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[PMID]:29399882
[Au] Autor:Mitra S; Chatterjee D; Das A; Gupta K; Radotra BD; Mandal AK
[Ad] Endereço:Department of Histopathology, PGIMER, Chandigarh, India.
[Ti] Título:Urothelial tumors with villous morphology: Histomorphology and role of immunohistochemistry in diagnosis.
[So] Source:APMIS;126(3):191-200, 2018 Mar.
[Is] ISSN:1600-0463
[Cp] País de publicação:Denmark
[La] Idioma:eng
[Ab] Resumo:Villous adenoma and urothelial carcinoma with villoglandular differentiation (UCVGD) are rare urothelial tumours showing villous morphology, the former being a preneoplastic entity and the latter being a malignant one. The detailed immunohistochemistry of these entities is previously not described in the literature. Moreover, a limited biopsy sample of UCVGD or a villous adenoma with or without adenocarcinoma may be difficult to distinguish on the basis of the histomorphology alone. An immunohistochemical panel comprising of GATA3, p63, ß-catenin, CK7 and CK20 was performed on five cases of UCVGD and three cases of villous adenoma with the aim of studying the expression of the proteins thereby aiding in the diagnosis of these entities in a limited surgical pathology specimen. The mean age of UCVGD was 66.8 years and all the patients were male. All the cases of UCVGD were associated with high grade papillary urothelial carcinoma with lamina propria invasion. The immunohistochemical panel showed strong nuclear GATA3 expression in the urothelial component of UCVGD. Interestingly, the high grade and the low grade villoglandular components of UCVGD also expressed GATA3 (nuclear) with a progressive loss of expression from the high grade to the low grade component. The villous adenomas showed negativity or aberrant cytoplasmic positivity for GATA3. The ß-catenin showed a gradual loss of membranous expression from villous adenoma to low grade and high grade villoglandular components of UCVGD with a patchy membranous expression in the urothelial component of the UCVGD. p63 showed strong nuclear positivity in the urothelial component and uniform negativity in the villous adenoma and villoglandular component of UCVGD irrespective of its grade, thereby distinguishing the villoglandular component from the urothelial component. The urothelial component of UCVGD showed strong membranous CK7 expression and was higher than the CK20 expression in the urothelial component. In contrast, CK20 expression was higher in villous adenoma as compared to CK7. There was no difference in the expression of CK7 and CK20 in the villoglandular components and low grade and high grade villoglandular areas. The above-mentioned immunohistochemical pattern may help to distinguish the UCVGD from the villous adenoma.
[Mh] Termos MeSH primário: Adenoma Viloso/diagnóstico
Fator de Transcrição GATA3/metabolismo
Queratina-7/metabolismo
Proteínas de Membrana/metabolismo
Neoplasias Urológicas/diagnóstico
beta Catenina/metabolismo
[Mh] Termos MeSH secundário: Adenoma Viloso/patologia
Idoso
Biomarcadores Tumorais/metabolismo
Feminino
Hematúria/patologia
Seres Humanos
Imuno-Histoquímica
Queratina-20/metabolismo
Masculino
Meia-Idade
Neoplasias Urológicas/patologia
Urotélio/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (CKAP4 protein, human); 0 (GATA3 Transcription Factor); 0 (GATA3 protein, human); 0 (KRT20 protein, human); 0 (KRT7 protein, human); 0 (Keratin-20); 0 (Keratin-7); 0 (Membrane Proteins); 0 (beta Catenin)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180206
[St] Status:MEDLINE
[do] DOI:10.1111/apm.12799


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[PMID]:29441916
[Au] Autor:Fan X; Wang P; Sun Y; Jiang J; Du H; Wang Z; Duan Z; Lei H; Li H
[Ti] Título:Oleanolic acid derivatives inhibit the Wnt/ß-catenin signaling pathway by promoting the phosphorylation of ß-catenin in human SMMC-7721 cells.
[So] Source:Pharmazie;71(7):398-401, 2016 Jul 07.
