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[PMID]:28457887
[Au] Autor:Gómez-Miragaya J; Palafox M; Paré L; Yoldi G; Ferrer I; Vila S; Galván P; Pellegrini P; Pérez-Montoyo H; Igea A; Muñoz P; Esteller M; Nebreda AR; Urruticoechea A; Morilla I; Pernas S; Climent F; Soler-Monso MT; Petit A; Serra V; Prat A; González-Suárez E
[Ad] Endereço:Cancer Epigenetics and Biology Program (PEBC), Bellvitge Biomedical Research Institute (IDIBELL), Avinguda de la Gran Via, 199 - 203, L'Hospitalet de Llobregat, 08908 Barcelona, Spain.
[Ti] Título:Resistance to Taxanes in Triple-Negative Breast Cancer Associates with the Dynamics of a CD49f+ Tumor-Initiating Population.
[So] Source:Stem Cell Reports;8(5):1392-1407, 2017 May 09.
[Is] ISSN:2213-6711
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Taxanes are a mainstay of treatment for breast cancer, but resistance often develops followed by metastatic disease and mortality. Aiming to reveal the mechanisms underlying taxane resistance, we used breast cancer patient-derived orthoxenografts (PDX). Mimicking clinical behavior, triple-negative breast tumors (TNBCs) from PDX models were more sensitive to docetaxel than luminal tumors, but they progressively acquired resistance upon continuous drug administration. Mechanistically, we found that a CD49f+ chemoresistant population with tumor-initiating ability is present in sensitive tumors and expands during the acquisition of drug resistance. In the absence of the drug, the resistant CD49f+ population shrinks and taxane sensitivity is restored. We describe a transcriptional signature of resistance, predictive of recurrent disease after chemotherapy in TNBC. Together, these findings identify a CD49f+ population enriched in tumor-initiating ability and chemoresistance properties and evidence a drug holiday effect on the acquired resistance to docetaxel in triple-negative breast cancer.
[Mh] Termos MeSH primário: Antineoplásicos/uso terapêutico
Resistência a Medicamentos Antineoplásicos
Integrina alfa6/metabolismo
Taxoides/uso terapêutico
Neoplasias de Mama Triplo Negativas/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/farmacologia
Linhagem Celular
Células Cultivadas
Feminino
Seres Humanos
Integrina alfa6/genética
Camundongos
Células-Tronco Neoplásicas/efeitos dos fármacos
Células-Tronco Neoplásicas/metabolismo
Células-Tronco Neoplásicas/transplante
Taxoides/farmacologia
Neoplasias de Mama Triplo Negativas/patologia
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Integrin alpha6); 0 (Taxoids); 15H5577CQD (docetaxel)
[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:170502
[St] Status:MEDLINE


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[PMID]:28806779
[Au] Autor:Crompton M; Purnell T; Tyrer HE; Parker A; Ball G; Hardisty-Hughes RE; Gale R; Williams D; Dean CH; Simon MM; Mallon AM; Wells S; Bhutta MF; Burton MJ; Tateossian H; Brown SDM
[Ad] Endereço:Mammalian Genetics Unit, MRC Harwell Institute, Harwell, Oxfordshire, United Kingdom.
[Ti] Título:A mutation in Nischarin causes otitis media via LIMK1 and NF-κB pathways.
[So] Source:PLoS Genet;13(8):e1006969, 2017 Aug.
