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  1 / 1083 MEDLINE  
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[PMID]:28899658
[Au] Autor:Chetty CJ; Ferreira E; Jovanovic K; Weiss SFT
[Ad] Endereço:School of Molecular and Cell Biology, University of the Witwatersrand, Private Bag 3, Wits 2050, Johannesburg, Republic of South Africa.
[Ti] Título:Knockdown of LRP/LR induces apoptosis in pancreatic cancer and neuroblastoma cells through activation of caspases.
[So] Source:Exp Cell Res;360(2):264-272, 2017 Nov 15.
[Is] ISSN:1090-2422
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The 37kDa/67kDa laminin receptor (LRP/LR) serves various physiological and pathological roles such as enhancing tumour-related processes including metastasis, angiogenesis, cellular viability and telomerase activation in cancerous cell lines. The present study investigates the effect of siRNA mediated downregulation of LRP/LR on pancreatic cancer (AsPC-1) and neuroblastoma (IMR-32) cells. MTT and BrdU assays revealed that siRNA mediated downregulation of LRP resulted in a significant reduction in cell viability and cell proliferation. In addition, knock-down of LRP resulted in phosphatidylserine externalization, diminished nuclear integrity and significantly enhanced caspase-3 activity, which is indicative of apoptosis. LRP downregulation resulted in a significant increase in caspase-8 activity in IMR-32 cells and enhanced caspase-8 and 9 activity in AsPC-1 cells. These data recommend siRNA mediated knock-down of LRP as a potential therapeutic avenue for the treatment of pancreatic cancer and neuroblastoma.
[Mh] Termos MeSH primário: Apoptose/genética
Caspases/metabolismo
Neuroblastoma/genética
Neoplasias Pancreáticas/genética
Receptores de Laminina/genética
[Mh] Termos MeSH secundário: Apoptose/efeitos dos fármacos
Ativação Enzimática/efeitos dos fármacos
Ativação Enzimática/genética
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Técnicas de Silenciamento de Genes
Seres Humanos
Neuroblastoma/patologia
Neoplasias Pancreáticas/patologia
RNA Interferente Pequeno/farmacologia
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (RNA, Small Interfering); 0 (Receptors, Laminin); EC 3.4.22.- (Caspases)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170914
[St] Status:MEDLINE


  2 / 1083 MEDLINE  
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[PMID]:28618937
[Au] Autor:Zhou Y; Wang Y; Zhao Z; Wang Y; Zhang N; Zhang H; Liu L
[Ad] Endereço:1 Department of Thoracic Surgery, Tangdu Hospital, The Fourth Military Medical University, Xi'an, China.
[Ti] Título:37LRP induces invasion in hypoxic lung adenocarcinoma cancer cells A549 through the JNK/ERK/c-Jun signaling cascade.
[So] Source:Tumour Biol;39(6):1010428317701655, 2017 Jun.
[Is] ISSN:1423-0380
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We previously reported that 37-kDa laminin receptor precursor involved in metastasis of lung adenocarcinoma cancer cells. In this study, we further revealed that hypoxia induced 37-kDa laminin receptor precursor expression and activation of extracellular signal-regulated protein kinase, c-Jun N-terminal kinase, and p38 mitogen-activated protein kinase in lung adenocarcinoma cancer cells. In addition, we further demonstrated that the c-Jun N-terminal kinase inhibitor SP600125 and extracellular signal-regulated protein kinase inhibitor U0126 blocked the c-Jun activity and abolished hypoxia-induced 37-kDa laminin receptor precursor expression and promoter activity in a concentration-dependent manner. However, the p38 mitogen-activated protein kinase inhibitor did not affect 37-kDa laminin receptor precursor expression and c-Jun activity in response to hypoxia. Furthermore, downregulated c-Jun expression by short interfering RNA could also inhibit hypoxia-induced 37-kDa laminin receptor precursor expression and transcriptional activity. The inhibition of 37-kDa laminin receptor precursor expression by SP600125 and U0126 could be rescued by c-Jun overexpression. Studies using luciferase promoter constructs revealed a significant increase in the activity of promoter binding in the cells exposed to hypoxia, which was lost in the cells with mutation of the activator protein 1 binding site. Electrophoresis mobility shift assay and chromatin immunoprecipitation demonstrated a functional activator protein 1 binding site within 37-kDa laminin receptor precursor gene regulatory sequence located at -271 relative to the transcriptional initiation point. Hypoxia-induced invasion of A549 cells was inhibited by the pharmacologic inhibitors of c-Jun N-terminal kinase (SP600125) and extracellular signal-regulated protein kinase (U0126) as well as 37-kDa laminin receptor precursor-specific siRNA or antibody. Our results suggest that hypoxia-elicited c-Jun/activator protein 1 regulates 37-kDa laminin receptor precursor expression, which modulates migration and invasion of lung adenocarcinoma cells.