[Is] ISSN:0031-7144
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Oleanolic acid, isolated from privet, has shown antitumor effects in several cancers. However, the underlying molecular mechanism associated with these effects is largely unknown. In this study, we explored the effect of oleanolic acid derivatives on the Wnt/ß-catenin signaling pathway in human hepatocellular carcinoma SMMC-7721 cells. The mRNA and protein levels of related genes were determined by real-time quantitative PCR and Western blot, respectively. Treatment of SMMC-7721 cells with oleanolic acid derivatives led to the downregulation of the mRNA and protein levels of ß-catenin, c-myc, and cyclin D1. Treatment with oleanolic acid derivatives decreased the levels of ß-catenin in both the cytoplasm and the nucleus. Moreover, oleanolic acid derivatives promoted the phosphorylation of ß-catenin (Ser33/37/Thr41) in the cytoplasm. Our results suggest that oleanolic acid derivatives inhibit the Wnt/ß-catenin signaling pathway by stimulating the phosphorylation of ß-catenin (Ser33/37/Thr41) in human SMMC-7721 cells.
[Mh] Termos MeSH primário: Ácido Oleanólico/análogos & derivados
Ácido Oleanólico/farmacologia
Via de Sinalização Wnt/efeitos dos fármacos
beta Catenina/efeitos dos fármacos
beta Catenina/metabolismo
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Núcleo Celular/efeitos dos fármacos
Núcleo Celular/metabolismo
Ciclina D1/antagonistas & inibidores
Ciclina D1/biossíntese
Citoplasma/efeitos dos fármacos
Citoplasma/metabolismo
Regulação para Baixo/efeitos dos fármacos
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Fosforilação/efeitos dos fármacos
Proteínas Proto-Oncogênicas c-myc/antagonistas & inibidores
Proteínas Proto-Oncogênicas c-myc/biossíntese
RNA Mensageiro/biossíntese
RNA Mensageiro/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CTNNB1 protein, human); 0 (Proto-Oncogene Proteins c-myc); 0 (RNA, Messenger); 0 (beta Catenin); 136601-57-5 (Cyclin D1); 6SMK8R7TGJ (Oleanolic Acid)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180215
[St] Status:MEDLINE
[do] DOI:10.1691/ph.2016.6536


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[PMID]:29267503
[Au] Autor:Wang ZK; Yang L; Wu LL; Mao H; Zhou YH; Zhang PF; Dai GH
[Ad] Endereço:The Second Department of Medical Oncology, Chinese People's Liberation Army General Hospital, Beijing, China.
[Ti] Título:Long non-coding RNA LINC00261 sensitizes human colon cancer cells to cisplatin therapy.
[So] Source:Braz J Med Biol Res;51(2):e6793, 2017 Dec 11.
[Is] ISSN:1414-431X
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:Colon cancer is one of the most common digestive tumors. The present study aimed to explore the functional role, as well as the underlying mechanism of long non-coding RNA LINC00261 in colon cancer. Expression of LINC00261 was analyzed in colon cancer cell lines and human normal cell lines. Acquired resistance cell lines were then built and the acquired resistance efficiency was detected by evaluating cell viability. Thereafter, the effects of LINC00261 overexpression on cisplatin-resistant colon cancer cells were measured, as well as cell apoptosis, viability, migration, and invasion. Subsequently, we investigated the interaction of LINC00261 and ß-catenin. The results showed that the LINC00261 gene was down-regulated in colon cancer cell lines and tissues, and in cisplatin-resistant cells. LINC00261 overexpression might relieve cisplatin resistance of colon cancer cells via promoting cell apoptosis, and inhibiting cell viability, migration, and invasion. Moreover, LINC00261 might down-regulate nuclear ß-catenin through restraining ß-catenin from cytoplasm into nuclei or it could also promote ß-catenin degradation and inhibit activation of Wnt pathway. Finally, LINC00261 reduced cisplatin resistance of colon cancer in vivo and enhanced the anti-colon cancer effect of cisplatin through reducing tumor volume and weight.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Cisplatino/farmacologia
Neoplasias do Colo/tratamento farmacológico
Neoplasias do Colo/genética
