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[PMID]: 29374703 [Au] Autor: Kang S; Oh SC; Min BW; Lee DH [Ad] Endereço: Department of Surgery, Korea University Guro Hospital, Seoul, Republic of Korea. [Ti] Título: Transglutaminase 2 Regulates Self-renewal and Stem Cell Marker of Human Colorectal Cancer Stem Cells. [So] Source: Anticancer Res;38(2):787-794, 2018 02. [Is] ISSN: 1791-7530 [Cp] País de publicação: Greece [La] Idioma: eng [Ab] Resumo: BACKGROUND/AIM: The aim of this study was to investigate the role of transglutaminase 2 (TGM2) in colorectal cancer stem cells (CCSCs). MATERIALS AND METHODS: We used the TU12 cell line possessing CD133-expressing CCSCs. After isolating CD133 (-) and CD133 (+) CCSCs, we overexpressed and knocked-down TGM2 to investigate its role in human CCSCs. RESULTS: The expression level of TGM2 was 25-fold higher in tumorigenic cells than non-tumorigenic cells. We found that knockdown of TGM2 by specific RNA interference markedly inhibited cell growth and caused down-regulation of the stemness markers, CD133, SOX2, and ß-catenin. We further demonstrated that knockdown of TGM2 inhibited cell metastatic abilities by down-regulating N-cadherin and vimentin and up-regulating E-cadherin. These findings revealed that TGM2 expression is markedly increased in human colorectal cancer and that down-regulation of TGM2 in tumors may serve as a treatment for colorectal cancer patients. Therefore, this study indicate that TGM2 affects the metastatic potential and stemness of CCSCs by regulating EMT- and stemness-related proteins. CONCLUSION: The metastatic potential of CSCs arises from highly expressed TGM2. [Mh] Termos MeSH primário: Neoplasias Colorretais/enzimologia Proteínas de Ligação ao GTP/biossíntese Células-Tronco Neoplásicas/enzimologia Transglutaminases/biossíntese [Mh] Termos MeSH secundário: Antígeno AC133/biossíntese Antígenos CD/metabolismo Biomarcadores Tumorais Caderinas/metabolismo Linhagem Celular Tumoral Movimento Celular/fisiologia Neoplasias Colorretais/genética Neoplasias Colorretais/patologia Regulação para Baixo Transição Epitelial-Mesenquimal Proteínas de Ligação ao GTP/genética Proteínas de Ligação ao GTP/metabolismo Técnicas de Silenciamento de Genes Seres Humanos Imuno-Histoquímica Invasividade Neoplásica Metástase Neoplásica Células-Tronco Neoplásicas/patologia Transglutaminases/genética Transglutaminases/metabolismo Células Tumorais Cultivadas Vimentina/metabolismo [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (AC133 Antigen); 0 (Antigens, CD); 0 (Biomarkers, Tumor); 0 (CDH1 protein, human); 0 (CDH2 protein, human); 0 (Cadherins); 0 (PROM1 protein, human); 0 (Vimentin); EC 2.3.2.- (transglutaminase 2); EC 2.3.2.13 (Transglutaminases); EC 3.6.1.- (GTP-Binding Proteins) [Em] Mês de entrada: 1802 [Cu] Atualização por classe: 180221 [Lr] Data última revisão: 180221 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 180129 [St] Status: MEDLINE

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[PMID]: 29307822 [Au] Autor: Hongdan L; Feng L [Ad] Endereço: Department of Cell Biology, Key Laboratory of Cell Biology, National Health and Family Planning Commission of the PRC, Key Laboratory of Medical Cell Biology, Ministry of Education of the PRC, China Medical University, No. 77, Puhe Road, Shenyang North New Area, Shenyang, Liaoning 110122, China. [Ti] Título: miR-3120-5p promotes colon cancer stem cell stemness and invasiveness through targeting Axin2. [So] Source: Biochem Biophys Res Commun;496(2):302-308, 2018 02 05. [Is] ISSN: 1090-2104 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: It is well known that colon cancer stemness and invasiveness are the main reasons for tumor recurrence and metastasis. MicroRNAs dysregulation can disrupt the balance of cell signaling and growth processes, resulting in cancer proliferation, invasion and metastasis, chemoresistance and so on. In this study, we used colon cancer cell lines HCT-116 and SW-480 to investigate the effects of miR-3120-5p on stemness and invasiveness of colon cancer. We found that