[Mh] Termos MeSH primário: Adenocarcinoma/genética
Proteínas Quinases JNK Ativadas por Mitógeno/genética
Neoplasias Pulmonares/genética
MAP Quinase Quinase 4/genética
Receptores de Laminina/genética
[Mh] Termos MeSH secundário: Células A549
Adenocarcinoma/patologia
Antracenos/administração & dosagem
Butadienos/administração & dosagem
Seres Humanos
Proteínas Quinases JNK Ativadas por Mitógeno/antagonistas & inibidores
Neoplasias Pulmonares/patologia
MAP Quinase Quinase 4/antagonistas & inibidores
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Nitrilos/administração & dosagem
Fosforilação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anthracenes); 0 (Butadienes); 0 (Nitriles); 0 (Receptors, Laminin); 0 (U 0126); 1TW30Y2766 (pyrazolanthrone); EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases); EC 2.7.12.2 (MAP Kinase Kinase 4)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170718
[Lr] Data última revisão:
170718
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170617
[St] Status:MEDLINE
[do] DOI:10.1177/1010428317701655


  3 / 1083 MEDLINE  
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[PMID]:28334989
[Au] Autor:Nunes AM; Wuebbles RD; Sarathy A; Fontelonga TM; Deries M; Burkin DJ; Thorsteinsdóttir S
[Ad] Endereço:Departamento de Biologia Animal, Centro de Ecologia, Evolução e Alterações Ambientais, Faculdade de Ciências, Universidade de Lisboa, 1749-016 Lisbon, Portugal.
[Ti] Título:Impaired fetal muscle development and JAK-STAT activation mark disease onset and progression in a mouse model for merosin-deficient congenital muscular dystrophy.
[So] Source:Hum Mol Genet;26(11):2018-2033, 2017 Jun 01.
[Is] ISSN:1460-2083
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Merosin-deficient congenital muscular dystrophy type 1A (MDC1A) is a dramatic neuromuscular disease in which crippling muscle weakness is evident from birth. Here, we use the dyW mouse model for human MDC1A to trace the onset of the disease during development in utero. We find that myotomal and primary myogenesis proceed normally in homozygous dyW-/- embryos. Fetal dyW-/- muscles display the same number of myofibers as wildtype (WT) muscles, but by E18.5 dyW-/- muscles are significantly smaller and muscle size is not recovered post-natally. These results suggest that fetal dyW-/- myofibers fail to grow at the same rate as WT myofibers. Consistent with this hypothesis between E17.5 and E18.5 dyW-/- muscles display a dramatic drop in the number of Pax7- and myogenin-positive cells relative to WT muscles, suggesting that dyW-/- muscles fail to generate enough muscle cells to sustain fetal myofiber growth. Gene expression analysis of dyW-/- E17.5 muscles identified a significant increase in the expression of the JAK-STAT target gene Pim1 and muscles from 2-day and 3-week old dyW-/- mice demonstrate a dramatic increase in pSTAT3 relative to WT muscles. Interestingly, myotubes lacking integrin α7ß1, a laminin-receptor, also show a significant increase in pSTAT3 levels compared with WT myotubes, indicating that α7ß1 can act as a negative regulator of STAT3 activity. Our data reveal for the first time that dyW-/- mice exhibit a myogenesis defect already in utero. We propose that overactivation of JAK-STAT signaling is part of the mechanism underlying disease onset and progression in dyW-/- mice.
