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[PMID]:27776018
[Au] Autor:Vartanian A; Baryshnikova M; Burova O; Afanasyeva D; Misyurin V; Belyаvsky A; Shprakh Z
[Ad] Endereço:Department of Experimental Diagnosis and Therapy of Tumors, N.N. Blokhin Russian Cancer Research Center, Moscow, Russia.
[Ti] Título:Inhibitor of vasculogenic mimicry restores sensitivity of resistant melanoma cells to DNA-damaging agents.
[So] Source:Melanoma Res;27(1):8-16, 2017 Feb.
[Is] ISSN:1473-5636
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The increasing incidence of melanoma makes this cancer an important public health problem. Therapeutic resistance is still a major obstacle to the therapy of patients with metastatic melanomas. The aim of this study was to develop the melanoma cell line resistant to DNA-alkylating agents and to elucidate the mechanisms involved in acquired drug resistance. We established a unique melanoma subline Mel MeR resistant to DNA-alkylating drug aranoza by continuous stepwise selection of the Mel Me/WT cell line with increasing concentrations of this drug. Mel MeR cells were also cross-resistant to streptozotocin or cisplatin. Here, we show that aranoza-resistant melanoma cells modulate the ABC transporter activity, upregulate the expression of PRAME, adopt a vascular-related phenotype and engage in vasculogenic mimicry. LCS1269, a vasculogenic mimicry low-molecular-weight inhibitor, reverses the sensitivity of resistant melanoma cells to DNA-damaging agents. In this study, we provide experimental evidence that LCS1269 might be considered as a new potential anticancer agent capable of overcoming multidrug resistance for DNA-damaging agents in melanoma.
[Mh] Termos MeSH primário: Antineoplásicos Alquilantes/farmacologia
Carbazóis/farmacologia
Linhagem Celular Tumoral
Resistência a Medicamentos Antineoplásicos
Glicosídeos/farmacologia
Melanoma/tratamento farmacológico
Melanoma/metabolismo
Metilnitrosoureia/análogos & derivados
Neovascularização Patológica/prevenção & controle
[Mh] Termos MeSH secundário: Membro 1 da Subfamília B de Cassetes de Ligação de ATP/metabolismo
Antígenos de Neoplasias/genética
Apoptose/efeitos dos fármacos
Antígeno CD24/metabolismo
Resistência a Medicamentos Antineoplásicos/genética
Endoglina/metabolismo
Corantes Fluorescentes/metabolismo
Expressão Gênica/efeitos dos fármacos
Seres Humanos
Receptores de Hialuronatos/metabolismo
Molécula 1 de Adesão Intercelular/metabolismo
Masculino
Melanoma/irrigação sanguínea
Melanoma/genética
Metilnitrosoureia/farmacologia
Meia-Idade
Proteínas de Neoplasias/genética
Células-Tronco Neoplásicas/metabolismo
Proteínas Nucleares/genética
Fenótipo
Fosfoproteínas Fosfatases/genética
Proteínas Proto-Oncogênicas c-kit/metabolismo
Rodamina 123/metabolismo
Tetraspanina 30/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ABCB5 protein, human); 0 (ATP-Binding Cassette, Sub-Family B, Member 1); 0 (Antigens, Neoplasm); 0 (Antineoplastic Agents, Alkylating); 0 (CD24 Antigen); 0 (CD24 protein, human); 0 (CD44 protein, human); 0 (CD63 protein, human); 0 (Carbazoles); 0 (ENG protein, human); 0 (Endoglin); 0 (Fluorescent Dyes); 0 (GAGE1 protein, human); 0 (Glycosides); 0 (Hyaluronan Receptors); 0 (LCS1269); 0 (Neoplasm Proteins); 0 (Nuclear Proteins); 0 (PRAME protein, human); 0 (Tetraspanin 30); 0 (aranoza); 126547-89-5 (Intercellular Adhesion Molecule-1); 1N3CZ14C5O (Rhodamine 123); 684-93-5 (Methylnitrosourea); EC 2.7.10.1 (Proto-Oncogene Proteins c-kit); EC 3.1.3.16 (CTDSP1 protein, human); EC 3.1.3.16 (Phosphoprotein Phosphatases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE
[do] DOI:10.1097/CMR.0000000000000308


  2 / 1128 MEDLINE  
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[PMID]:29355544
[Au] Autor:Li X; Zhou N; Wang J; Liu Z; Wang X; Zhang Q; Liu Q; Gao L; Wang R
[Ad] Endereço:Key Laboratory of Pharmacology, Chifeng University, Hongshan, Chifeng, Inner Mongolia 024000, China.
