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[PMID]:29195074
[Au] Autor:Kortlever RM; Sodir NM; Wilson CH; Burkhart DL; Pellegrinet L; Brown Swigart L; Littlewood TD; Evan GI
[Ad] Endereço:Department of Biochemistry, University of Cambridge, 80 Tennis Court Road, Cambridge CB2 1GA, UK; Department of Pathology and Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, San Francisco, CA 94143, USA.
[Ti] Título:Myc Cooperates with Ras by Programming Inflammation and Immune Suppression.
[So] Source:Cell;171(6):1301-1315.e14, 2017 Nov 30.
[Is] ISSN:1097-4172
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The two oncogenes KRas and Myc cooperate to drive tumorigenesis, but the mechanism underlying this remains unclear. In a mouse lung model of KRas -driven adenomas, we find that co-activation of Myc drives the immediate transition to highly proliferative and invasive adenocarcinomas marked by highly inflammatory, angiogenic, and immune-suppressed stroma. We identify epithelial-derived signaling molecules CCL9 and IL-23 as the principal instructing signals for stromal reprogramming. CCL9 mediates recruitment of macrophages, angiogenesis, and PD-L1-dependent expulsion of T and B cells. IL-23 orchestrates exclusion of adaptive T and B cells and innate immune NK cells. Co-blockade of both CCL9 and IL-23 abrogates Myc-induced tumor progression. Subsequent deactivation of Myc in established adenocarcinomas triggers immediate reversal of all stromal changes and tumor regression, which are independent of CD4 CD8 T cells but substantially dependent on returning NK cells. We show that Myc extensively programs an immune suppressive stroma that is obligatory for tumor progression.
[Mh] Termos MeSH primário: Adenocarcinoma/imunologia
Adenoma/imunologia
Neoplasias Pulmonares/genética
Neoplasias Pulmonares/imunologia
Proteínas Proto-Oncogênicas c-myc/metabolismo
Proteínas Proto-Oncogênicas p21(ras)/metabolismo
[Mh] Termos MeSH secundário: Adenocarcinoma/metabolismo
Adenocarcinoma/patologia
Adenoma/genética
Adenoma/patologia
Animais
Carcinogênese
Quimiocinas CC/imunologia
Modelos Animais de Doenças
Feminino
Inflamação/imunologia
Inflamação/metabolismo
Interleucina-23/imunologia
Neoplasias Pulmonares/patologia
Proteínas Inflamatórias de Macrófagos/imunologia
Macrófagos/imunologia
Masculino
Camundongos
Microambiente Tumoral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ccl9 protein, mouse); 0 (Chemokines, CC); 0 (Interleukin-23); 0 (Macrophage Inflammatory Proteins); 0 (Myc protein, mouse); 0 (Proto-Oncogene Proteins c-myc); EC 3.6.5.2 (Kras2 protein, mouse); EC 3.6.5.2 (Proto-Oncogene Proteins p21(ras))
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171222
[Lr] Data última revisão:
171222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171202
[St] Status:MEDLINE


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[PMID]:28108624
[Au] Autor:Li J; Zhou Z; Zhang X; Zheng L; He D; Ye Y; Zhang QQ; Qi CL; He XD; Yu C; Shao CK; Qiao L; Wang L
[Ad] Endereço:Vascular Biology Research Institute, School of Basic Course, Guangdong Pharmaceutical University, Guangzhou, China.
[Ti] Título:Inflammatory Molecule, , Deficiency Activates Macrophages to Promote Colorectal Cancer Growth through NFκB Signaling.
[So] Source:Mol Cancer Res;15(4):467-477, 2017 Apr.