the population of CD133 + and Lgr5+ stem cells in both cell lines expressed miR-3120-5p highly, and introducing miR-3120-5p into both cell lines increased the population of cancer stem cells, as measured by flow cytometry, qRT-PCR and sphere formation assays. Transwell assay, Gelatin zymography assay and Western blot assays further revealed that miR-3120-5p promotes colon cancer cells invasive ability. By the target prediction algorithm TargetScan, we found Axin2 is a potential target for miR-3120-5p, and luciferase reporter assay demonstrated that miR-3120-5p reduces Axin2 expression. Transfection of siRNA against Axin2 into colon cancer cells promoted the stemness and invasion of colon cancer cells. Furthermore, Axin2 overexpression partially reversed the promotion of stemness and invasiveness caused by miR-3120-5p in colon cancer cells. Together, all the results demonstrated miR-3120-5p promotes stemness and invasiveness of colon cancer cells through direct targeting of Axin2. They suggest that antago-miR-3120-5p plays important roles on treatment strategy for colon cancer. [Mh] Termos MeSH primário: Proteína Axina/genética Biomarcadores Tumorais/genética Regulação Neoplásica da Expressão Gênica MicroRNAs/genética Células-Tronco Neoplásicas/metabolismo Esferoides Celulares/metabolismo [Mh] Termos MeSH secundário: Antígeno AC133/genética Antígeno AC133/metabolismo Antagomirs/genética Antagomirs/metabolismo Proteína Axina/antagonistas & inibidores Proteína Axina/metabolismo Biomarcadores Tumorais/antagonistas & inibidores Biomarcadores Tumorais/metabolismo Linhagem Celular Tumoral Movimento Celular Proliferação Celular Genes Reporter Células HCT116 Seres Humanos Luciferases/genética Luciferases/metabolismo MicroRNAs/antagonistas & inibidores MicroRNAs/metabolismo Células-Tronco Neoplásicas/patologia RNA Interferente Pequeno/genética RNA Interferente Pequeno/metabolismo Receptores Acoplados a Proteínas-G/genética Receptores Acoplados a Proteínas-G/metabolismo Transdução de Sinais Esferoides Celulares/patologia [Pt] Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nome de substância: 0 (AC133 Antigen); 0 (AXIN2 protein, human); 0 (Antagomirs); 0 (Axin Protein); 0 (Biomarkers, Tumor); 0 (LGR5 protein, human); 0 (MicroRNAs); 0 (PROM1 protein, human); 0 (RNA, Small Interfering); 0 (Receptors, G-Protein-Coupled); EC 1.13.12.- (Luciferases) [Em] Mês de entrada: 1802 [Cu] Atualização por classe: 180214 [Lr] Data última revisão: 180214 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 180109 [St] Status: MEDLINE

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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

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[PMID]: 28452069 [Au] Autor: Chao OS; Chang TC; Di Bella MA; Alessandro R; Anzanello F; Rappa G; Goodman OB; Lorico A [Ad] Endereço: College of Medicine, Roseman University, Las Vegas, Nevada, 89135. [Ti] Título: The HDAC6 Inhibitor Tubacin Induces Release of CD133 Extracellular Vesicles From Cancer Cells. [So] Source: J Cell Biochem;118(12):4414-4424, 2017 Dec. [Is] ISSN: 1097-4644 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Tumor-derived extracellular vesicles (EVs) are emerging as an important mode of intercellular communication, capable of transferring biologically active molecules that facilitate the malignant growth and metastatic process. CD133 (Prominin-1), a stem cell marker implicated in tumor initiation, differentiation and resistance to anti-cancer therapy, is reportedly associated with EVs in various types of cancer. However, little is known about the factors that regulate the release of these CD133 EVs. Here, we report that the HDAC6 inhibitor tubacin promoted the extracellular release of CD133 EVs from human FEMX-I metastatic melanoma and Caco-2 colorectal carcinoma cells, with a concomitant downregulation of intracellular CD133. This effect was specific for tubacin, as inhibition of HDAC6 deacetylase activity by another selective HDAC6 inhibitor, ACY-1215 or the pan-HDAC inhibitor trichostatin A (TSA), and knockdown of HDAC6 did not enhance the release of CD133 EVs. The tubacin-induced EV release was associated with changes in cellular lipid composition, loss of clonogenic capacity and decrease in the ability to form multicellular aggregates. These findings indicate a novel potential anti-tumor mechanism for tubacin in CD133-expressing malignancies. J. Cell. Biochem. 