell proliferation is not fully understood. The aim of this study is to investigate the role of CD147 in cell proliferation associated with the TGF-ß/Smad4 signaling pathway. Here, we used cell viability and clone formation assays in LNCaP prostate cancer cells to demonstrate that CD147 promotes cell proliferation. The luciferase assay and western blotting show that silencing CD147 using shRNA enhances transcription and expression of p21 . Using immunofluorescence and nuclear-cytoplasmic separation, we show that this is primarily attributed to transport of Smad4 from the cytoplasm to nucleus. Other assays (GST pull-down, co-immunoprecipitation and immunofluorescence) demonstrate that Smad4 is a new interaction partner of CD147, with the Smad4 MH2 domain and CD147 intracellular domain (CD147-ICD) being involved in the interaction. Furthermore, we report that a phosphoserine (pSer) in CD147 (pSer252) is responsible for this interaction and inhibition of the Smad4/p21 signal that promotes cell proliferation. Our results provide a novel molecular mechanism for CD147-induced cell proliferation associated with Smad4 signal inhibition.
[Mh] Termos MeSH primário: Basigina/genética
Proliferação Celular/genética
Regiões Promotoras Genéticas/genética
Transdução de Sinais/genética
Proteína Smad4/metabolismo
[Mh] Termos MeSH secundário: Basigina/metabolismo
Linhagem Celular Tumoral
Núcleo Celular/metabolismo
Citoplasma/metabolismo
Seres Humanos
Transativadores/metabolismo
Fator de Crescimento Transformador beta/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (BSG protein, human); 0 (SMAD4 protein, human); 0 (Smad4 Protein); 0 (Trans-Activators); 0 (Transforming Growth Factor beta); 136894-56-9 (Basigin)
[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:170708
[St] Status:MEDLINE


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[PMID]:28666119
[Au] Autor:Rusu V; Hoch E; Mercader JM; Tenen DE; Gymrek M; Hartigan CR; DeRan M; von Grotthuss M; Fontanillas P; Spooner A; Guzman G; Deik AA; Pierce KA; Dennis C; Clish CB; Carr SA; Wagner BK; Schenone M; Ng MCY; Chen BH; Centeno-Cruz F; Zerrweck C; Orozco L; Altshuler DM; Schreiber SL; Florez JC; Jacobs SBR; Lander ES; MEDIA Consortium; SIGMA T2D Consortium
[Ad] Endereço:Program in Biological and Biomedical Sciences, Harvard Medical School, Boston, MA 02115, USA; Program in Medical and Population Genetics, Broad Institute of Harvard and MIT, Cambridge, MA 02142, USA.
[Ti] Título:Type 2 Diabetes Variants Disrupt Function of SLC16A11 through Two Distinct Mechanisms.
[So] Source:Cell;170(1):199-212.e20, 2017 Jun 29.
[Is] ISSN:1097-4172
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Type 2 diabetes (T2D) affects Latinos at twice the rate seen in populations of European descent. We recently identified a risk haplotype spanning SLC16A11 that explains ∼20% of the increased T2D prevalence in Mexico. Here, through genetic fine-mapping, we define a set of tightly linked variants likely to contain the causal allele(s). We show that variants on the T2D-associated haplotype have two distinct effects: (1) decreasing SLC16A11 expression in liver and (2) disrupting a key interaction with basigin, thereby reducing cell-surface localization. Both independent mechanisms reduce SLC16A11 function and suggest SLC16A11 is the causal gene at this locus. To gain insight into how SLC16A11 disruption impacts T2D risk, we demonstrate that SLC16A11 is a proton-coupled monocarboxylate transporter and that genetic perturbation of SLC16A11 induces changes in fatty acid and lipid metabolism that are associated with increased T2D risk. Our findings suggest that increasing SLC16A11 function could be therapeutically beneficial for T2D. VIDEO ABSTRACT.
[Mh] Termos MeSH primário: Diabetes Mellitus Tipo 2/metabolismo
Transportadores de Ácidos Monocarboxílicos/genética
Transportadores de Ácidos Monocarboxílicos/metabolismo
[Mh] Termos MeSH secundário: Basigina/metabolismo
Membrana Celular/metabolismo
Cromossomos Humanos Par 17/metabolismo
Técnicas de Silenciamento de Genes
Haplótipos
Hepatócitos/metabolismo
Heterozigoto
Código das Histonas
Seres Humanos
Fígado/metabolismo
Modelos Moleculares
Transportadores de Ácidos Monocarboxílicos/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (BSG protein, human); 0 (Monocarboxylic Acid Transporters); 0 (SLC16A11 protein, human); 136894-56-9 (Basigin)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170701
[St] Status:MEDLINE



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