[Is] ISSN:1557-3125
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:P-selectin glycoprotein ligand 1 (SELPLG/ ) is an inflammatory molecule that is functionally related to immune cell differentiation and leukocyte mobilization. However, the role of in tumor development remains unknown. Therefore, this study investigates the mechanistic role of in the development of intestinal tumors in colorectal cancer. Apc mice are highly susceptible to spontaneous intestinal adenoma formation, and were crossbred with PSGL1-null mice to generate compound transgenic mice with a Apc ; genotype. The incidence and pathologic features of the intestinal tumors were compared between the Apc mice and Apc ; mice. Importantly, -deficient mice showed increased susceptibility to develop intestinal tumors and accelerated tumor growth. Mechanistically, increased production of the mouse chemokine ligand 9 (CCL9/MIP-1γ) was found in the -deficient mice, and the macrophages are likely the major source of macrophage inflammatory protein-1 gamma (MIP-1γ). Studies demonstrated that macrophage-derived MIP-1γ promoted colorectal cancer tumor cell growth through activating NFκB signaling. Conversely, restoration of the signaling via bone marrow transplantation reduced MIP-1γ production and attenuated the ability of Apc ; mice to generate intestinal tumors. In human colorectal cancer clinical specimens, the presence of -positive cells was associated with a favorable tumor-node-metastasis staging and decreased lymph node metastasis. deficiency and inflammation render intestinal tissue more vulnerable to develop colorectal tumors through a MIP-1γ/NFκB signaling axis. .
[Mh] Termos MeSH primário: Quimiocinas CC/metabolismo
Neoplasias Colorretais/patologia
Proteínas Inflamatórias de Macrófagos/metabolismo
Macrófagos/patologia
Glicoproteínas de Membrana/deficiência
NF-kappa B/metabolismo
[Mh] Termos MeSH secundário: Adenoma/metabolismo
Animais
Linhagem Celular Tumoral
Proliferação Celular
Neoplasias Colorretais/metabolismo
Feminino
Células HCT116
Seres Humanos
Ativação de Macrófagos
Macrófagos/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Camundongos Transgênicos
Invasividade Neoplásica
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chemokines, CC); 0 (Macrophage Inflammatory Proteins); 0 (Membrane Glycoproteins); 0 (NF-kappa B); 0 (P-selectin ligand protein)
[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:170122
[St] Status:MEDLINE
[do] DOI:10.1158/1541-7786.MCR-16-0309


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[PMID]:27843299
[Au] Autor:Lin CH; Lee SY; Zhang CC; Du YF; Hung HC; Wu HT; Ou HY
[Ad] Endereço:Department of Internal Medicine, Division of Endocrinology and Metabolism, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan.
[Ti] Título:Fenretinide inhibits macrophage inflammatory mediators and controls hypertension in spontaneously hypertensive rats via the peroxisome proliferator-activated receptor gamma pathway.
[So] Source:Drug Des Devel Ther;10:3591-3597, 2016.
[Is] ISSN:1177-8881
[Cp] País de publicação:New Zealand
[La] Idioma:eng
[Ab] Resumo:Fenretinide is a novel anticancer agent reported to exhibit anti-invasive and antimetastatic activities. It has also been shown to improve obesity and diabetes, although the effects of fenretinide on hypertension are still unknown, and the detailed mechanisms remain unclear. In this study, we have shown that treatment with lipopolysaccharide (LPS) decreased the expression of peroxisome proliferator-activated receptor γ (PPARγ) in RAW264.7 macrophages, and pretreatment with fenretinide reversed the effect of LPS on PPARγ expression. In addition, LPS-induced pro-inflammatory cytokine production, including tumor necrosis factor-α, interleukin 6, and monocyte chemoattractant protein 1 were dose-dependently reversed by fenretinide, and the effects of fenretinide on LPS-induced pro-inflammatory cytokine production were blocked by treatment with PPARγ antagonist. Moreover, fenretinide decreased LPS-induced inducible nitric oxide synthase expression and nitrogen oxide production. These effects were blocked by the pretreatment with PPARγ antagonist in a dose-dependent manner, indicating fenretinide activated PPARγ to exert anti-inflammation activity. In view of the role of inflammation in hypertension and the anti-inflammatory action of fenretinide, we found that administration of fenretinide in spontaneously hypertensive rats significantly decreased blood pressure. Taken together, these results indicate that fenretinide might be a potent antihypertensive agent that works by suppressing inflammation via activating PPARγ.