118: 4414-4424, 2017. © 2017 Wiley Periodicals, Inc. [Mh] Termos MeSH primário: Antígeno AC133/metabolismo Anilidas/farmacologia Micropartículas Derivadas de Células/metabolismo Desacetilase 6 de Histona/antagonistas & inibidores Inibidores de Histona Desacetilases/farmacologia Ácidos Hidroxâmicos/farmacologia Proteínas de Neoplasias/metabolismo Neoplasias/metabolismo [Mh] Termos MeSH secundário: Linhagem Celular Tumoral Desacetilase 6 de Histona/metabolismo Seres Humanos [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (AC133 Antigen); 0 (Anilides); 0 (Histone Deacetylase Inhibitors); 0 (Hydroxamic Acids); 0 (Neoplasm Proteins); 0 (PROM1 protein, human); 02C2G1D30D (tubacin); EC 3.5.1.98 (HDAC6 protein, human); EC 3.5.1.98 (Histone Deacetylase 6) [Em] Mês de entrada: 1801 [Cu] Atualização por classe: 180102 [Lr] Data última revisão: 180102 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170429 [St] Status: MEDLINE [do] DOI: 10.1002/jcb.26095

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[PMID]: 29049740 [Au] Autor: Doherty RE; Sisley K; Hammond DW; Rennie IG; Cross NA [Ad] Endereço: Academic Unit of Ophthalmology and Orthoptics, Department of Oncology and Metabolism, School of Medicine and Biomedical Sciences, University of Sheffield, Royal Hallamshire Hospital, Sheffield, United Kingdom. [Ti] Título: Phenotypic Plasticity in Uveal Melanoma Is Not Restricted to a Tumor Subpopulation and Is Unrelated to Cancer Stem Cell Characteristics. [So] Source: Invest Ophthalmol Vis Sci;58(12):5387-5395, 2017 Oct 01. [Is] ISSN: 1552-5783 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Purpose: Uveal melanoma (UM) is the most common primary intraocular malignancy in adults and approximately half of those diagnosed will die of metastasis. This study investigates whether UM progression is driven by a subpopulation of stem-like cells, termed "cancer stem cells" (CSCs). Methods: Expression of postulated stem cell markers aldehyde dehydrogenase (ALDH), CD44, and CD133 was analyzed in UM cell lines and primary UM short-term cultures (STCs) established from tumor samples. Additionally, the notion of a "cellular hierarchy" within UM was investigated. Finally, the phenomenon of phenotypic plasticity in response to environmental factors was explored. Results: We demonstrate that expression of ALDH, CD44, and CD133 does not select for a subpopulation of stem-like cells in either UM cell lines or UM STCs. Furthermore, there is an absence of a cellular hierarchy in cell lines and all cells in culture are able to drive tumor progression. Last, we show that established UM cell lines and UM STCs are plastic in nature and switch their phenotype in response to environmental stimuli. Conclusions: We hypothesize that this capacity to undergo phenotypic plasticity may be a consequence of neural crest lineage and renders the exploration of the CSC hypothesis extremely challenging in UM. [Mh] Termos MeSH primário: Plasticidade Celular Melanoma/patologia Células-Tronco Neoplásicas/patologia Neoplasias Uveais/patologia [Mh] Termos MeSH secundário: Antígeno AC133/metabolismo Aldeído Desidrogenase/metabolismo Biomarcadores Tumorais/metabolismo Linhagem Celular Tumoral Citometria de Fluxo Seres Humanos Receptores de Hialuronatos/metabolismo Melanoma/metabolismo Células-Tronco Neoplásicas/metabolismo Fenótipo Ensaio Tumoral de Célula-Tronco Neoplasias Uveais/metabolismo [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (AC133 Antigen); 0 (Biomarkers, Tumor); 0 (CD44 protein, human); 0 (Hyaluronan Receptors); 0 (PROM1 protein, human); EC 1.2.1.3 (Aldehyde Dehydrogenase) [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: 171020 [St] Status: MEDLINE [do] DOI: 10.1167/iovs.17-22272