[Is] ISSN:1553-7404
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Otitis media (OM), inflammation of the middle ear (ME), is a common cause of conductive hearing impairment. Despite the importance of the disease, the aetiology of chronic and recurrent forms of middle ear inflammatory disease remains poorly understood. Studies of the human population suggest that there is a significant genetic component predisposing to the development of chronic OM, although the underlying genes are largely unknown. Using N-ethyl-N-nitrosourea mutagenesis we identified a recessive mouse mutant, edison, that spontaneously develops a conductive hearing loss due to chronic OM. The causal mutation was identified as a missense change, L972P, in the Nischarin (NISCH) gene. edison mice develop a serous or granulocytic effusion, increasingly macrophage and neutrophil rich with age, along with a thickened, inflamed mucoperiosteum. We also identified a second hypomorphic allele, V33A, with only modest increases in auditory thresholds and reduced incidence of OM. NISCH interacts with several proteins, including ITGA5 that is thought to have a role in modulating VEGF-induced angiogenesis and vascularization. We identified a significant genetic interaction between Nisch and Itga5; mice heterozygous for Itga5-null and homozygous for edison mutations display a significantly increased penetrance and severity of chronic OM. In order to understand the pathological mechanisms underlying the OM phenotype, we studied interacting partners to NISCH along with downstream signalling molecules in the middle ear epithelia of edison mouse. Our analysis implicates PAK1 and RAC1, and downstream signalling in LIMK1 and NF-κB pathways in the development of chronic OM.
[Mh] Termos MeSH primário: Peptídeos e Proteínas de Sinalização Intracelular/genética
Quinases Lim/metabolismo
Mutação de Sentido Incorreto
NF-kappa B/metabolismo
Otite Média/genética
[Mh] Termos MeSH secundário: Alelos
Animais
Mapeamento Cromossômico
Doença Crônica
Modelos Animais de Doenças
Orelha Média/metabolismo
Etilnitrosoureia/toxicidade
Feminino
Técnicas de Genotipagem
Heterozigoto
Homozigoto
Seres Humanos
Inflamação/genética
Integrina alfa6/genética
Integrina alfa6/metabolismo
Peptídeos e Proteínas de Sinalização Intracelular/metabolismo
Quinases Lim/genética
Masculino
Camundongos
Camundongos Knockout
NF-kappa B/genética
Neuropeptídeos/genética
Neuropeptídeos/metabolismo
Otite Média/metabolismo
Penetrância
Análise de Sequência de DNA
Regulação para Cima
Fator A de Crescimento do Endotélio Vascular/genética
Fator A de Crescimento do Endotélio Vascular/metabolismo
Quinases Ativadas por p21/genética
Quinases Ativadas por p21/metabolismo
Proteínas rac1 de Ligação ao GTP/genética
Proteínas rac1 de Ligação ao GTP/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Integrin alpha6); 0 (Intracellular Signaling Peptides and Proteins); 0 (NF-kappa B); 0 (Neuropeptides); 0 (Nisch protein, mouse); 0 (Rac1 protein, mouse); 0 (Vascular Endothelial Growth Factor A); 0 (vascular endothelial growth factor A, mouse); EC 2.7.11.1 (Lim Kinases); EC 2.7.11.1 (Limk1 protein, mouse); EC 2.7.11.1 (Pak1 protein, mouse); EC 2.7.11.1 (p21-Activated Kinases); EC 3.6.5.2 (rac1 GTP-Binding Protein); P8M1T4190R (Ethylnitrosourea)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170913
[Lr] Data última revisão:
170913
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170815
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pgen.1006969


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[PMID]:28795417
[Au] Autor:Henry G; Malewska A; Mauck R; Gahan J; Hutchinson R; Torrealba J; Francis F; Roehrborn C; Strand D
[Ad] Endereço:Department of Urology, UT Southwestern Medical Center, Dallas, Texas.
[Ti] Título:Molecular pathogenesis of human prostate basal cell hyperplasia.
[So] Source:Prostate;77(13):1344-1355, 2017 May.