[Mh] Termos MeSH primário: Anti-Inflamatórios/farmacologia
Anti-Hipertensivos/farmacologia
Pressão Sanguínea/efeitos dos fármacos
Fenretinida/farmacologia
Hipertensão/tratamento farmacológico
Proteínas Inflamatórias de Macrófagos/metabolismo
Macrófagos/efeitos dos fármacos
PPAR gama/agonistas
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Relação Dose-Resposta a Droga
Hipertensão/imunologia
Hipertensão/metabolismo
Hipertensão/fisiopatologia
Lipopolissacarídeos/farmacologia
Proteínas Inflamatórias de Macrófagos/imunologia
Macrófagos/imunologia
Macrófagos/metabolismo
Camundongos
Óxido Nítrico/metabolismo
Óxido Nítrico Sintase Tipo II/metabolismo
PPAR gama/metabolismo
Células RAW 264.7
Ratos Endogâmicos SHR
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Antihypertensive Agents); 0 (Lipopolysaccharides); 0 (Macrophage Inflammatory Proteins); 0 (PPAR gamma); 187EJ7QEXL (Fenretinide); 31C4KY9ESH (Nitric Oxide); EC 1.14.13.39 (Nitric Oxide Synthase Type II); EC 1.14.13.39 (Nos2 protein, mouse)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170321
[Lr] Data última revisão:
170321
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161116
[St] Status:MEDLINE


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[PMID]:27311921
[Au] Autor:Yang T; Xie Z; Li H; Yue L; Pang Z; MacNeil AJ; Tremblay ML; Tang JT; Lin TJ
[Ad] Endereço:The Institute of Medical Biology, Chinese Academy of Medical Sciences and Peking Union Medical College, 935 Jiaoling Road, Kunming, Yunnan 650118, China.
[Ti] Título:Protein tyrosine phosphatase 1B (PTP1B) is dispensable for IgE-mediated cutaneous reaction in vivo.
[So] Source:Cell Immunol;306-307:9-16, 2016 Aug-Sep.
[Is] ISSN:1090-2163
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Mast cells play a critical role in allergic reactions. The cross-linking of FcεRI-bound IgE with multivalent antigen initiates a cascade of signaling events leading to mast cell activation. It has been well-recognized that cross linking of FcεRI mediates tyrosine phosphorylation. However, the mechanism involved in tyrosine dephosphorylation in mast cells is less clear. Here we demonstrated that protein tyrosine phosphatase 1B (PTP1B)-deficient mast cells showed increased IgE-mediated phosphorylation of the signal transducer and activator of transcription 5 (STAT5) and enhanced production of CCL9 (MIP-1γ) and IL-6 in IgE-mediated mast cells activation in vitro. However, IgE-mediated calcium mobilization, ß-hexaosaminidase release (degranulation), and phosphorylation of IκB and MAP kinases were not affected by PTP1B deficiency. Furthermore, PTP1B deficient mice showed normal IgE-dependent passive cutaneous anaphylaxis and late phase cutaneous reactions in vivo. Thus, PTP1B specifically regulates IgE-mediated STAT5 pathway, but is redundant in influencing mast cell function in vivo.