[Ti] Título:Quercetin suppresses breast cancer stem cells (CD44 /CD24 ) by inhibiting the PI3K/Akt/mTOR-signaling pathway.
[So] Source:Life Sci;196:56-62, 2018 Mar 01.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: Cancer stem cells (CSCs) are considered the prime source of cancer recurrence, metastasis, and progression and represent important targets for developing novel anticancer agents and therapeutic strategies. The aim of this study was to investigate the effect of treating breast CSCs with the anticancer flavonoid, quercetin. MAIN METHODS: We examined changes in the cluster of differentiation CD44 /CD24 CSC population and behavior using the breast cancer cell line MCF-7. KEY FINDINGS: Our results indicated that cell viability, clone formation, mammosphere generation, and nude mice tumor metastasis were inhibited in the CD44 /CD24 population and that MCF-7 cells exhibited G1-phase arrest after quercetin treatment. Additionally, CyclinD1 and B cell lymphoma-2 expression were suppressed and Bcl-2-like protein-4 expression was enhanced after quercetin treatment. We also observed that estrogen receptor α and phosphatidylinositol-3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) signaling were downregulated concurrently with the inhibition of CD44 /CD24 viability and clone formation. Our findings suggested that quercetin treatment promoted weaker malignant activity associated with CSCs relative to that observed in normal cancer cells through its inhibition of the PI3K/Akt/mTOR-signaling pathway. SIGNIFICANCE: These results indicated that CSCs are potential therapeutic targets for quercetin treatment of breast cancer.
[Mh] Termos MeSH primário: Antioxidantes/farmacologia
Antígeno CD24/efeitos dos fármacos
Receptores de Hialuronatos/efeitos dos fármacos
Proteína Oncogênica v-akt/antagonistas & inibidores
Fosfatidilinositol 3-Quinases/antagonistas & inibidores
Quercetina/farmacologia
Transdução de Sinais/efeitos dos fármacos
Serina-Treonina Quinases TOR/antagonistas & inibidores
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Feminino
Fase G1/efeitos dos fármacos
Seres Humanos
Células MCF-7
Camundongos Nus
Proteínas Proto-Oncogênicas c-bcl-2/antagonistas & inibidores
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (CD24 Antigen); 0 (CD44 protein, human); 0 (Hyaluronan Receptors); 0 (Proto-Oncogene Proteins c-bcl-2); 9IKM0I5T1E (Quercetin); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.1.1 (MTOR protein, human); EC 2.7.1.1 (TOR Serine-Threonine Kinases); EC 2.7.11.1 (Oncogene Protein v-akt)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180123
[St] Status:MEDLINE


  3 / 1128 MEDLINE  
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[PMID]:28461108
[Au] Autor:Santaguida MG; Gatto I; Mangino G; Virili C; Stramazzo I; Fallahi P; Antonelli A; Segni M; Romeo G; Centanni M
[Ad] Endereço:Department of Medico-Surgical Sciences and Biotechnologies, "Sapienza" University of Rome, Latina, Italy.
[Ti] Título:BREG cells in Hashimoto's thyroiditis isolated or associated to further organ-specific autoimmune diseases.
[So] Source:Clin Immunol;184:42-47, 2017 11.