[Mh] Termos MeSH primário: Desenvolvimento Muscular/fisiologia
Distrofias Musculares/metabolismo
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Janus Quinase 1/metabolismo
Laminina/metabolismo
Camundongos
Fibras Musculares Esqueléticas/metabolismo
Músculo Esquelético/metabolismo
Distrofias Musculares/embriologia
Distrofias Musculares/genética
Distrofia Muscular Animal/embriologia
Distrofia Muscular Animal/metabolismo
Miogenina/metabolismo
Fator de Transcrição PAX7/metabolismo
Receptores de Laminina
Fator de Transcrição STAT3/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Laminin); 0 (Myogenin); 0 (PAX7 Transcription Factor); 0 (Pax7 protein, mouse); 0 (Receptors, Laminin); 0 (STAT3 Transcription Factor); 0 (Stat3 protein, mouse); EC 2.7.10.2 (Jak1 protein, mouse); EC 2.7.10.2 (Janus Kinase 1)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171017
[Lr] Data última revisão:
171017
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170324
[St] Status:MEDLINE
[do] DOI:10.1093/hmg/ddx083


  4 / 1083 MEDLINE  
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[PMID]:28154178
[Au] Autor:Kumazoe M; Nakamura Y; Yamashita M; Suzuki T; Takamatsu K; Huang Y; Bae J; Yamashita S; Murata M; Yamada S; Shinoda Y; Yamaguchi W; Toyoda Y; Tachibana H
[Ad] Endereço:From the Division of Applied Biological Chemistry, Department of Bioscience and Biotechnology, Faculty of Agriculture, Kyushu University, Fukuoka 812-8581 and.
[Ti] Título:Green Tea Polyphenol Epigallocatechin-3-gallate Suppresses Toll-like Receptor 4 Expression via Up-regulation of E3 Ubiquitin-protein Ligase RNF216.
[So] Source:J Biol Chem;292(10):4077-4088, 2017 Mar 10.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Toll-like receptor 4 (TLR4) plays an essential role in innate immunity through inflammatory cytokine induction. Recent studies demonstrated that the abnormal activation of TLR4 has a pivotal role in obesity-induced inflammation, which is associated with several diseases, including hyperinsulinemia, hypertriglyceridemia, and cardiovascular disease. Here we demonstrate that (-)-epigallocatechin-3- -gallate, a natural agonist of the 67-kDa laminin receptor (67LR), suppressed TLR4 expression through E3 ubiquitin-protein ring finger protein 216 (RNF216) up-regulation. Our data indicate cyclic GMP mediates 67LR agonist-dependent RNF216 up-regulation. Moreover, we show that the highly absorbent 67LR agonist (-)-epigallocatechin-3- -(3- -methyl)-gallate (EGCG3″Me) significantly attenuated TLR4 expression in the adipose tissue. EGCG3″Me completely inhibited the high-fat/high-sucrose (HF/HS)-induced up-regulation of tumor necrosis factor α in adipose tissue and serum monocyte chemoattractant protein-1 increase. Furthermore, this agonist intake prevented HF/HS-induced hyperinsulinemia and hypertriglyceridemia. Taken together, 67LR presents an attractive target for the relief of obesity-induced inflammation.