[Mh] Termos MeSH primário: Mastócitos/imunologia
Anafilaxia Cutânea Passiva/imunologia
Proteína Tirosina Fosfatase não Receptora Tipo 1/metabolismo
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Quimiocinas CC/metabolismo
Seres Humanos
Imunoglobulina E/metabolismo
Interleucina-4/metabolismo
Interleucina-6/metabolismo
Proteínas Inflamatórias de Macrófagos/metabolismo
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Knockout
Fosforilação/genética
Proteína Tirosina Fosfatase não Receptora Tipo 1/genética
Fator de Transcrição STAT5/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ccl9 protein, mouse); 0 (Chemokines, CC); 0 (Interleukin-6); 0 (Macrophage Inflammatory Proteins); 0 (STAT5 Transcription Factor); 207137-56-2 (Interleukin-4); 37341-29-0 (Immunoglobulin E); EC 3.1.3.48 (Protein Tyrosine Phosphatase, Non-Receptor Type 1); EC 3.1.3.48 (Ptpn1 protein, mouse)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170626
[Lr] Data última revisão:
170626
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160618
[St] Status:MEDLINE


  5 / 2430 MEDLINE  
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[PMID]:27295859
[Au] Autor:Luo YJ; Li RB; Ma SY; Lü MY
[Ti] Título:[Progress on Hypoxic-ischemic Brain Damage Associated with CCR2 and CCL2].
[So] Source:Fa Yi Xue Za Zhi;32(1):54-7, 2016 Feb.
[Is] ISSN:1004-5619
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:Hypoxic-ischemic brain damage (HIBD) is referred to a common type of cerebral damage, which is caused by injury, leading to shallow bleeding in the cortex with intact cerebral pia mater. In recent years, studies show that a various kinds of immune cells and immune cellular factors are involved in the occurrence of HIBD. CC chemokine receptor 2 (CCR2) is a representative of CC chemokine receptor, and is widely distributed in cerebral neuron, astrocyte, and microglial cells, and is the main chemo-tactic factor receptor in brain tissue. CC chemokine ligand 2 (CCL2) is a kind of basophilic protein and the ligand of CCR2, and plays an important role in inflammation. In order to provide evidence for correlational studies in HIBD, this review will introduce the biological characteristics of CCR2 and CCL2, and illustrate the relationship between the immunoreactivity and HIBD.
[Mh] Termos MeSH primário: Lesões Encefálicas/metabolismo
Quimiocina CCL2/metabolismo
Hipóxia-Isquemia Encefálica/metabolismo
[Mh] Termos MeSH secundário: Animais
Lesões Encefálicas/tratamento farmacológico
Lesões Encefálicas/patologia
Córtex Cerebral/metabolismo
Córtex Cerebral/patologia
Córtex Cerebral/fisiopatologia
Quimiocina CCL2/genética
Quimiocinas CC/metabolismo
Proteínas Inflamatórias de Macrófagos/metabolismo
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Ratos
Ratos Sprague-Dawley
Receptores CCR2/antagonistas & inibidores
Receptores CCR2/genética
Receptores CCR2/metabolismo
[Pt] Tipo de publicação:ENGLISH ABSTRACT; JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (CCL15 protein, human); 0 (Ccr2 protein, rat); 0 (Chemokine CCL2); 0 (Chemokines, CC); 0 (Macrophage Inflammatory Proteins); 0 (RNA, Messenger); 0 (Receptors, CCR2)
[Em] Mês de entrada:1607
[Cu] Atualização por classe:160614
[Lr] Data última revisão:
160614
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160615
[St] Status:MEDLINE


  6 / 2430 MEDLINE  
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[PMID]:26875556
[Au] Autor:Huang FJ; Zhou XY; Ye L; Fei XC; Wang S; Wang W; Ning G
[Ad] Endereço:Shanghai Key Laboratoryfor Endocrine Tumors, Shanghai Clinical Center for Endocrine and Metabolic Diseases, Shanghai Institute of Endocrine and Metabolic Diseases and Shanghai E-institute for Endocrinology, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, 197 Ruijin 2nd Road, Shan
[Ti] Título:Follicular thyroid carcinoma but not adenoma recruits tumor-associated macrophages by releasing CCL15.
[So] Source:BMC Cancer;16:98, 2016 Feb 15.