[Is] ISSN:1521-7035
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Hashimoto thyroiditis (HT) may occur isolated or associated with other non-endocrine autoimmune disorders (NEAD). No data are available about Breg cells in these disorders and this represented the aim of the study. Th17 and Breg cells subset were characterized on peripheral blood mononuclear cells isolated from 18 healthy donors (HD), 19 patients with isolated HT and 26 patients with HT+NEAD. Th17 were higher in patients with isolated HT than in HD but no further changes were seen in patients with HT+NEAD. CD24 CD38 unstimulated Breg cells were similar in HT patients and in HD, but significantly higher in patients with HT+NEAD than in both HT and in HD. CD19 CD24 CD27 Breg memory phenotype was similar in HD and in HT patients, but decreased in patients with HT+NEAD (23.4%vs38.5%). Upon CpG-stimulation, CD24 CD38 IL-10 Breg cells were higher in HT patients than in HD (3.9%vs1.8%) but similar in patients with HT+NEAD (2.4%).
[Mh] Termos MeSH primário: Linfócitos B Reguladores/imunologia
Doença Celíaca/imunologia
Gastrite Atrófica/imunologia
Doença de Hashimoto/imunologia
Células Th17/imunologia
Vitiligo/imunologia
[Mh] Termos MeSH secundário: ADP-Ribosil Ciclase 1/imunologia
Adulto
Antígenos CD19/imunologia
Doenças Autoimunes/complicações
Doenças Autoimunes/imunologia
Antígeno CD24/imunologia
Estudos de Casos e Controles
Doença Celíaca/complicações
Feminino
Gastrite Atrófica/complicações
Doença de Hashimoto/complicações
Seres Humanos
Interleucina-10/imunologia
Masculino
Glicoproteínas de Membrana/imunologia
Meia-Idade
Membro 7 da Superfamília de Receptores de Fatores de Necrose Tumoral/imunologia
Vitiligo/complicações
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD19); 0 (CD19 molecule, human); 0 (CD24 Antigen); 0 (CD24 protein, human); 0 (IL10 protein, human); 0 (Membrane Glycoproteins); 0 (Tumor Necrosis Factor Receptor Superfamily, Member 7); 130068-27-8 (Interleukin-10); EC 3.2.2.5 (CD38 protein, human); EC 3.2.2.6 (ADP-ribosyl Cyclase 1)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:180206
[Lr] Data última revisão:
180206
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE


  4 / 1128 MEDLINE  
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[PMID]:29227074
[Au] Autor:Minchenko OH; Tsymbal DO; Minchenko DO; Riabovol OO; Ratushna OO; Karbovskyi LL
[Ti] Título:Hypoxic regulation of the expression of cell proliferation related genes in U87 glioma cells upon inhibition of ire1 signaling enzyme
[So] Source:Ukr Biochem J;88(1):11-21, 2016 Ja-Feb.
[Is] ISSN:2409-4943
[Cp] País de publicação:Ukraine
[La] Idioma:eng
[Ab] Resumo:We have studied the effect of inhibition of IRE1 (inositol requiring enzyme 1), which is a central mediator of endoplasmic reticulum stress and a controller of cell proliferation and tumor growth, on hypoxic regulation of the expression of different proliferation related genes in U87 glioma cells. It was shown that hypoxia leads to up-regulation of the expression of IL13RA2, CD24, ING1, ING2, ENDOG, and POLG genes and to down-regulation ­ of KRT18, TRAPPC3, TSFM, and MTIF2 genes at the mRNA level in control glioma cells. Changes for ING1 and CD24 genes were more significant. At the same time, inhibition of IRE1 modifies the effect of hypoxia on the expression of all studied genes. In particular, it increases sensitivity to hypoxia of the expression of IL13RA2, TRAPPC3, ENDOG, and PLOG genes and suppresses the effect of hypoxia on the expression of ING1 gene. Additionally, it eliminates hypoxic regulation of KRT18, CD24, ING2, TSFM, and MTIF2 genes expressions and introduces sensitivity to hypoxia of the expression of BET1 gene in glioma cells. The present study demonstrates that hypoxia, which often contributes to tumor growth, affects the expression of almost all studied genes. Additionally, inhibition of IRE1 can both enhance and suppress the hypoxic regulation of these gene expressions in a gene specific manner and thus possibly contributes to slower glioma growth, but several aspects of this regulation must be further clarified.