[Is] ISSN:1097-0045
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Understanding the molecular pathogenesis of distinct phenotypes in human benign prostatic hyperplasia (BPH) is essential to improving therapeutic intervention. Current therapies target smooth muscle and luminal epithelia for relief of lower urinary tract symptoms (LUTS) due to BPH, but basal cell hyperplasia (BCH) remains untargeted. The incidence of has been reported at 8-10%, but a molecular and cellular characterization has not been performed on this phenotype. METHODS: Using freshly digested tissue from surgical specimens, we performed RNA-seq analysis of flow cytometry-purified basal epithelia from 3 patients with and 4 patients without a majority BCH phenotype. qPCR was performed on 28 genes identified as significant from 13 non-BCH and 7 BCH specimens to confirm transcriptomic analysis. IHC was performed on several non-BCH and BCH specimens for 3 proteins identified as significant by transcriptomic analysis. RESULTS: A total of 141 human BPH specimens were analyzed for the presence of BCH. Clinical characteristics of non-BCH and BCH cohorts revealed no significant differences in age, PSA, prostate volume, medical treatment, or comorbidities. Quantitation of cellular subsets by flow cytometry in 11 BCH patients vs. 11 non-BCH patients demonstrated a significant increase in the ratio of basal to luminal epithelia in patients with BCH (P <0.05), but no significant differences in the total number of leukocytes. RNA-seq data from flow cytometry isolated basal epithelia from patients with and without BCH were subjected to gene set enrichment analysis of differentially expressed genes, which revealed increased expression of members of the epidermal differentiation complex. Transcriptomic data were complemented by immunohistochemistry for members of the epidermal differentiation complex, revealing a morphological similarity to other stratified squamous epithelial layers. CONCLUSIONS: Increased expression of epidermal differentiation complex members and altered epithelial stratification resembles the progression of other metaplastic diseases. These data provide insight into the plasticity of the human prostate epithelium and suggest a classification of basal cell hyperplasia as a metaplasia.
[Mh] Termos MeSH primário: Células Epiteliais/patologia
Integrina alfa6/genética
Proteínas de Membrana/genética
Neoplasia de Células Basais
Próstata/patologia
Hiperplasia Prostática
[Mh] Termos MeSH secundário: Idoso
Gerenciamento Clínico
Progressão da Doença
Perfilação da Expressão Gênica/métodos
Seres Humanos
Imuno-Histoquímica
Masculino
Metaplasia/genética
Metaplasia/patologia
Meia-Idade
Neoplasia de Células Basais/tratamento farmacológico
Neoplasia de Células Basais/genética
Neoplasia de Células Basais/patologia
Tamanho do Órgão
Hiperplasia Prostática/tratamento farmacológico
Hiperplasia Prostática/genética
Hiperplasia Prostática/patologia
Análise de Sequência de RNA/métodos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CKAP4 protein, human); 0 (Integrin alpha6); 0 (Membrane Proteins)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170921
[Lr] Data última revisão:
170921
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170811
[St] Status:MEDLINE
[do] DOI:10.1002/pros.23394


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[PMID]:28760342
[Au] Autor:Shin HC; Park JY; Lim HD; Namgung U
[Ad] Endereço:Department of Oriental Medicine, Daejeon University, Daejeon 34520, Republic of Korea. Electronic address: hcshin2507@naver.com.
[Ti] Título:Induction of α6 and ß1 integrins by acupuncture stimulation in rats.
[So] Source:Biochem Biophys Res Commun;491(3):629-635, 2017 Sep 23.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Acupuncture therapy is performed by applying the needle insertion at discrete cutaneous locations and used for the treatments of diverse symptoms and disorders. In order to elucidate mechanistic basis on how acupuncture stimulation (AS) produces therapeutic effects, it is primarily important to understand tissue responses locally at the acupuncture site (acupoint). Here, we investigated integrin protein as molecular target responding to and integrating AS. Signals of α6 and ß1 integrins were clearly induced at zusanli acupoint 24 h after AS in areas of nuclear clusters around the needle track. Induction levels of integrin were largely reduced by needle insertion at non-acupuncture point or without needle rotation. Phospho-Erk1/2 was initially decreased below the basal level after AS but increased 24 h later. Induction pattern of phospho-Erk1/2 was as similar as that of α6 integrin in its selectivity to needling procedure and tissue distribution. We further found that mRNA expression of P2X3 purinergic receptor was upregulated in the dorsal root ganglion (DRG) after AS, but decreased by the inhibition of Erk1/2 activity at the acupuncture area. Moreover, AS-mediated integrin activation was required for Erk1/2 activation at the acupuncture site and regulation of pain sensitivity in the hind paw. The present results provide a new evidence on acupuncture-specific tissue response in terms of integrin induction, and further suggest that integrin activation may be involved in transmitting mechanosensory signals from the acupoint to afferent nerve fiber.