[Mh] Termos MeSH primário: Catequina/análogos & derivados
Regulação da Expressão Gênica/efeitos dos fármacos
Macrófagos Peritoneais/efeitos dos fármacos
Receptores de Laminina/metabolismo
Chá/química
Receptor 4 Toll-Like/metabolismo
Ubiquitina-Proteína Ligases/metabolismo
[Mh] Termos MeSH secundário: Animais
Catequina/farmacologia
Células Cultivadas
Hiperinsulinismo/metabolismo
Hiperinsulinismo/prevenção & controle
Hipertrigliceridemia/metabolismo
Hipertrigliceridemia/prevenção & controle
Inflamação/etiologia
Inflamação/prevenção & controle
Lipopolissacarídeos/farmacologia
Macrófagos Peritoneais/citologia
Macrófagos Peritoneais/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
NF-kappa B/genética
NF-kappa B/metabolismo
Obesidade/etiologia
Obesidade/prevenção & controle
Receptores de Laminina/agonistas
Receptores de Laminina/genética
Transdução de Sinais/efeitos dos fármacos
Receptor 4 Toll-Like/genética
Ativação Transcricional
Fator de Necrose Tumoral alfa/genética
Fator de Necrose Tumoral alfa/metabolismo
Ubiquitina-Proteína Ligases/genética
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Lipopolysaccharides); 0 (NF-kappa B); 0 (Receptors, Laminin); 0 (Tea); 0 (Tlr4 protein, mouse); 0 (Toll-Like Receptor 4); 0 (Tumor Necrosis Factor-alpha); 8R1V1STN48 (Catechin); BQM438CTEL (epigallocatechin gallate); EC 2.3.2.27 (RNF216 protein, mouse); EC 2.3.2.27 (Ubiquitin-Protein Ligases)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170727
[Lr] Data última revisão:
170727
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170204
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M116.755959


  5 / 1083 MEDLINE  
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[PMID]:28118986
[Au] Autor:Munien C; Rebelo TM; Ferreira E; Weiss SF
[Ad] Endereço:From the School of Molecular and Cell Biology, University of the Witwatersrand, Johannesburg, South Africa. Electronic address: 727874@students.wits.ac.za.
[Ti] Título:IgG1-iS18 impedes the adhesive and invasive potential of early and late stage malignant melanoma cells.
[So] Source:Exp Cell Res;351(2):135-141, 2017 Feb 15.
[Is] ISSN:1090-2422
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The 37kDa/67kDa laminin receptor (LRP/LR) is a non-integrin laminin receptor which is overexpressed in tumorigenic cells and supports progression of cancer via promoting metastasis, angiogenesis and telomerase activity and impediment of apoptosis. The present study investigates the role of LRP/LR on the metastatic potential of early (A375) and late (A375SM) stage malignant melanoma cells. Flow cytometry revealed that both early and late stage malignant melanoma cells display high levels of LRP/LR on their cell surface. Flow cytometry and western blot analysis showed that late stage malignant melanoma cells display significantly higher total and cell surface LRP/LR levels in comparison to early stage malignant melanoma cells and the poorly invasive breast cancer (MCF-7) control cell line. Targeting LRP/LR using the LRP/LR specific antibody IgG1-iS18 resulted in a significant reduction of the adhesive potential to laminin-1 and the invasive potential through the 'ECM-simulating' Matrigel™ of both early and late stage malignant melanoma cells. Furthermore, Pearson's correlation coefficient confirmed that increased LRP levels correlate with the increased invasive and adhesive potential in early and late stage melanoma cells. Thus, blocking LRP/LR using the IgG1-iS18 antibody may therefore be a promising therapeutic strategy for early and late stage malignant melanoma treatment.
[Mh] Termos MeSH primário: Anticorpos Antineoplásicos/farmacologia
Anticorpos Neutralizantes/farmacologia
Regulação Neoplásica da Expressão Gênica
Imunoglobulina G/farmacologia
Melanoma/imunologia
Receptores de Laminina/antagonistas & inibidores
[Mh] Termos MeSH secundário: Adesão Celular/efeitos dos fármacos
Movimento Celular/efeitos dos fármacos
Colágeno/química
Combinação de Medicamentos
Feminino
Citometria de Fluxo
Seres Humanos
Laminina/química
Células MCF-7
Melanoma/genética
Melanoma/patologia
Estadiamento de Neoplasias
Proteoglicanas/química
Receptores de Laminina/genética
Receptores de Laminina/imunologia
Transdução de Sinais
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Neoplasm); 0 (Antibodies, Neutralizing); 0 (Drug Combinations); 0 (Immunoglobulin G); 0 (Laminin); 0 (Proteoglycans); 0 (Receptors, Laminin); 0 (laminin 1); 119978-18-6 (matrigel); 9007-34-5 (Collagen)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170518
[Lr] Data última revisão:
170518
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170126
[St] Status:MEDLINE


  6 / 1083 MEDLINE  
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[PMID]:27884119
[Au] Autor:Rebelo TM; Chetty CJ; Ferreira E; Weiss SF
[Ad] Endereço:School of Molecular and Cell Biology, University of the Witwatersrand, Johannesburg, Republic of South Africa (RSA).