[Is] ISSN:1471-2407
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The differential diagnosis of follicular thyroid carcinoma (FTC) and follicular adenoma (FA) before surgery is a clinical challenge. Many efforts have been made but most focusing on tumor cells, while the roles of tumor associated macrophages (TAMs) remained unclear in FTC. Here we analyzed the differences between TAMs in FTC and those in FA. METHODS: We first analyzed the density of TAMs by CD68 immunostaining in 59 histologically confirmed FTCs and 47 FAs. Cytokines produced by FTC and FA were profiled using antibody array, and validated by quantitative PCR. Chemotaxis of monocyte THP-1 was induced by condition medium of FTC cell lines (FTC133 and WRO82-1) with and without anti-CCL15 neutralizing antibody. Finally, we analyzed CCL15 protein level in FTC and FA by immunohistochemistry. RESULTS: The average density of CD68(+) cells was 9.5 ± 5.4/field in FTC, significantly higher than that in FA (4.9 ± 3.4/field, p < 0.001). Subsequently profiling showed that CCL15 was the most abundant chemokine in FTC compared with FA. CCL15 mRNA in FTC was 51.4-folds of that in FA. CM of FTC cell lines induced THP-1 cell chemotaxis by 33 ~ 77%, and anti-CCL15 neutralizing antibody reduced THP-1 cell migration in a dose-dependent manner. Moreover, we observed positive CCL15 immunostaining in 67.8% of FTCs compared with 23.4% of FAs. CONCLUSION: Our study suggested FTC might induce TAMs infiltration by producing CCL15. Measurement of TAMs and CCL15 in follicular thyroid lesions may be applied clinically to differentiate FTC from FA pre-operation.
[Mh] Termos MeSH primário: Adenocarcinoma Folicular/diagnóstico
Adenoma/diagnóstico
Quimiocinas CC/biossíntese
Diagnóstico Diferencial
Proteínas Inflamatórias de Macrófagos/biossíntese
[Mh] Termos MeSH secundário: Adenocarcinoma Folicular/genética
Adenocarcinoma Folicular/patologia
Adenoma/genética
Adenoma/patologia
Biópsia por Agulha Fina
Quimiocinas CC/genética
Feminino
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Proteínas Inflamatórias de Macrófagos/genética
Macrófagos/patologia
Masculino
Período Pré-Operatório
RNA Mensageiro/biossíntese
Análise Serial de Tecidos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CCL15 protein, human); 0 (Chemokines, CC); 0 (Macrophage Inflammatory Proteins); 0 (RNA, Messenger)
[Em] Mês de entrada:1609
[Cu] Atualização por classe:160217
[Lr] Data última revisão:
160217
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160216
[St] Status:MEDLINE
[do] DOI:10.1186/s12885-016-2114-7


  7 / 2430 MEDLINE  
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[PMID]:26763650
[Au] Autor:Gao Y; Zhou Z; Lu S; Huang X; Zhang C; Jiang R; Yao A; Sun B; Wang X
[Ad] Endereço:Liver Transplantation Center, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu Province, People's Republic of China.
[Ti] Título:Chemokine CCL15 Mediates Migration of Human Bone Marrow-Derived Mesenchymal Stem Cells Toward Hepatocellular Carcinoma.
[So] Source:Stem Cells;34(4):1112-22, 2016 Apr.
[Is] ISSN:1549-4918
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mesenchymal stem cells (MSCs) possess the ability to migrate toward tumor sites and are regarded as promising gene delivery vehicles for cancer therapeutics. However, the factors that mediate this tropism have yet to be completely elucidated. In this study, through cytokine array analysis, chemokine CCL15 was found to be the most abundant protein differentially expressed in hepatocellular carcinoma (HCC) cell lines compared with a normal liver cell line. Serum CCL15 levels in HCC patients determined by enzyme linked immunosorbent assay were shown to be profoundly elevated compared with healthy controls. Immunohistochemical analysis indicated that CCL15 expression was much stronger in HCC tumor tissues than in adjacent nontumor tissues. Transwell migration assay suggested that CCL15 may be involved in chemotaxis of human MSCs (hMSCs) toward HCC in vitro and that this chemotactic effect of CCL15 is mediated via CCR1 receptors on hMSCs. Orthotopic animal models of HCC were established to investigate the role of CCL15 in hMSCs migration toward HCC in vivo. Both histological and flow cytometric analysis showed that significantly fewer hMSCs localized within 97H-CCL15-shRNA xenografts compared with 97H-green fluorescent protein xenografts after intravenous delivery. Finally, the possible effects of hMSCs on HCC tumor growth were also evaluated. Coculture experiments showed that hMSCs had no apparent effect on the proliferation of HCC cells in vitro In addition, systemic administration of hMSCs did not affect HCC tumor progression in vivo. Our data in this study help to elucidate the mechanism underlying the homing capacity of hMSCs toward HCC.