[Mh] Termos MeSH primário: Terapia por Acupuntura/métodos
Integrina alfa6/imunologia
Integrina beta1/imunologia
Sistema de Sinalização das MAP Quinases/imunologia
Neuralgia/imunologia
Neuralgia/terapia
[Mh] Termos MeSH secundário: Pontos de Acupuntura
Animais
Masculino
Mecanotransdução Celular/imunologia
Neuralgia/diagnóstico
Estimulação Física/métodos
Ratos
Ratos Sprague-Dawley
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Integrin alpha6); 0 (Integrin beta1)
[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:170802
[St] Status:MEDLINE


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[PMID]:28656629
[Au] Autor:Laudato S; Patil N; Abba ML; Leupold JH; Benner A; Gaiser T; Marx A; Allgayer H
[Ad] Endereço:Department of Experimental Surgery-Cancer Metastasis, Medical Faculty Mannheim, University of Heidelberg, Germany.
[Ti] Título:P53-induced miR-30e-5p inhibits colorectal cancer invasion and metastasis by targeting ITGA6 and ITGB1.
[So] Source:Int J Cancer;141(9):1879-1890, 2017 Nov 01.
[Is] ISSN:1097-0215
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The tumor suppressor P53 is a critical regulator of normal cellular homeostasis whose function is either distorted or lost in several cancer types including colorectal cancer (CRC). A small group of microRNAs have come to be recognized as essential mediators of P53 function. In a genome-wide systematic approach, we explored miRNAs that are substantially altered by P53 loss and found miR-30e to be the most significantly deregulated miRNA in P53-knockout human CRC cells. We identified miR-30e-5p to be a novel direct transcriptional target of P53 with gain and loss of function experiments revealing miR-30e-5p to be a significant regulator of tumor cell migration, invasion and in vivo metastasis mediated in part by integrins alpha-6 and beta-1 as novel targets. MiR-30e-5p also significantly reduced tumor cell proliferation by causing G1/S cell cycle arrest, which was achieved by inducing P21 and P27 expression. Finally, we found miR-30e-5p to be lost in resected CRC tumors as compared to normal colon tissues. Taken together, miR-30e-5p is a novel effector of P53-induced suppression of migration, invasion and metastasis.
[Mh] Termos MeSH primário: Neoplasias Colorretais/genética
Integrina alfa6/genética
Peptídeos e Proteínas de Sinalização Intracelular/genética
Proteínas de Membrana/genética
MicroRNAs/genética
Proteína Supressora de Tumor p53/genética
[Mh] Termos MeSH secundário: Animais
Pontos de Checagem do Ciclo Celular/genética
Linhagem Celular Tumoral
Proliferação Celular/genética
Neoplasias Colorretais/patologia
Inibidor de Quinase Dependente de Ciclina p21/genética
Inibidor de Quinase Dependente de Ciclina p27/genética
Regulação Neoplásica da Expressão Gênica
Células HCT116
Seres Humanos
Camundongos
Invasividade Neoplásica/genética
Invasividade Neoplásica/patologia
Metástase Neoplásica
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CDKN1A protein, human); 0 (Cyclin-Dependent Kinase Inhibitor p21); 0 (ITGA6 protein, human); 0 (ITGB1BP1 protein, human); 0 (Integrin alpha6); 0 (Intracellular Signaling Peptides and Proteins); 0 (MIRN30 microRNA, human); 0 (Membrane Proteins); 0 (MicroRNAs); 0 (TP53 protein, human); 0 (Tumor Suppressor Protein p53); 147604-94-2 (Cyclin-Dependent Kinase Inhibitor p27)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171009
[Lr] Data última revisão:
171009
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170629
[St] Status:MEDLINE
[do] DOI:10.1002/ijc.30854


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[PMID]:28604746
[Au] Autor:Zhang K; Myllymäki SM; Gao P; Devarajan R; Kytölä V; Nykter M; Wei GH; Manninen A
[Ad] Endereço:Biocenter Oulu, Centre of Excellence in Cell-Extracellular Matrix Research, Faculty of Biochemistry and Molecular Medicine, University of Oulu, Oulu, Finland.