[Mh] Termos MeSH primário: Estresse do Retículo Endoplasmático/genética
Endorribonucleases/genética
Regulação Neoplásica da Expressão Gênica
Neuroglia/metabolismo
Proteínas Serina-Treonina Quinases/genética
RNA Mensageiro/genética
Transdução de Sinais/genética
[Mh] Termos MeSH secundário: Antígeno CD24/genética
Antígeno CD24/metabolismo
Hipóxia Celular
Linhagem Celular Tumoral
Proliferação Celular
DNA Polimerase gama/genética
DNA Polimerase gama/metabolismo
Endodesoxirribonucleases/genética
Endodesoxirribonucleases/metabolismo
Endorribonucleases/antagonistas & inibidores
Endorribonucleases/metabolismo
Fatores de Iniciação em Eucariotos/genética
Fatores de Iniciação em Eucariotos/metabolismo
Proteínas de Homeodomínio/genética
Proteínas de Homeodomínio/metabolismo
Seres Humanos
Proteína 1 Inibidora do Crescimento/genética
Proteína 1 Inibidora do Crescimento/metabolismo
Subunidade alfa2 de Receptor de Interleucina-13/genética
Subunidade alfa2 de Receptor de Interleucina-13/metabolismo
Queratina-18/genética
Queratina-18/metabolismo
Proteínas Mitocondriais/genética
Proteínas Mitocondriais/metabolismo
Neuroglia/patologia
Fatores de Alongamento de Peptídeos/genética
Fatores de Alongamento de Peptídeos/metabolismo
Proteínas Serina-Treonina Quinases/antagonistas & inibidores
Proteínas Serina-Treonina Quinases/metabolismo
Proteínas Qc-SNARE/genética
Proteínas Qc-SNARE/metabolismo
RNA Mensageiro/metabolismo
Receptores Citoplasmáticos e Nucleares/genética
Receptores Citoplasmáticos e Nucleares/metabolismo
Proteínas Supressoras de Tumor/genética
Proteínas Supressoras de Tumor/metabolismo
Proteínas de Transporte Vesicular/genética
Proteínas de Transporte Vesicular/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (BET1L protein, human); 0 (CD24 Antigen); 0 (Eukaryotic Initiation Factors); 0 (Homeodomain Proteins); 0 (ING1 protein, human); 0 (ING2 protein, human); 0 (Inhibitor of Growth Protein 1); 0 (Interleukin-13 Receptor alpha2 Subunit); 0 (KRT18 protein, human); 0 (Keratin-18); 0 (MTIF2 protein, human); 0 (Mitochondrial Proteins); 0 (Peptide Elongation Factors); 0 (Qc-SNARE Proteins); 0 (RNA, Messenger); 0 (Receptors, Cytoplasmic and Nuclear); 0 (TRAPPC3 protein, human); 0 (TSFM protein, human); 0 (Tumor Suppressor Proteins); 0 (Vesicular Transport Proteins); EC 2.7.11.1 (ERN1 protein, human); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.7.7 (DNA Polymerase gamma); EC 2.7.7.7 (POLG protein, human); EC 3.1.- (Endodeoxyribonucleases); EC 3.1.- (Endoribonucleases); EC 3.1.21.- (endonuclease G)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180116
[Lr] Data última revisão:
180116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171212
[St] Status:MEDLINE
[do] DOI:10.15407/ubj88.01.011


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[PMID]:29277789
[Au] Autor:Spelt L; Sasor A; Ansari D; Hilmersson KS; Andersson R
[Ad] Endereço:Department of Surgery, Clinical Sciences Lund, Lund University and Skåne University Hospital, Lund, Sweden lidewij.spelt@med.lu.se.