[Ti] Título:Anti-LRP/LR-specific antibody IgG1-iS18 impedes adhesion and invasion of pancreatic cancer and neuroblastoma cells.
[So] Source:BMC Cancer;16(1):917, 2016 11 24.
[Is] ISSN:1471-2407
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Cancer has become a global burden due to its high incidence and mortality rates, with an estimated 14.1 million cancer cases reported worldwide in 2012 particularly as a result of metastasis. Metastasis involves two crucial steps: adhesion and invasion, and the non-integrin receptor; the 37-kDa/67-kDa laminin receptor precursor/ high affinity laminin receptor (LRP/LR) has been shown to be overexpressed on the surface of tumorigenic cells, thus being implicated in the enhancement of these two crucial steps. The current study investigated the role of LRP/LR on the aggressiveness of pancreatic cancer (AsPC-1) and neuroblastoma (IMR-32) cells with respect to their adhesive and invasive potential. METHODS: AsPC-1 and IMR-32 cells were utilized as the experimental cell lines for the study. Cell surface LRP/LR levels were visualised and quantified on the experimental and control (MCF-7) cell lines via confocal microscopy and flow cytometry, respectively. Total LRP/LR levels in the cell lines were assessed by Western blotting and the adhesive and invasive potential of the above-mentioned cell lines was determined before and after supplementation with the anti-LRP/LR specific antibody IgG1-iS18. Statistical significance of the data was confirmed via the use of the two-tailed student's t-test and Pearson's correlation coefficient. RESULTS: Flow cytometry revealed that AsPC-1 and IMR-32 cells displayed significantly higher cell surface LRP/LR levels in comparison to the MCF-7 control cell line. However, Western blotting and subsequent densitometric analysis revealed that all three tumorigenic cell lines displayed no significant difference in total LRP/LR levels. The treatment of AsPC-1 and IMR-32 cells with IgG1-iS18 caused a significant reduction in the adhesive and invasive potential of the cells to laminin-1 and through the ECM-like Matrigel™, respectively. Pearson's correlation coefficients indicated a high correlation, thus suggesting a directly proportional relationship between cell surface LRP/LR levels and the adhesive and invasive potential of AsPC-1 and IMR-32 cells. CONCLUSION: These findings suggest that through the interference of the LRP/LR-laminin-1 interaction, the anti-LRP/LR specific antibody IgG1-iS18 may act as an alternative therapeutic tool for the treatment of metastatic pancreatic cancer and neuroblastoma.
[Mh] Termos MeSH primário: Anticorpos Monoclonais/farmacologia
Adesão Celular/efeitos dos fármacos
Imunoglobulina G/imunologia
Neuroblastoma/prevenção & controle
Neoplasias Pancreáticas/prevenção & controle
Receptores de Laminina/antagonistas & inibidores
[Mh] Termos MeSH secundário: Apoptose/efeitos dos fármacos
Biomarcadores Tumorais/genética
Biomarcadores Tumorais/metabolismo
Western Blotting
Movimento Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Seres Humanos
Invasividade Neoplásica
Neuroblastoma/metabolismo
Neuroblastoma/patologia
Neoplasias Pancreáticas/metabolismo
Neoplasias Pancreáticas/patologia
RNA Mensageiro/genética
Reação em Cadeia da Polimerase em Tempo Real
Receptores de Laminina/imunologia
Receptores de Laminina/metabolismo
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Biomarkers, Tumor); 0 (Immunoglobulin G); 0 (RNA, Messenger); 0 (Receptors, Laminin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171121
[Lr] Data última revisão:
171121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161126
[St] Status:MEDLINE


  7 / 1083 MEDLINE  
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[PMID]:27832636
[Au] Autor:Wang QM; Wang H; Li YF; Xie ZY; Ma Y; Yan JJ; Gao YF; Wang ZM; Wang LS
[Ad] Endereço:Department of Cardiology, the First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
[Ti] Título:Inhibition of EMMPRIN and MMP-9 Expression by Epigallocatechin-3-Gallate through 67-kDa Laminin Receptor in PMA-Induced Macrophages.