Neoplasias do Colo/patologia
RNA Longo não Codificante/fisiologia
[Mh] Termos MeSH secundário: Análise de Variância
Apoptose/efeitos dos fármacos
Apoptose/fisiologia
Proteínas Reguladoras de Apoptose/efeitos dos fármacos
Proteínas Reguladoras de Apoptose/fisiologia
Western Blotting
Ensaios de Migração Celular
Proliferação Celular/efeitos dos fármacos
Proliferação Celular/fisiologia
Regulação para Baixo
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Regulação Neoplásica da Expressão Gênica/fisiologia
Células HCT116
Células HT29
Seres Humanos
RNA Longo não Codificante/análise
RNA Longo não Codificante/efeitos dos fármacos
RNA Longo não Codificante/genética
Reprodutibilidade dos Testes
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Transdução de Sinais/efeitos dos fármacos
Transdução de Sinais/fisiologia
Sais de Tetrazólio
Tiazóis
beta Catenina/efeitos dos fármacos
beta Catenina/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Apoptosis Regulatory Proteins); 0 (RNA, Long Noncoding); 0 (Tetrazolium Salts); 0 (Thiazoles); 0 (beta Catenin); 0 (long non-coding RNA 00261, human); EUY85H477I (thiazolyl blue); Q20Q21Q62J (Cisplatin)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171222
[St] Status:MEDLINE


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[PMID]:29429160
[Au] Autor:Zhao M; Wang YB; Yan YJ; Wang W; Ru GQ; He XL
[Ad] Endereço:Department of Pathology, Zhejiang Provincial People's Hospital, People's Hospital of Hangzhou Medical College, Hangzhou 310014, China.
[Ti] Título:[Clinicopathologic features of atypical spindle cell lipomatous tumor].
[So] Source:Zhonghua Bing Li Xue Za Zhi;47(2):99-104, 2018 Feb 08.
[Is] ISSN:0529-5807
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:To investigate the clinicopathologic characteristics, immunophenotype, differential and diagnostic features of atypical spindle cell lipomatous tumor (ASLT). Three cases of ASLT were collected from January 2010 to March 2017 at Zhejiang Provincial People's Hospital. The clinical and imaging features, histomorphology, immunophenotype and prognosis were analyzed. Fluorescence in situ hybridization (FISH) was used to detect MDM2 gene amplification, and relevant literature was reviewed. All three patients were adult males, aged 38, 43 and 54 years, respectively. One tumor originated in the subcutaneous soft tissue in the head and neck, one was located in the left primary bronchus and one in the latissimus dorsi muscle. Grossly, all three tumors were circumscribed and ranged from 4.0 to 5.8 cm in size. Microscopically, all showed a focally infiltrative front. These tumors were composed of variable proportions of spindle-shaped and adipocytic cells in a background of variable fibrous and edematous matrix. Scattered lipoblasts were easily seen. One tumor was composed predominately of spindle tumor cells, one of adipocytic cells, and one of equally mixed cell populations. The spindle tumor cells were generally bland-appearing with focal nuclear enlargement and hyperchromasia noted in one case. Mitosis was not seen in neither the spindle cells nor the adipocytic cells. By immunohistochemistry, diffuse and strong reactivity to CD34 of the spindle cells was noted in all cases, definite loss of Rb expression was noted in one of three cases, and S-100 protein was expressed only in the adipocytic cells. INI-1 was intact and Ki-67 index was 1% to 3%. All other markers including CDK4, MDM2, STAT6, SOX10, CD99, bcl-2, ß-catenin, CD117, GFAP, CK, EMA, SMA and desmin were negative. FISH of MDM2 was done in two cases, and both showed no amplification. The ASLT in the head and neck had two recurrences during 17 months of follow-up, whereas the tumor in the latissimus dorsi was free of disease during 33 months of follow-up. ASLT is a rare subtype of low-grade adipocytic neoplasm and is distinctive from atypical lipomatous tumor/well-differentiated liposarcoma. The histomorpholgy of ASLT has significant heterogeneity and forms a continuous spectrum. ASLT needs to be distinguished from a series of benign and malignant soft tissue tumors.