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[PMID]: 28918838 [Au] Autor: Erdogan S; Doganlar ZB; Doganlar O; Turkekul K; Serttas R [Ad] Endereço: Department of Medical Biology, School of Medicine, Trakya University, Balkan Campus, Edirne, Turkey. Electronic address: suaterdogan@trakya.edu.tr. [Ti] Título: Inhibition of Midkine Suppresses Prostate Cancer CD133 Stem Cell Growth and Migration. [So] Source: Am J Med Sci;354(3):299-309, 2017 Sep. [Is] ISSN: 1538-2990 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: BACKGROUND: Midkine (MDK) is a tumor-promoting factor that is often overexpressed in various human carcinomas, and the role of MDK has not yet been fully investigated in prostate cancer stem cells. MATERIALS AND METHODS: Prostate cancer CD133 stem cells (PCSCs) were isolated from human castration-resistant PC3 cells. PCSCs were treated with different concentrations of MDK inhibitor, iMDK, for 24-72 hours. The IC values were determined by the MTT test. Endogenous MDK messenger RNA expression was knocked down by small interfering RNA. Quantitative reverse transcription polymerase chain reaction, Western blot analyses and image-based cytometry were used to investigate apoptosis and cell cycle progression as well as their underlying molecular mechanisms. Cell migration was evaluated by the wound healing test. RESULTS: iMDK caused dose- and time-dependent inhibition of PCSC survival. Similar growth inhibition was also obtained by small interfering RNA-mediated knockdown of endogenous MDK expression. iMDK was shown to preferentially induce cell cycle arrest at the S and G2/M phases. Suppressed PCSC growth was also accompanied by increases in p53 and the cell cycle inhibitor p21 genes. Combinatorial treatment of iMDK with docetaxel significantly inhibited cell proliferation versus either of the agents used alone. Inhibition of MDK expression strongly suppressed the migration of PCSCs compared to untreated and docetaxel-treated cells. iMDK and the knockdown of MDK decreased p-Akt and significantly upregulated the expression of PI3K/phosphatase/tensin homolog. CONCLUSIONS: Our data indicate that MDK plays a crucial role in controlling PCSC proliferation and migration. Therefore, suppression of endogenous expression of MDK would, in combination with traditional chemotherapy drugs, be a potential treatment for PCSCs. [Mh] Termos MeSH primário: Antígeno AC133/imunologia Antineoplásicos/farmacologia Movimento Celular/efeitos dos fármacos Proliferação Celular/efeitos dos fármacos Cumarínicos/farmacologia Células-Tronco Neoplásicas/efeitos dos fármacos Fatores de Crescimento Neural/antagonistas & inibidores Neoplasias da Próstata/patologia Tiazóis/farmacologia [Mh] Termos MeSH secundário: Sobrevivência Celular/efeitos dos fármacos Células Cultivadas Relação Dose-Resposta a Droga Técnicas de Silenciamento de Genes Seres Humanos Masculino Células-Tronco Neoplásicas/imunologia Células-Tronco Neoplásicas/metabolismo Células-Tronco Neoplásicas/patologia Fatores de Crescimento Neural/genética Neoplasias da Próstata/imunologia Neoplasias da Próstata/metabolismo RNA Interferente Pequeno/genética Fatores de Tempo [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (3-(2-(4-fluorobenzyl)imidazo(2,1-beta)(1),(3)thiazol-6-yl)-2H-chromen-2-one); 0 (AC133 Antigen); 0 (Antineoplastic Agents); 0 (Coumarins); 0 (MDK protein, human); 0 (Nerve Growth Factors); 0 (PROM1 protein, human); 0 (RNA, Small Interfering); 0 (Thiazoles) [Em] Mês de entrada: 1709 [Cu] Atualização por classe: 170925 [Lr] Data última revisão: 170925 [Sb] Subgrupo de revista: AIM; IM [Da] Data de entrada para processamento: 170919 [St] Status: MEDLINE