[So] Source:Cell Physiol Biochem;39(6):2308-2319, 2016.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: It is well documented that overexpression of EMMPRIN (extracellular matrix metalloproteinase inducer) and MMPs (matrix metalloproteinases) by monocytes/macrophages plays an important role in atherosclerotic plaque rupture. Green tea polyphenol epigallocatechin-3-gallate (EGCG) has a variety of pharmacological properties and exerts cardiovascular protective effects. Recently, the 67-kD laminin receptor (67LR) has been identified as a cell surface receptor of EGCG. The aim of the present study was to evaluate the effects of EGCG on the expression of EMMPRIN and MMP-9 in PMA-induced macrophages, and the potential mechanisms underlying its effects. METHODS: Human monocytic THP-1 cells were induced to differentiate into macrophages with phorbol 12-myristate 13-acetate (PMA). Protein expression and MMP-9 activity were assayed by Western blot and Gelatin zymography, respectively. Real-time PCR was used to examine EMMPRIN and MMP-9 mRNA expression. RESULTS: We showed that EGCG (10-50µmol/L) significantly inhibited the expression of EMMPRIN and MMP-9 and activation of extracellular signal-regulated kinase 1/2 (ERK1/2), p38 and c-Jun N-terminal kinase (JNK) in PMA-induced macrophages. Downregulation of EMMPRIN by gene silencing hindered PMA-induced MMP-9 secretion and expression, indicating an important role of EMMPRIN in the inhibition of MMP-9 by EGCG. Moreover, 67LR was involved in EGCG-mediated suppression of EMMPRIN and MMP-9 expression. Anti-67LR antibody treatment led to abrogation of the inhibitory action of EGCG on the expression of EMMPRIN and MMP-9 and activation of ERK1/2, p38, and JNK. CONCLUSION: Our results indicate that EGCG restrains EMMPRIN and MMP-9 expression via 67LR in PMA-induced macrophages, which also suggests that EGCG may be a possible therapeutic agent for stabilizing atherosclerotic plaque.
[Mh] Termos MeSH primário: Basigina/metabolismo
Catequina/análogos & derivados
Macrófagos/metabolismo
Metaloproteinase 9 da Matriz/metabolismo
Receptores de Laminina/metabolismo
Acetato de Tetradecanoilforbol/farmacologia
[Mh] Termos MeSH secundário: Catequina/química
Catequina/farmacologia
Morte Celular/efeitos dos fármacos
Diferenciação Celular/efeitos dos fármacos
Linhagem Celular
Seres Humanos
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Macrófagos/efeitos dos fármacos
Macrófagos/enzimologia
Inibidores de Proteínas Quinases/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Protein Kinase Inhibitors); 0 (Receptors, Laminin); 136894-56-9 (Basigin); 8R1V1STN48 (Catechin); BQM438CTEL (epigallocatechin gallate); EC 3.4.24.35 (Matrix Metalloproteinase 9); NI40JAQ945 (Tetradecanoylphorbol Acetate)
[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:161111
[St] Status:MEDLINE


  8 / 1083 MEDLINE  
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[PMID]:27748570
[Au] Autor:Wu H; Li J; Xu D; Jv D; Meng X; Qiao P; Cui T; Shi B
[Ad] Endereço:Department of Neurosurgery, The First Affiliated Hospital, and College of Clinical Medicine of Henan University of Science and Technology, Luoyang, China, 471003. hongjiewu8@yahoo.com.