[Mh] Termos MeSH primário: Neoplasias Brônquicas/patologia
Neoplasias de Cabeça e Pescoço/patologia
Lipoma/patologia
Neoplasias Musculares/patologia
[Mh] Termos MeSH secundário: Adulto
Neoplasias Brônquicas/química
Neoplasias de Cabeça e Pescoço/química
Seres Humanos
Imuno-Histoquímica
Hibridização in Situ Fluorescente
Lipoma/química
Lipossarcoma/química
Lipossarcoma/patologia
Masculino
Meia-Idade
Neoplasias Musculares/química
Recidiva Local de Neoplasia
Proteínas S100/análise
Fator de Transcrição STAT6/análise
Músculos Superficiais do Dorso
beta Catenina/análise
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CTNNB1 protein, human); 0 (S100 Proteins); 0 (STAT6 Transcription Factor); 0 (STAT6 protein, human); 0 (beta Catenin)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180213
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.0529-5807.2018.02.004


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[PMID]:29381400
[Au] Autor:Song ZY; Wang F; Cui SX; Qu XJ
[Ad] Endereço:a Department of Pharmacology, School of Basic Medical Sciences , Capital Medical University , Beijing , China.
[Ti] Título:Knockdown of CXCR4 Inhibits CXCL12-Induced Angiogenesis in HUVECs through Downregulation of the MAPK/ERK and PI3K/AKT and the Wnt/ß-Catenin Pathways.
[So] Source:Cancer Invest;36(1):10-18, 2018 Jan 02.
[Is] ISSN:1532-4192
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:CXCL12 is an extracellular chemokine binding to cell surface receptor CXCR4. We found that activation of CXCL12/CXCR4 axis stimulated angiogenesis in endothelial cells. Knockdown of CXCR4 in endothelial cells prevented the branch points of angiogenesis. Endothelial cells exposed to CXCL12 presented high level of epidermal growth factor receptor (EGFR), vascular endothelial growth factor (VEGF), and matrix metalloproteinase MMP-2, but not in CXCR4 knockdown cells. Further studies revealed that activation of CXCL12/CXCR4 axis in vascular endothelial cells stimulates the angiogenesis through upregulation of the MAPK/ERK and PI3K/AKT and Wnt/ß-catenin pathways. Conclusion, downregulation of CXCR4 could inhibit angiogenesis in cancer tissues.
[Mh] Termos MeSH primário: Quimiocina CXCL12/genética
Regulação para Baixo/genética
Regulação Neoplásica da Expressão Gênica/genética
Neovascularização Patológica/genética
Receptores CXCR4/genética
Transdução de Sinais/genética
[Mh] Termos MeSH secundário: Linhagem Celular
Células Endoteliais/metabolismo
Células Endoteliais da Veia Umbilical Humana
Seres Humanos
Sistema de Sinalização das MAP Quinases/genética
Metaloproteinase 2 da Matriz/genética
Proteínas Quinases Ativadas por Mitógeno/genética
Fosfatidilinositol 3-Quinases/genética
Proteínas Proto-Oncogênicas c-akt/genética
Receptor do Fator de Crescimento Epidérmico/genética
Regulação para Cima/genética
Fator A de Crescimento do Endotélio Vascular/genética
Via de Sinalização Wnt/genética
beta Catenina/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CXCL12 protein, human); 0 (CXCR4 protein, human); 0 (Chemokine CXCL12); 0 (Receptors, CXCR4); 0 (Vascular Endothelial Growth Factor A); 0 (beta Catenin); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.10.1 (Receptor, Epidermal Growth Factor); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 2.7.11.24 (Mitogen-Activated Protein Kinases); EC 3.4.24.24 (Matrix Metalloproteinase 2)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180131
[St] Status:MEDLINE
[do] DOI:10.1080/07357907.2017.1422512


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[PMID]:28467300
[Au] Autor:Ku AT; Shaver TM; Rao AS; Howard JM; Rodriguez CN; Miao Q; Garcia G; Le D; Yang D; Borowiak M; Cohen DN; Chitsazzadeh V; Diwan AH; Tsai KY; Nguyen H
[Ad] Endereço:Stem Cell and Regenerative Medicine Center, Baylor College of Medicine, Houston, United States.