[Ti] Título:The Prognostic Role of Cancer Stem Cell Markers for Long-term Outcome After Resection of Colonic Liver Metastases.
[So] Source:Anticancer Res;38(1):313-320, 2018 01.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIM: To assess the expression of cancer stem cell (CSC) markers CD44, CD133 and CD24 in colon cancer liver metastases and analyse their predictive value for overall survival (OS) and disease-free survival (DFS) after liver resection. MATERIALS AND METHODS: Patients operated on for colon cancer liver metastases were included. CSC marker expression was determined through immunohistochemistry analysis. OS and DFS were compared between marker-positive and marker-negative patients. Multivariate analysis was performed to select predictive variables for OS and DFS. RESULTS: CD133-positive patients had a worse DFS than CD133-negative patients, with a median DFS of 12 and 25 months (p=0.051). Multivariate analysis selected CD133 expression as a significant predictor for DFS. CD44 and CD24 were not found to predict OS or DFS. CONCLUSION: CD133 expression in colonic liver metastases is a negative prognostic factor for DFS after liver resection. In the future, CD133 could be used as a biomarker for risk stratification, and possibly for developing novel targeted therapy.
[Mh] Termos MeSH primário: Antígeno AC133/metabolismo
Antígeno CD24/metabolismo
Neoplasias do Colo/patologia
Receptores de Hialuronatos/metabolismo
Neoplasias Hepáticas/secundário
Células-Tronco Neoplásicas/metabolismo
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Biomarcadores Tumorais
Colo/patologia
Intervalo Livre de Doença
Feminino
Hepatectomia
Seres Humanos
Fígado/patologia
Fígado/cirurgia
Neoplasias Hepáticas/mortalidade
Neoplasias Hepáticas/cirurgia
Masculino
Meia-Idade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (AC133 Antigen); 0 (Biomarkers, Tumor); 0 (CD24 Antigen); 0 (CD24 protein, human); 0 (CD44 protein, human); 0 (Hyaluronan Receptors); 0 (PROM1 protein, human)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180104
[Lr] Data última revisão:
180104
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171227
[St] Status:MEDLINE


  6 / 1128 MEDLINE  
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[PMID]:29183942
[Au] Autor:Urbanska M; Winzi M; Neumann K; Abuhattum S; Rosendahl P; Müller P; Taubenberger A; Anastassiadis K; Guck J
[Ad] Endereço:Cellular Machines, Biotechnology Center, Center for Molecular and Cellular Bioengineering, Technische Universität Dresden, Tatzberg 47-49, Dresden 01307, Germany marta.urbanska@tu-dresden.de jochen.guck@tu-dresden.de.
[Ti] Título:Single-cell mechanical phenotype is an intrinsic marker of reprogramming and differentiation along the mouse neural lineage.
[So] Source:Development;144(23):4313-4321, 2017 Dec 01.
[Is] ISSN:1477-9129
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Cellular reprogramming is a dedifferentiation process during which cells continuously undergo phenotypical remodeling. Although the genetic and biochemical details of this remodeling are fairly well understood, little is known about the change in cell mechanical properties during the process. In this study, we investigated changes in the mechanical phenotype of murine fetal neural progenitor cells (fNPCs) during reprogramming to induced pluripotent stem cells (iPSCs). We find that fNPCs become progressively stiffer en route to pluripotency, and that this stiffening is mirrored by iPSCs becoming more compliant during differentiation towards the neural lineage. Furthermore, we show that the mechanical phenotype of iPSCs is comparable with that of embryonic stem cells. These results suggest that mechanical properties of cells are inherent to their developmental stage. They also reveal that pluripotent cells can differentiate towards a more compliant phenotype, which challenges the view that pluripotent stem cells are less stiff than any cells more advanced developmentally. Finally, our study indicates that the cell mechanical phenotype might be utilized as an inherent biophysical marker of pluripotent stem cells.