[Ti] Título:The 37-kDa laminin receptor precursor regulates the malignancy of human glioma cells.
[So] Source:Cell Biochem Funct;34(7):516-521, 2016 Oct.
[Is] ISSN:1099-0844
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Glioma is one of the most common brain tumors and one of the most aggressive cancers. Although extensive progress has been made regarding to the diagnosis and treatment, the mortality in glioma patients is still high. Therefore, finding new therapeutic targets to the glioma is critical to the advancement in cancer treatment. Recently, the 37-kDa laminin receptor precursor (37LRP) was reported to play important roles in occurrence of some types of cancer, indicating that this molecule may function as a key regulator in the tumor migration and metastasis. However, there is still no report to elucidate the correlation between 37LRP expression and glioma genesis and development. In this study, we found the higher expression of 37LRP in the glioma cells compared with the normal brain cells. We also indicated that the downregulation of 37LRP could affect the glioma biomarker expression and also weaken the proliferative, migratory, and metastatic capacity of glioma cells in vitro. Furthermore, 37LRP silencing inhibited the glioma tumor growth in vivo. Collectively, these data demonstrated that 37LRP regulates the metastasis of glioma cells in vitro and tumor growth in vivo, suggesting that 37LRP may function as a potential molecular target in the glioma treatment.
[Mh] Termos MeSH primário: Neoplasias Encefálicas/metabolismo
Neoplasias Encefálicas/patologia
Glioma/metabolismo
Glioma/patologia
Receptores de Laminina/metabolismo
[Mh] Termos MeSH secundário: Animais
Neoplasias Encefálicas/genética
Linhagem Celular Tumoral
Movimento Celular/genética
Proliferação Celular
Regulação para Baixo/genética
Ativação Enzimática
Regulação Neoplásica da Expressão Gênica
Inativação Gênica
Glioma/genética
Seres Humanos
Camundongos Nus
Proteínas Quinases Ativadas por Mitógeno/metabolismo
Invasividade Neoplásica
Fosforilação
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
RNA Interferente Pequeno/metabolismo
Receptores de Laminina/genética
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (RNA, Messenger); 0 (RNA, Small Interfering); 0 (Receptors, Laminin); EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170123
[Lr] Data última revisão:
170123
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161018
[St] Status:MEDLINE
[do] DOI:10.1002/cbf.3225


  9 / 1083 MEDLINE  
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[PMID]:27576948
[Au] Autor:Li Y; Li D; Chen J; Wang S
[Ad] Endereço:Institute of Hepatobiliary Surgery, Southwest Hospital, Third Military Medical University, Chongqing, China.
[Ti] Título:A polysaccharide from Pinellia ternata inhibits cell proliferation and metastasis in human cholangiocarcinoma cells by targeting of Cdc42 and 67kDa Laminin Receptor (LR).
[So] Source:Int J Biol Macromol;93(Pt A):520-525, 2016 Dec.
[Is] ISSN:1879-0003
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:In this study, we isolated and purified a polysaccharide (PTPA) from the tubers of Pinellia ternate. We aimed to evaluate the cytotoxic effects of PTPA on human cholangiocarcinoma (CCA) cell lines and to identify the underlying molecular mechanism. PTPA at the dose from 25 to 200µg/mL showed significant inhibitory effect on the proliferation of four cancer cell lines (SNU-245, CL-6, Sk-ChA-1 and MZ-ChA-1), among which Sk-ChA-1 was a most sensitive cell line to PTPA treatment via induction of apoptosis. Interestingly, RNA interference of Sk-ChA-1 cells with 67LR or Cdc42-targeted shRNAs resulted a similar potency in decreasing cell viability and causing apoptotic death. Moreover, PTPA (100µg/mL) or 67LR or Cdc42 special shRNAs increased the ratio of pro-apoptotic Bax to anti-apoptotic Bcl-2, induced the activation of caspase-9 and caspase-3, but not caspsase-8, and inhibited the expression of 67LR or Cdc42 protein in Sk-ChA-1 cells. Taken together, the inhibitory effect of PTPA on the cell growth of Sk-ChA-1 cells was at least in part mediated via the activation of the intrinsic mitochondrial apoptotic pathway and the downregulation of 67LR or Cdc42 protein expression. Thus, PTPA may be developed as a promising candidate for chemopreventive agent in the prevention and treatment of human CCA.