[Ti] Título:TCF7L1 promotes skin tumorigenesis independently of ß-catenin through induction of LCN2.
[So] Source:Elife;6, 2017 05 03.
[Is] ISSN:2050-084X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The transcription factor is an embryonic stem cell signature gene that is upregulated in multiple aggressive cancer types, but its role in skin tumorigenesis has not yet been defined. Here we document TCF7L1 upregulation in skin squamous cell carcinoma (SCC) and demonstrate that TCF7L1 overexpression increases tumor incidence, tumor multiplicity, and malignant progression in the chemically induced mouse model of skin SCC. Additionally, we show that downregulation of TCF7L1 and its paralogue TCF7L2 reduces tumor growth in a xenograft model of human skin SCC. Using separation-of-function mutants, we show that TCF7L1 promotes tumor growth, enhances cell migration, and overrides oncogenic RAS-induced senescence independently of its interaction with ß-catenin. Through transcriptome profiling and combined gain- and loss-of-function studies, we identified LCN2 as a major downstream effector of TCF7L1 that drives tumor growth. Our findings establish a tumor-promoting role for TCF7L1 in skin and elucidate the mechanisms underlying its tumorigenic capacity.
[Mh] Termos MeSH primário: Carcinogênese
Carcinoma de Células Escamosas/fisiopatologia
Lipocalina-2/metabolismo
Neoplasias Cutâneas/fisiopatologia
Proteína 1 Semelhante ao Fator 7 de Transcrição/metabolismo
beta Catenina/metabolismo
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Perfilação da Expressão Gênica
Xenoenxertos
Seres Humanos
Camundongos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (CTNNB1 protein, human); 0 (LCN2 protein, human); 0 (Lipocalin-2); 0 (TCF7L1 protein, human); 0 (Transcription Factor 7-Like 1 Protein); 0 (beta Catenin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE


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[PMID]:28463112
[Au] Autor:Edens BM; Yan J; Miller N; Deng HX; Siddique T; Ma YC
[Ad] Endereço:Department of Pediatrics, Northwestern University Feinberg School of Medicine, Ann & Robert H Lurie Children's Hospital of Chicago, Chicago, United States.
[Ti] Título:A novel ALS-associated variant in regulates motor axon morphogenesis.
[So] Source:Elife;6, 2017 05 02.
[Is] ISSN:2050-084X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The etiological underpinnings of amyotrophic lateral sclerosis (ALS) are complex and incompletely understood, although contributions to pathogenesis by regulators of proteolytic pathways have become increasingly apparent. Here, we present a novel variant in that is associated with ALS and show that its expression compromises motor axon morphogenesis in mouse motor neurons and in zebrafish. We further demonstrate that the ALS-associated variant impairs proteasomal function, and identify the Wnt signaling pathway effector beta-catenin as a substrate. Inhibition of beta-catenin function rescues the variant-induced motor axon phenotypes. These findings provide a strong link between the regulation of axonal morphogenesis and a new ALS-associated gene variant mediated by protein degradation pathways.
[Mh] Termos MeSH primário: Esclerose Amiotrófica Lateral/genética
Esclerose Amiotrófica Lateral/patologia
Proteínas de Transporte/genética
Morfogênese
Neurônios Motores/citologia
Proteínas Nucleares/genética
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Camundongos
Complexo de Endopeptidases do Proteassoma/metabolismo
Proteólise
Peixe-Zebra
beta Catenina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Carrier Proteins); 0 (Nuclear Proteins); 0 (UBQLN4 protein, human); 0 (beta Catenin); EC 3.4.25.1 (Proteasome Endopeptidase Complex)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE


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[PMID]:28460484
[Au] Autor:Wiese M; Walther N; Diederichs C; Schill F; Monecke S; Salinas G; Sturm D; Pfister SM; Dressel R; Johnsen SA; Kramm CM
[Ad] Endereço:Division of Pediatric Hematology and Oncology, Department of Child and Adolescent Health, University Medical Center Goettingen, Goettingen, Germany.