[Mh] Termos MeSH primário: Diferenciação Celular/fisiologia
Reprogramação Celular/fisiologia
Células-Tronco Neurais/citologia
Células-Tronco Neurais/fisiologia
[Mh] Termos MeSH secundário: Animais
Biomarcadores/metabolismo
Fenômenos Biomecânicos
Antígeno CD24/metabolismo
Diferenciação Celular/genética
Linhagem da Célula/genética
Linhagem da Célula/fisiologia
Reprogramação Celular/genética
Células-Tronco Pluripotentes Induzidas/classificação
Células-Tronco Pluripotentes Induzidas/citologia
Células-Tronco Pluripotentes Induzidas/fisiologia
Antígeno Lewis X/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Células-Tronco Neurais/classificação
Fenótipo
Análise de Célula Única
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (CD24 Antigen); 0 (Cd24a protein, mouse); 0 (Lewis X Antigen)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171204
[Lr] Data última revisão:
171204
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171130
[St] Status:MEDLINE
[do] DOI:10.1242/dev.155218


  7 / 1128 MEDLINE  
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[PMID]:28746471
[Au] Autor:Wanandi SI; Yustisia I; Neolaka GMG; Jusman SWA
[Ad] Endereço:Department of Biochemistry and Molecular Biology, Faculty of Medicine, Universitas Indonesia, Jakarta, Indonesia.
[Ti] Título:Impact of extracellular alkalinization on the survival of human CD24-/CD44+ breast cancer stem cells associated with cellular metabolic shifts.
[So] Source:Braz J Med Biol Res;50(8):e6538, 2017 Jul 20.
[Is] ISSN:1414-431X
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:Cancer stem cells reside in a distinct region within the tumor microenvironment that it is believed to play a fundamental role in regulating stemness, proliferation, survival, and metabolism of cancer cells. This study aimed to analyze the effect of extracellular alkalinization on metabolism and survival of human CD24-/CD44+ breast cancer stem cells (BCSCs). BCSCs were cultured in alkalinized DMEM-F12 and incubated at 37°C, 5% CO2, and 20% O2 for 30 min, 6, 24, and 48 h. After each incubation period, we analyzed the modulation of various mRNA expressions related to pH and cellular metabolic regulation using the qRT-PCR. Metabolic state was measured using colorimetric and fluorometric assays. To examine cell proliferation and apoptosis, we used trypan blue and annexin V/propidium iodide assay, respectively. This study demonstrated that alkalinization could stimulate extracellular carbonic anhydrase (CAe) activity, as well as CA9 and HIF1α expression. Under alkaline pH and HIF1α regulation, glucose consumption, extracellular lactate production, and LDH activity of BCSCs were upregulated while O2 consumption was downregulated. These metabolic shifts seemed to promote apoptosis and suppress the proliferation of BCSCs. To conclude, modulation of the extracellular environment through alkalinization could change the metabolic states of BCSCs, which in turn affect the cell survival.
[Mh] Termos MeSH primário: Neoplasias da Mama/metabolismo
Antígeno CD24/metabolismo
Receptores de Hialuronatos/metabolismo
Células-Tronco Neoplásicas/metabolismo
[Mh] Termos MeSH secundário: Apoptose
Proliferação Celular
Sobrevivência Celular
Espaço Extracelular
Feminino
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Reação em Cadeia da Polimerase Via Transcriptase Reversa
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD24 Antigen); 0 (CD24 protein, human); 0 (CD44 protein, human); 0 (Hyaluronan Receptors)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171204
[Lr] Data última revisão:
171204
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE


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[PMID]:28793333
[Au] Autor:Belogortseva N; Krezalek M; Guyton K; Labno C; Poroyko V; Zaborina O; Alverdy JC
[Ad] Endereço:Department of Surgery, University of Chicago, Chicago, Illinois, United States of America.
[Ti] Título:Media from macrophages co-incubated with Enterococcus faecalis induces epithelial cell monolayer reassembly and altered cell morphology.