[Mh] Termos MeSH primário: Carcinoma Hepatocelular/terapia
Quimiocinas CC/genética
Técnicas de Transferência de Genes
Neoplasias Hepáticas/terapia
Proteínas Inflamatórias de Macrófagos/genética
Células Mesenquimais Estromais/metabolismo
[Mh] Termos MeSH secundário: Animais
Células da Medula Óssea/citologia
Células da Medula Óssea/metabolismo
Carcinoma Hepatocelular/genética
Linhagem Celular Tumoral
Movimento Celular/genética
Quimiocinas CC/biossíntese
Quimiocinas CC/uso terapêutico
Quimiotaxia/genética
Regulação Neoplásica da Expressão Gênica
Proteínas de Fluorescência Verde/genética
Seres Humanos
Neoplasias Hepáticas/genética
Proteínas Inflamatórias de Macrófagos/biossíntese
Proteínas Inflamatórias de Macrófagos/uso terapêutico
Células Mesenquimais Estromais/química
Células Mesenquimais Estromais/citologia
Camundongos
RNA Interferente Pequeno/genética
RNA Interferente Pequeno/uso terapêutico
Receptores CCR1/biossíntese
Receptores CCR1/genética
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CCL15 protein, human); 0 (Chemokines, CC); 0 (Macrophage Inflammatory Proteins); 0 (RNA, Small Interfering); 0 (Receptors, CCR1); 147336-22-9 (Green Fluorescent Proteins)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170111
[Lr] Data última revisão:
170111
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160115
[St] Status:MEDLINE
[do] DOI:10.1002/stem.2275


  8 / 2430 MEDLINE  
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[PMID]:26643668
[Au] Autor:Li Y; Yu HP; Zhang P
[Ad] Endereço:Department of Clinical Laboratory, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, The National "863" Program of Clinical Research Laboratory, Tianjin, 300060, People's Republic of China.
[Ti] Título:CCL15 overexpression predicts poor prognosis for hepatocellular carcinoma.
[So] Source:Hepatol Int;10(3):488-92, 2016 May.
[Is] ISSN:1936-0541
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: The purpose of this study was to study the expression of CCL15 in hepatocellular carcinoma (HCC) and explore its clinicopathological significance, and study relationships between expressions of CCL15 and malignant behaviors of HCC. METHODS: The SP immunohistochemical method was used to detect expression of CCL15 in routinely paraffin-embedded sections from 80 cases of HCC, 80 of adjacent cancerous specimens and 50 of normal liver tissue. In these patients with HCC, Kaplan-Meier was used to assess survival outcomes. RESULTS: The positive rates and scores of CCL15 were significantly higher in HCC than adjacent cancerous specimens and normal liver tissue (p < 0.05), but not significantly higher between adjacent cancerous specimens and normal liver tissue (p > 0.05). The expression of CCL15 was significantly correlated to tumor size, tumor thrombi in portal vein of HCC, capsule and TNM stage (p < 0.05), but not to sex, age, liver cirrhosis and the level of AFP so on (p > 0.05). Survival time of the patients with positive CCL15 expression was significantly decreased, and multivariate analysis indicated CCL15 expression was one of the independent predictors of survival (p = 0.042). CONCLUSION: The expression of CCL15 was significantly correlated with malignant behaviors of HCC, and CCL15 might be important biological markers for reflecting the carcinogenesis, progression, biological behaviors and prognosis of HCC.