[Ti] Título:The ß-catenin/CBP-antagonist ICG-001 inhibits pediatric glioma tumorigenicity in a Wnt-independent manner.
[So] Source:Oncotarget;8(16):27300-27313, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Pediatric high-grade gliomas (pedHGG) belong to the most aggressive cancers in children with a poor prognosis due to a lack of efficient therapeutic strategies. The ß-catenin/Wnt-signaling pathway was shown to hold promising potential as a treatment target in adult high-grade gliomas by abrogating tumor cell invasion and the acquisition of stem cell-like characteristics. Since pedHGG differ from their adult counterparts in genetically and biologically we aimed to investigate the effects of ß-catenin/Wnt-signaling pathway-inhibition by the ß-catenin/CBP antagonist ICG-001 in pedHGG cell lines. In contrast to adult HGG, pedHGG cells displayed minimal detectable canonical Wnt-signaling activity. Nevertheless, low doses of ICG-001 inhibited cell migration/invasion, tumorsphere- and colony formation, proliferation in vitro as well as tumor growth in vivo/ovo, suggesting that ICG-001 affects pedHGG tumor cell characteristics independent of ß-catenin/Wnt-signaling. RNA-sequencing analyses support a Wnt/ß-catenin-independent effect of ICG-001 on target gene transcription, revealing strong effects on genes involved in cellular metabolic/biosynthetic processes and cell cycle progression. Among these, high mRNA expression of cell cycle regulator JDP2 was found to confer a better prognosis for pedHGG patients. In conclusion, ICG-001 might offer an effective treatment option for pedHGG patients functioning to regulate cell phenotype and gene expression programs in absence of Wnt/ß-catenin signaling-activity.
[Mh] Termos MeSH primário: Compostos Bicíclicos Heterocíclicos com Pontes/farmacologia
Proteína de Ligação a CREB/antagonistas & inibidores
Transformação Celular Neoplásica/efeitos dos fármacos
Transformação Celular Neoplásica/metabolismo
Glioma/metabolismo
Pirimidinonas/farmacologia
Via de Sinalização Wnt/efeitos dos fármacos
beta Catenina/antagonistas & inibidores
[Mh] Termos MeSH secundário: Adolescente
Animais
Linhagem Celular Tumoral
Movimento Celular/efeitos dos fármacos
Movimento Celular/genética
Autorrenovação Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Transformação Celular Neoplásica/genética
Embrião de Galinha
Criança
Pré-Escolar
Bases de Dados Genéticas
Modelos Animais de Doenças
Glioma/genética
Glioma/mortalidade
Glioma/patologia
Seres Humanos
Estimativa de Kaplan-Meier
Células-Tronco Neoplásicas/citologia
Células-Tronco Neoplásicas/efeitos dos fármacos
Células-Tronco Neoplásicas/metabolismo
Prognóstico
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bridged Bicyclo Compounds, Heterocyclic); 0 (ICG 001); 0 (Pyrimidinones); 0 (beta Catenin); EC 2.3.1.48 (CREB-Binding Protein); EC 2.3.1.48 (CREBBP protein, human)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.15934


  9 / 15191 MEDLINE  
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[PMID]:28743796
[Au] Autor:Roberts SL; Dun XP; Doddrell RDS; Mindos T; Drake LK; Onaitis MW; Florio F; Quattrini A; Lloyd AC; D'Antonio M; Parkinson DB
[Ad] Endereço:Plymouth University Peninsula Schools of Medicine and Dentistry, John Bull Building, Plymouth Science Park, Plymouth PL6 8BU, UK.
[Ti] Título:Sox2 expression in Schwann cells inhibits myelination and induces influx of macrophages to the nerve.
[So] Source:Development;144(17):3114-3125, 2017 09 01.