[So] Source:PLoS One;12(8):e0182825, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Signal exchange between intestinal epithelial cells, microbes and local immune cells is an important mechanism of intestinal homeostasis. Given that intestinal macrophages are in close proximity to both the intestinal epithelium and the microbiota, their pathologic interactions may result in epithelial damage. The present study demonstrates that co-incubation of murine macrophages with E. faecalis strains producing gelatinase (GelE) and serine protease (SprE) leads to resultant condition media (CM) capable of inducing reassembly of primary colonic epithelial cell monolayers. Following the conditioned media (CM) exposure, some epithelial cells are shed whereas adherent cells are observed to undergo dissolution of cell-cell junctions and morphologic transformation with actin cytoskeleton reorganization resulting in flattened and elongated shapes. These cells exhibit marked filamentous filopodia and lamellipodia formation. Cellular reorganization is not observed when epithelial monolayers are exposed to: CM from macrophages co-incubated with E. faecalis GelE/SprE-deficient mutants, CM from macrophages alone, or E. faecalis (GelE/SprE) alone. Flow cytometry analysis reveals increased expression of CD24 and CD44 in cells treated with macrophage/E. faecalis CM. This finding in combination with the appearance colony formation in matrigel demonstrate that the cells treated with macrophage/E. faecalis CM contain a higher proportion progenitor cells compared to untreated control. Taken together, these findings provide evidence for a triangulated molecular dialogue between E. faecalis, macrophages and colonic epithelial cells, which may have important implications for conditions in the gut that involve inflammation, injury or tumorigenesis.
[Mh] Termos MeSH primário: Enterococcus faecalis/metabolismo
Células Epiteliais/citologia
Mucosa Intestinal/citologia
Macrófagos/citologia
[Mh] Termos MeSH secundário: Animais
Antígeno CD24/metabolismo
Linhagem Celular
Forma Celular/fisiologia
Meios de Cultura
Células Epiteliais/metabolismo
Células Epiteliais/microbiologia
Gelatinases/metabolismo
Receptores de Hialuronatos/metabolismo
Mucosa Intestinal/metabolismo
Mucosa Intestinal/microbiologia
Macrófagos/metabolismo
Macrófagos/microbiologia
Camundongos
Serina Endopeptidases/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD24 Antigen); 0 (Culture Media); 0 (Hyaluronan Receptors); EC 3.4.21.- (Serine Endopeptidases); EC 3.4.24.- (Gelatinases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170810
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0182825


  9 / 1128 MEDLINE  
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[PMID]:28683133
[Au] Autor:Bautista-Caro MB; de Miguel E; Peiteado D; Plasencia-Rodríguez C; Villalba A; Monjo-Henry I; Puig-Kröger A; Sánchez-Mateos P; Martín-Mola E; Miranda-Carús ME
[Ad] Endereço:Department of Rheumatology, Hospital Universitario La Paz-IdiPAZ, Madrid, Spain.
[Ti] Título:Increased frequency of circulating CD19+CD24hiCD38hi B cells with regulatory capacity in patients with Ankylosing spondylitis (AS) naïve for biological agents.
[So] Source:PLoS One;12(7):e0180726, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Our objective was to study the frequency of circulating CD19+CD24hiCD38hi B cells (Breg) in AS patients. To this end, peripheral blood was drawn from AS patients naïve for TNF blockers (AS/nb) (n = 42) and healthy controls (HC) (n = 42). Six patients donated blood for a second time, 6 months after initiating treatment with anti-TNFα drugs. After isolation by Ficoll-Hypaque, PBMCs were stained with antibodies to CD3, CD4, CD19, CD24, and CD38, and examined by cytometry. For functional studies, total CD19+ B cells were isolated from PBMCs of 3 HC by magnetical sorting. Breg-depleted CD19+ B cells were obtained after CD19+CD24hiCD38hi B cells were removed from total CD19+ cells by cytometry. Total CD19+ B cells or Breg-depleted CD19+ B cells were established in culture and stimulated through their BCR. Secretion of IFNγ was determined by ELISA in culture supernatants. When compared with HC, AS/nb patients demonstrated a significantly increased frequency of Breg cells, which was independent of disease activity. Anti-TNFα drugs induced a significant reduction of circulating Breg numbers, which were no longer elevated after six months of treatment. Functional in vitro studies showed that the secretion of IFNγ was significantly higher in Breg-depleted as compared with total CD19+ B cells, indicating that Breg can downmodulate B cell pro-inflammatory cytokine secretion. In summary, an increased frequency of circulating CD19+CD24hiCD38hi B cells is observed in AS/nb patients, that is not related with disease activity; anti-TNFα drugs are able to downmodulate circulating Breg numbers in AS.