[Mh] Termos MeSH primário: Carcinoma Hepatocelular/diagnóstico
Quimiocinas CC/metabolismo
Neoplasias Hepáticas/diagnóstico
Proteínas Inflamatórias de Macrófagos/metabolismo
[Mh] Termos MeSH secundário: Adulto
Idoso
Carcinoma Hepatocelular/química
Carcinoma Hepatocelular/metabolismo
Quimiocinas CC/análise
Feminino
Seres Humanos
Estimativa de Kaplan-Meier
Fígado/química
Fígado/metabolismo
Neoplasias Hepáticas/química
Neoplasias Hepáticas/metabolismo
Proteínas Inflamatórias de Macrófagos/análise
Masculino
Meia-Idade
Prognóstico
Análise de Sobrevida
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CCL15 protein, human); 0 (Chemokines, CC); 0 (Macrophage Inflammatory Proteins)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:171108
[Lr] Data última revisão:
171108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151209
[St] Status:MEDLINE
[do] DOI:10.1007/s12072-015-9683-4


  9 / 2430 MEDLINE  
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[PMID]:26501423
[Au] Autor:Li Y; Wu J; Zhang P
[Ad] Endereço:Department of Clinical Laboratory, National Clinical Research Center for Cancer, Tianjin Medical University Cancer Institute and Hospital, Tianjin, 300060, People's Republic of China. kesaqi@163.com.
[Ti] Título:CCL15/CCR1 axis is involved in hepatocellular carcinoma cells migration and invasion.
[So] Source:Tumour Biol;37(4):4501-7, 2016 Apr.
[Is] ISSN:1423-0380
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The identification of new biomarkers for the early detection of hepatocellular carcinoma is critical in the development of tumor-targeted therapy, which is possibly advantageous on the prognosis of this disease. Results from our previous study indicated that CCL15 can be a specific proteomic biomarker of hepatocellular carcinoma, which plays an important role in tumorigenesis and tumor invasion. In this study, we found that CCL15 can induce hepatocellular carcinoma cell migration and invasion. Furthermore, CCR1, the receptor of CCL15, was demonstrated to play a critical role in metastatic hepatocellular carcinoma. CCR1 short hairpin RNA significantly inhibited CCL15-induced chemotaxis and invasion of HepG2 cells. Moreover, CCR1 knockdown significantly limited the activity and expression of matrix metalloproteinase-2 (MMP-2) and MMP-9. These findings suggest that CCR1 plays critical roles in hepatocellular carcinoma metastasis, which indicates that CCR1 may be a potential molecular target in hepatocellular carcinoma therapy.
[Mh] Termos MeSH primário: Carcinoma Hepatocelular/metabolismo
Quimiocinas CC/metabolismo
Quimiotaxia
Neoplasias Hepáticas/metabolismo
Proteínas Inflamatórias de Macrófagos/metabolismo
Receptores CCR1/metabolismo
[Mh] Termos MeSH secundário: Carcinoma Hepatocelular/patologia
Indução Enzimática
Regulação Neoplásica da Expressão Gênica
Células Hep G2
Seres Humanos
Neoplasias Hepáticas/patologia
Metaloproteinase 2 da Matriz/genética
Metaloproteinase 2 da Matriz/metabolismo
Metaloproteinase 9 da Matriz/genética
Metaloproteinase 9 da Matriz/metabolismo
Invasividade Neoplásica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCL15 protein, human); 0 (CCR1 protein, human); 0 (Chemokines, CC); 0 (Macrophage Inflammatory Proteins); 0 (Receptors, CCR1); 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:1702
[Cu] Atualização por classe:171111
[Lr] Data última revisão:
171111
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151027
[St] Status:MEDLINE
[do] DOI:10.1007/s13277-015-4287-0


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[PMID]:26341919
[Au] Autor:Inamoto S; Itatani Y; Yamamoto T; Minamiguchi S; Hirai H; Iwamoto M; Hasegawa S; Taketo MM; Sakai Y; Kawada K
[Ad] Endereço:Department of Surgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
[Ti] Título:Loss of SMAD4 Promotes Colorectal Cancer Progression by Accumulation of Myeloid-Derived Suppressor Cells through the CCL15-CCR1 Chemokine Axis.