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[PMID]: 28843521 [Au] Autor: Liu T; Chi H; Chen J; Chen C; Huang Y; Xi H; Xue J; Si Y [Ad] Endereço: Shanghai Geriatric Institute of Chinese Medicine, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200031, China; Department of Pathology, Yale University School of Medicine, New Haven 06520, USA; Shanghai Tenth People's Hospital, Medical School, Tongji University, Sha [Ti] Título: Curcumin suppresses proliferation and in vitro invasion of human prostate cancer stem cells by ceRNA effect of miR-145 and lncRNA-ROR. [So] Source: Gene;631:29-38, 2017 Oct 05. [Is] ISSN: 1879-0038 [Cp] País de publicação: Netherlands [La] Idioma: eng [Ab] Resumo: Many studies have demonstrated that curcumin can effectively inhibit the proliferation, invasion, and tumorigenesis of prostate cancer cells in vitro and in vivo. In this study, CD44 /CD133 human prostate cancer stem cells (HuPCaSCs) were isolated from the prostate cancer cell lines Du145 and 22RV1. Curcumin treatment of these cells resulted in the inhibition of in vitro proliferation and invasion, and cell cycle arrest. The expression levels of cell cycle proteins (Ccnd1 and Cdk4) and stem cell markers (Oct4, CD44, and CD133) were decreased in curcumin-treated HuPCaSCs. Microarray analysis and northern blotting assays indicated that miR-145 was overexpressed in curcumin-treated HuPCaSCs. Insights of the mechanism of competitive endogenous RNAs (ceRNAs) were gained from bioinformatic analysis, bioinformatics analysis and luciferase activity assays showed that the lncRNA-ROR and Oct4 mRNA both contain miR-145 binding sites, and Oct4 and lncRNA-ROR directly compete for microRNA binding. Curcumin induced high miR-145 expression and inhibited the expression of lncRNA-ROR. The tumorigenicity of curcumin- treated HuPCaSCs in nude mice was significantly reduced. In summary, reducing the expression of endogenous lncRNA-ROR could effectively increase the available concentration of miR-145 in HuPCaSCs, where miR-145 prevents cell proliferation by decreasing Oct4 expression. In particular, we hypothesized that lncRNA-ROR may act as a ceRNA, effectively becoming a sink for miR-145, thereby activating the derepression of core transcription factors Oct4. Thus, curcumin suppresses the proliferation, in vitro invasion, and tumorigenicity of HuPCaSCs through ceRNA effect of miR-145 and lncRNA-ROR caused. [Mh] Termos MeSH primário: Antineoplásicos Fitogênicos/farmacologia Proliferação Celular/efeitos dos fármacos Curcumina/farmacologia MicroRNAs/metabolismo Neoplasias da Próstata/tratamento farmacológico RNA Longo não Codificante/metabolismo RNA Neoplásico/efeitos dos fármacos [Mh] Termos MeSH secundário: Antígeno AC133 Animais Ligação Competitiva Biomarcadores/metabolismo Proteínas de Ciclo Celular/metabolismo Linhagem Celular Tumoral Seres Humanos Receptores de Hialuronatos Masculino Camundongos Endogâmicos BALB C Camundongos Nus Invasividade Neoplásica Neoplasias da Próstata/imunologia Ensaios Antitumorais Modelo de Xenoenxerto [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (AC133 Antigen); 0 (Antineoplastic Agents, Phytogenic); 0 (Biomarkers); 0 (Cell Cycle Proteins); 0 (Hyaluronan Receptors); 0 (Linc-RNA-RoR, human); 0 (MIRN145 microRNA, human); 0 (MicroRNAs); 0 (PROM1 protein, human); 0 (RNA, Long Noncoding); 0 (RNA, Neoplasm); IT942ZTH98 (Curcumin) [Em] Mês de entrada: 1709 [Cu] Atualização por classe: 171116 [Lr] Data última revisão: 171116 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170828 [St] Status: MEDLINE

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[PMID]: 28817605 [Au] Autor: Mei D; Lv B; Chen B; Xiao S; Jiang J; Xie Y; Jiang L [Ad] Endereço: Department of Clinical Medicine, School of Medicine, Shandong University, Jinan, China. [Ti] Título: All-trans retinoic acid suppresses malignant characteristics of CD133-positive thyroid cancer stem cells and induces apoptosis. [So] Source: PLoS One;12(8):e0182835, 2017. [Is] ISSN: 1932-6203 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Recently, diagnoses of radioiodine-refractory differentiated thyroid cancer (RAI-R DTC) have become more common; prognosis is poor. It has been suggested that cancer stem cells account for radiotherapy resistance. By flow cytometry, different expression percents of CD133 and OCT4 in thyroid cancer cell lines were detected. By real-time quantitative PCR, different mRNA expression of