[Is] ISSN:1477-9129
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Correct myelination is crucial for the function of the peripheral nervous system. Both positive and negative regulators within the axon and Schwann cell function to ensure the correct onset and progression of myelination during both development and following peripheral nerve injury and repair. The Sox2 transcription factor is well known for its roles in the development and maintenance of progenitor and stem cell populations, but has also been proposed as a negative regulator of myelination in Schwann cells. We wished to test fully whether Sox2 regulates myelination and show here that, in mice, sustained Sox2 expression blocks myelination in the peripheral nerves and maintains Schwann cells in a proliferative non-differentiated state, which is also associated with increased inflammation within the nerve. The plasticity of Schwann cells allows them to re-myelinate regenerated axons following injury and we show that re-myelination is also blocked by Sox2 expression in Schwann cells. These findings identify Sox2 as a physiological regulator of Schwann cell myelination and its potential to play a role in disorders of myelination in the peripheral nervous system.
[Mh] Termos MeSH primário: Macrófagos/metabolismo
Bainha de Mielina/metabolismo
Nervos Periféricos/metabolismo
Fatores de Transcrição SOXB1/metabolismo
Células de Schwann/metabolismo
[Mh] Termos MeSH secundário: Animais
Biomarcadores/metabolismo
Caderinas/metabolismo
Proliferação Celular
Proteína 2 de Resposta de Crescimento Precoce/metabolismo
Proteínas de Fluorescência Verde/metabolismo
Camundongos Transgênicos
Atividade Motora
Condução Nervosa
Traumatismos dos Nervos Periféricos/metabolismo
Traumatismos dos Nervos Periféricos/patologia
Nervos Periféricos/patologia
Nervos Periféricos/ultraestrutura
Proteínas Proto-Oncogênicas c-jun/metabolismo
Ratos
Recuperação de Função Fisiológica
Células de Schwann/patologia
Transgenes
beta Catenina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Biomarkers); 0 (Cadherins); 0 (Early Growth Response Protein 2); 0 (Proto-Oncogene Proteins c-jun); 0 (SOXB1 Transcription Factors); 0 (beta Catenin); 147336-22-9 (Green Fluorescent Proteins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE
[do] DOI:10.1242/dev.150656


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[PMID]:29271667
[Au] Autor:Fan R; He H; Yao W; Zhu Y; Zhou X; Gui M; Lu J; Xi H; Deng Z; Fan M
[Ad] Endereço:1 Department of Cardiology, Yueyang Hospital Integrated Traditional Chinese and Western Medicine, Shanghai University of Traditional Chinese Medicine , Shanghai, China .
[Ti] Título:SOX7 Suppresses Wnt Signaling by Disrupting ß-Catenin/BCL9 Interaction.
[So] Source:DNA Cell Biol;37(2):126-132, 2018 Feb.
[Is] ISSN:1557-7430
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The Wnt signaling is involved in angiogenesis and tumor development. ß-catenin is the core component of the Wnt pathway, which mediates oncogenic transcription and regulated by a series of proteins. Sex-determining region Y-box 7 (SOX7) is a member of high-mobility-group transcription factor family, which inhibits oncogenic Wnt signaling in lots of tumor cells with unknown mechanism. By coimmunoprecipitation (co-IP) and super Topflash reporter assay, SOX7 can bind ß-catenin and inhibit ß-catenin/T cell factor (TCF)-mediated transcription. Meanwhile, B cell lymphoma 9 (BCL9) drives Wnt signaling path through direct binding-mediated ß-catenin. Finally, we found that SOX7 inhibits oncogenic ß-catenin-mediated transcription by disrupting the ß-catenin/BCL9 interaction. Mechanistically, SOX7 compete with BCL9 to bind ß-catenin. Our results show SOX7 inhibited Wnt signaling as suppressor and could be an important target for anticancer therapy.
[Mh] Termos MeSH primário: Proteínas de Neoplasias/metabolismo
Fatores de Transcrição SOXF/fisiologia
beta Catenina/metabolismo
[Mh] Termos MeSH secundário: Proliferação Celular
Células HEK293
Seres Humanos
Ligação Proteica
Transcrição Genética
Via de Sinalização Wnt
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (BCL9 protein, human); 0 (CTNNB1 protein, human); 0 (Neoplasm Proteins); 0 (SOX7 protein, human); 0 (SOXF Transcription Factors); 0 (beta Catenin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171223
[St] Status:MEDLINE
[do] DOI:10.1089/dna.2017.3866



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