[So] Source:Clin Cancer Res;22(2):492-501, 2016 Jan 15.
[Is] ISSN:1078-0432
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE: We previously reported that loss of SMAD4 promotes chemokine CCL15 expression to recruit CCR1(+) myeloid cells via the CCL15-CCR1 axis, which facilitates metastasis of colorectal cancer to the liver. The purposes of this study were to investigate whether essentially the same mechanism works in tumor invasion of the primary colorectal cancer and to evaluate the clinical importance of CCL15 expression and CCR1(+) cell accumulation. EXPERIMENTAL DESIGN: Using human colorectal cancer cell lines with reduced expression of SMAD4 or CCL15, we investigated tumor growth activities in vivo. We used immunohistochemistry (IHC) to investigate expression of SMAD4, CCL15, and CCR1 with 333 clinical specimens of primary colorectal cancer. We next characterized the CCR1(+) cells using double immunofluorescence staining with several specific cell-type markers. Finally, we determined the serum CCL15 levels in 132 colorectal cancer patients. RESULTS: In an orthotopic xenograft model, CCL15 secreted from SMAD4-deficient colorectal cancer cells recruited CCR1(+) cells, resulting in aggressive tumor growth. IHC indicated that loss of SMAD4 was significantly associated with CCL15 expression, and that CCL15-positive primary colorectal cancers recruited approximately 2.2 times more numbers of CCR1(+) cells at their invasion front than CCL15-negative colorectal cancers. Importantly, these CCR1(+) cells were of the myeloid-derived suppressor cell (MDSC) phenotype (CD11b(+), CD33(+), and HLA-DR(-)). Most CCR1(+) cells showed the granulocytic-MDSC phenotype (CD15(+)), whereas some showed the monocytic-MDSC phenotype (CD14(+)). Serum CCL15 levels in colorectal cancer patients were significantly higher than in controls. CONCLUSIONS: Blocking the recruitment of CCR1(+) MDSCs may represent a novel molecular-targeted therapy, and serum CCL15 concentration can be a novel biomarker for colorectal cancer.
[Mh] Termos MeSH primário: Quimiocinas CC/metabolismo
Quimiocinas/metabolismo
Neoplasias Colorretais/metabolismo
Neoplasias Colorretais/patologia
Proteínas Inflamatórias de Macrófagos/metabolismo
Células Mieloides/patologia
Receptores CCR1/metabolismo
Proteína Smad4/metabolismo
[Mh] Termos MeSH secundário: Antígeno CD11b/metabolismo
Linhagem Celular Tumoral
Progressão da Doença
Antígenos HLA-DR/metabolismo
Células HT29
Seres Humanos
Células Mieloides/metabolismo
Lectina 3 Semelhante a Ig de Ligação ao Ácido Siálico/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CCL15 protein, human); 0 (CCR1 protein, human); 0 (CD11b Antigen); 0 (CD33 protein, human); 0 (Chemokines); 0 (Chemokines, CC); 0 (HLA-DR Antigens); 0 (Macrophage Inflammatory Proteins); 0 (Receptors, CCR1); 0 (SMAD4 protein, human); 0 (Sialic Acid Binding Ig-like Lectin 3); 0 (Smad4 Protein)
[Em] Mês de entrada:1610
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150906
[St] Status:MEDLINE
[do] DOI:10.1158/1078-0432.CCR-15-0726



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