CD133, OCT4, GLUT1, thyroglobulin (TG), thyroperoxidase (TPO) and sodium iodine symporter (NIS) was analyzed; the localization of CD133, OCT4, and NIS expression was examined using immunofluorescence confocal microscopy. Different expression of CD133, OCT4, and NIS in 21 human thyroid cancer and nodule tissues was investigated using immunohistochemistry. CD133-positive cells were isolated by magnetic sorting. Stronger colony formation ability of CD133-positive and weaker ability of CD133-negative cells in vivo were examined by colony formation. The effects of all-trans retinoic acid (ATRA) on CD133-positive cells in vivo were explored with Cell Counting Kit-8, colony formation, apoptosis, cell cycle, and ethynyl deoxyuridine assays. The ARO cell line and RAI-R DTC tissue specimens had more CD133-positive cells. NIS expression was significantly lower in RAI-R DTC tissue compared to radioiodine-sensitive DTC (RAI-DTC) tissue and specimens from patients with thyroid nodule. ATRA inhibited the stem cell characteristics of CD133-positive cells and induced CD133-positive cell differentiation to CD133-negative cells, and promoted CD133-positive cell apoptosis. [Mh] Termos MeSH primário: Antígeno AC133/genética Antineoplásicos/farmacologia Apoptose Células-Tronco Neoplásicas/efeitos dos fármacos Neoplasias da Glândula Tireoide/patologia Tretinoína/farmacologia [Mh] Termos MeSH secundário: Antígeno AC133/metabolismo Linhagem Celular Tumoral Transportador de Glucose Tipo 1/genética Transportador de Glucose Tipo 1/metabolismo Seres Humanos Células-Tronco Neoplásicas/metabolismo Células-Tronco Neoplásicas/patologia Fator 3 de Transcrição de Octâmero/genética Fator 3 de Transcrição de Octâmero/metabolismo Tireoglobulina/genética Tireoglobulina/metabolismo Neoplasias da Glândula Tireoide/metabolismo [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (AC133 Antigen); 0 (Antineoplastic Agents); 0 (Glucose Transporter Type 1); 0 (Octamer Transcription Factor-3); 0 (POU5F1 protein, human); 5688UTC01R (Tretinoin); 9010-34-8 (Thyroglobulin) [Em] Mês de entrada: 1710 [Cu] Atualização por classe: 171016 [Lr] Data última revisão: 171016 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170818 [St] Status: MEDLINE [do] DOI: 10.1371/journal.pone.0182835

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[PMID]: 28771552 [Au] Autor: Chen J; Mao S; Li H; Zheng M; Yi L; Lin JM; Lin ZX [Ad] Endereço: Department of Neurosurgery, The First Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian, China. [Ti] Título: The pathological structure of the perivascular niche in different microvascular patterns of glioblastoma. [So] Source: PLoS One;12(8):e0182183, 2017. [Is] ISSN: 1932-6203 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: The perivascular niche is critical for intercellular communication between resident cell types in glioblastoma (GBM), and it plays a vital role in maintaining the glioma stem cell (GSC) microenvironment. It is shown in abundant research that different microvascular patterns exist in GBM; and it can be implied that different microvascular patterns are associated with different pathological structures in the perivascular niche. However, the pathological structure of the perivascular niche is still not clear. Here, we investigated the distribution and biological characteristics of different microvascular pattern niches (MVPNs) in GBM by detecting the expression of CD34, CD133, Nestin, α-SMA, GFAP and CD14 in the perivascular niche using multiple -fluorescence. The four basic microvascular patterns are microvascular sprouting (MS), vascular cluster (VC), vascular garland (VG), and glomeruloid vascular proliferation (GVP). By analyzing the proportion of the area of each marker in four types of formations, the results indicated that the expression of CD34, CD133 and Nestin in MS and VC was significantly lower than that in VG and GVP (P<0.05). Furthermore, the results showed that α-SMA expression different in the MS, VC, VG and GVP (P<0.05). However, the expression of GFAP and CD14 in each type of formation exhibited