[Mh] Termos MeSH primário: Antineoplásicos Fitogênicos/farmacologia
Colangiocarcinoma/tratamento farmacológico
Colangiocarcinoma/metabolismo
Proteínas de Neoplasias/antagonistas & inibidores
Pinellia/química
Polissacarídeos/farmacologia
Proteína cdc42 de Ligação ao GTP/antagonistas & inibidores
[Mh] Termos MeSH secundário: Antineoplásicos Fitogênicos/química
Linhagem Celular Tumoral
Técnicas de Reprogramação Celular
Colangiocarcinoma/patologia
Seres Humanos
Proteínas de Neoplasias/metabolismo
Polissacarídeos/química
Receptores de Laminina/antagonistas & inibidores
Receptores de Laminina/metabolismo
Proteína cdc42 de Ligação ao GTP/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents, Phytogenic); 0 (Lamr1 protein, human); 0 (Neoplasm Proteins); 0 (Polysaccharides); 0 (Receptors, Laminin); EC 3.6.5.2 (cdc42 GTP-Binding Protein)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170317
[Lr] Data última revisão:
170317
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160901
[St] Status:MEDLINE


  10 / 1083 MEDLINE  
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[PMID]:27273766
[Au] Autor:Poitelon Y; Lopez-Anido C; Catignas K; Berti C; Palmisano M; Williamson C; Ameroso D; Abiko K; Hwang Y; Gregorieff A; Wrana JL; Asmani M; Zhao R; Sim FJ; Wrabetz L; Svaren J; Feltri ML
[Ad] Endereço:Department of Biochemistry, Hunter James Kelly Research Institute, Jacobs School of Medicine and Biomedical Sciences, State University of New York at Buffalo, Buffalo, New York, USA.
[Ti] Título:YAP and TAZ control peripheral myelination and the expression of laminin receptors in Schwann cells.
[So] Source:Nat Neurosci;19(7):879-87, 2016 Jul.
[Is] ISSN:1546-1726
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Myelination is essential for nervous system function. Schwann cells interact with neurons and the basal lamina to myelinate axons using known receptors, signals and transcription factors. In contrast, the transcriptional control of axonal sorting and the role of mechanotransduction in myelination are largely unknown. Yap and Taz are effectors of the Hippo pathway that integrate chemical and mechanical signals in cells. We describe a previously unknown role for the Hippo pathway in myelination. Using conditional mutagenesis in mice, we show that Taz is required in Schwann cells for radial sorting and myelination and that Yap is redundant with Taz. Yap and Taz are activated in Schwann cells by mechanical stimuli and regulate Schwann cell proliferation and transcription of basal lamina receptor genes, both necessary for radial sorting of axons and subsequent myelination. These data link transcriptional effectors of the Hippo pathway and of mechanotransduction to myelin formation in Schwann cells.
[Mh] Termos MeSH primário: Proteínas Adaptadoras de Transdução de Sinal/metabolismo
Movimento Celular/fisiologia
Proliferação Celular/fisiologia
Bainha de Mielina/metabolismo
Fosfoproteínas/metabolismo
Células de Schwann/metabolismo
Fatores de Transcrição/metabolismo
[Mh] Termos MeSH secundário: Animais
Axônios/fisiologia
Axônios/ultraestrutura
Células Cultivadas
Mecanotransdução Celular/fisiologia
Camundongos Endogâmicos C57BL
Neurogênese/fisiologia
Receptores de Laminina/metabolismo
Células de Schwann/citologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (Phosphoproteins); 0 (Receptors, Laminin); 0 (Taz protein, mouse); 0 (Transcription Factors); 0 (Yap protein, mouse)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170818
[Lr] Data última revisão:
170818
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160609
[St] Status:MEDLINE
[do] DOI:10.1038/nn.4316



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