[Mh] Termos MeSH primário: ADP-Ribosil Ciclase 1/imunologia
Antígenos CD19/imunologia
Linfócitos B/imunologia
Fatores Biológicos/uso terapêutico
Antígeno CD24/imunologia
Espondilite Anquilosante/imunologia
[Mh] Termos MeSH secundário: Adulto
Feminino
Seres Humanos
Masculino
Meia-Idade
Espondilite Anquilosante/tratamento farmacológico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD19); 0 (Biological Factors); 0 (CD24 Antigen); EC 3.2.2.6 (ADP-ribosyl Cyclase 1)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170707
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0180726


  10 / 1128 MEDLINE  
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[PMID]:28674079
[Au] Autor:Duex JE; Owens C; Chauca-Diaz A; Dancik GM; Vanderlinden LA; Ghosh D; Leivo MZ; Hansel DE; Theodorescu D
[Ad] Endereço:Departments of Surgery and Pharmacology, University of Colorado, Aurora, Colorado.
[Ti] Título:Nuclear CD24 Drives Tumor Growth and Is Predictive of Poor Patient Prognosis.
[So] Source:Cancer Res;77(18):4858-4867, 2017 Sep 15.
[Is] ISSN:1538-7445
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Elevated tumor expression of the cell surface GPI-linked CD24 protein signals poor patient prognosis in many tumor types. However, some cancer cells selected to be negative for surface CD24 (surCD24 ) still retain aggressive phenotypes and Here, we resolve this apparent paradox with the discovery of biologically active, nuclear CD24 (nucCD24) and finding that its levels are unchanged in surCD24 cells. Using the complementary techniques of biochemical cellular fractionation and immunofluorescence, we demonstrate a signal for CD24 in the nucleus in cells from various histologic types of cancer. Nuclear-specific expression of CD24 (NLS-CD24) increased anchorage-independent growth and tumor formation Immunohistochemistry of patient tumor samples revealed the presence of nucCD24, whose signal intensity correlated positively with the presence of metastatic disease. Analysis of gene expression between cells expressing CD24 and NLS-CD24 revealed a unique nucCD24 transcriptional signature. The median score derived from this signature was able to stratify overall survival in four patient datasets from bladder cancer and five patient datasets from colorectal cancer. Patients with high scores (more nucCD24-like) had reduced survival. These findings define a novel and functionally important intracellular location of CD24; they explain why surCD24 cells can remain aggressive, and they highlight the need to consider nucCD24 in both fundamental research and therapeutic development. .
[Mh] Termos MeSH primário: Biomarcadores Tumorais/metabolismo
Antígeno CD24/metabolismo
Núcleo Celular/metabolismo
Proliferação Celular
Neoplasias da Bexiga Urinária/patologia
[Mh] Termos MeSH secundário: Animais
Apoptose
Seres Humanos
Metástase Linfática
Camundongos
Camundongos Nus
Invasividade Neoplásica
Estadiamento de Neoplasias
Prognóstico
Taxa de Sobrevida
Células Tumorais Cultivadas
Neoplasias da Bexiga Urinária/metabolismo
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (CD24 Antigen); 0 (CD24 protein, human)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170705
[St] Status:MEDLINE
[do] DOI:10.1158/0008-5472.CAN-17-0367



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