no significant difference (P>0.05). According to the area distributions of different markers, we mapped four precise simulation diagrams to provide an effective foundation for the accurate simulation of glioblastoma in vitro. [Mh] Termos MeSH primário: Neoplasias Encefálicas/patologia Glioblastoma/patologia Microvasos/patologia [Mh] Termos MeSH secundário: Antígeno AC133/metabolismo Actinas/metabolismo Adolescente Adulto Idoso Antígenos CD34/metabolismo Feminino Proteína Glial Fibrilar Ácida/metabolismo Seres Humanos Receptores de Lipopolissacarídeos/metabolismo Masculino Microscopia de Fluorescência Microvasos/metabolismo Meia-Idade Nestina/metabolismo Adulto Jovem [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (AC133 Antigen); 0 (ACTA2 protein, human); 0 (Actins); 0 (Antigens, CD34); 0 (Glial Fibrillary Acidic Protein); 0 (Lipopolysaccharide Receptors); 0 (Nestin) [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: 170804 [St] Status: MEDLINE [do] DOI: 10.1371/journal.pone.0182183

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MEDLINE

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[PMID]: 28749943 [Au] Autor: Moussy A; Cosette J; Parmentier R; da Silva C; Corre G; Richard A; Gandrillon O; Stockholm D; Páldi A [Ad] Endereço: Ecole Pratique des Hautes Etudes, PSL Research University, UMRS 951, INSERM, Univ-Evry, Evry, France. [Ti] Título: Integrated time-lapse and single-cell transcription studies highlight the variable and dynamic nature of human hematopoietic cell fate commitment. [So] Source: PLoS Biol;15(7):e2001867, 2017 Jul. [Is] ISSN: 1545-7885 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Individual cells take lineage commitment decisions in a way that is not necessarily uniform. We address this issue by characterising transcriptional changes in cord blood-derived CD34+ cells at the single-cell level and integrating data with cell division history and morphological changes determined by time-lapse microscopy. We show that major transcriptional changes leading to a multilineage-primed gene expression state occur very rapidly during the first cell cycle. One of the 2 stable lineage-primed patterns emerges gradually in each cell with variable timing. Some cells reach a stable morphology and molecular phenotype by the end of the first cell cycle and transmit it clonally. Others fluctuate between the 2 phenotypes over several cell cycles. Our analysis highlights the dynamic nature and variable timing of cell fate commitment in hematopoietic cells, links the gene expression pattern to cell morphology, and identifies a new category of cells with fluctuating phenotypic characteristics, demonstrating the complexity of the fate decision process (which is different from a simple binary switch between 2 options, as it is usually envisioned). [Mh] Termos MeSH primário: Regulação da Expressão Gênica no Desenvolvimento Células-Tronco Hematopoéticas/metabolismo Células-Tronco Multipotentes/metabolismo Transcrição Genética [Mh] Termos MeSH secundário: Antígeno AC133/genética Antígeno AC133/metabolismo Antígenos CD34/genética Antígenos CD34/metabolismo Biomarcadores/metabolismo Diferenciação Celular Linhagem da Célula Proliferação Celular Forma Celular Rastreamento de Células Células Cultivadas Sangue Fetal/citologia Perfilação da Expressão Gênica Células-Tronco Hematopoéticas/citologia Seres Humanos Processamento de Imagem Assistida por Computador Microscopia Confocal Células-Tronco Multipotentes/citologia Análise de Componente Principal Análise de Célula Única Antígenos Thy-1/genética Antígenos Thy-1/metabolismo Imagem com Lapso de Tempo [Pt] Tipo de publicação: COMPARATIVE STUDY; JOURNAL ARTICLE [Nm] Nome de substância: 0 (AC133 Antigen); 0 (Antigens, CD34); 0 (Biomarkers); 0 (PROM1 protein, human); 0 (Thy-1 Antigens) [Em] Mês de entrada: 1708 [Cu] Atualização por classe: 171116 [Lr] Data última revisão: 171116 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170728 [St] Status: MEDLINE [do] DOI: 10.1371/journal.pbio.2001867

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