[Ti] Título:Oncogenic K-Ras upregulates ITGA6 expression via FOSL1 to induce anoikis resistance and synergizes with αV-Class integrins to promote EMT.
[So] Source:Oncogene;36(41):5681-5694, 2017 Oct 12.
[Is] ISSN:1476-5594
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:In many cancer types, integrin-mediated signaling regulates proliferation, survival and invasion of tumorigenic cells. However, it is still unclear how integrins crosstalk with oncogenes to regulate tumorigenesis and metastasis. Here we show that oncogenic K-Ras upregulates α6-integrin expression in Madin-Darby canine kidney (MDCK) cells via activation of the mitogen-activated protein kinase/extracellular signal-regulated kinase (ERK)/Fos-related antigen 1-signaling cascade. Activated α6-integrins promoted metastatic capacity and anoikis resistance, and led to perturbed growth of MDCK cysts. Transcriptomic analysis of K-Ras -transformed MDCK cells also revealed robust downregulation of αV-class integrins. Re-expression of αV-integrin in K-Ras -transformed MDCK cells synergistically upregulated the expression of Zinc finger E-box-binding homeobox 1 and Twist-related protein 1 and triggered epithelial-mesenchymal transition leading to induced cell motility and invasion. These results delineate the signaling cascades connecting oncogenic K-Ras with α6- and αV-integrin functions to modulate cancer cell survival and tumorigenesis, and reveal new possible strategies to target highly oncogenic K-Ras mutants.
[Mh] Termos MeSH primário: Transição Epitelial-Mesenquimal/genética
Integrina alfaV/genética
Neoplasias/genética
Proteínas Proto-Oncogênicas c-fos/genética
[Mh] Termos MeSH secundário: Animais
Anoikis/genética
Proliferação Celular/genética
Cães
Seres Humanos
Integrina alfa6/genética
Células Madin Darby de Rim Canino
Neoplasias/patologia
Proteínas Proto-Oncogênicas p21(ras)/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ITGA6 protein, human); 0 (Integrin alpha6); 0 (Integrin alphaV); 0 (KRAS protein, human); 0 (Proto-Oncogene Proteins c-fos); 0 (fos-related antigen 1); EC 3.6.5.2 (Proto-Oncogene Proteins p21(ras))
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170613
[St] Status:MEDLINE
[do] DOI:10.1038/onc.2017.177


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[PMID]:28603917
[Au] Autor:Sackmann Sala L; Boutillon F; Menara G; De Goyon-Pélard A; Leprévost M; Codzamanian J; Lister N; Pencik J; Clark A; Cagnard N; Bole-Feysot C; Moriggl R; Risbridger GP; Taylor RA; Kenner L; Guidotti JE; Goffin V
[Ad] Endereço:Institut Necker Enfants Malades (INEM), Inserm U1151-CNRS UMR 8253, University Paris Descartes, Sorbonne Paris Cité, Faculty of Medicine, Paris, France.
[Ti] Título:A rare castration-resistant progenitor cell population is highly enriched in Pten-null prostate tumours.
[So] Source:J Pathol;243(1):51-64, 2017 Sep.
[Is] ISSN:1096-9896
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Castration-resistant prostate cancer is a lethal disease. The cell type(s) that survive androgen deprivation remain poorly described, despite global efforts to understand the various mechanisms of therapy resistance. We recently identified in wild-type (WT) mouse prostates a rare population of luminal progenitor cells that we called LSC according to their FACS profile (Lin /Sca-1 /CD49f ). Here, we investigated the prevalence and castration resistance of LSC in various mouse models of prostate tumourigenesis (Pb-PRL, Pten , and Hi-Myc mice). LSC prevalence is low (∼8%, similar to WT) in Hi-Myc mice, where prostatic androgen receptor signalling is unaltered, but is significantly higher in the two other models, where androgen receptor signalling is decreased, rising up to more than 80% in Pten prostates. LSC tolerate androgen deprivation and persist or are enriched 2-3 weeks after castration. The tumour-initiating properties of LSC from Pten mice were demonstrated by regeneration of tumours in vivo. Transcriptomic analysis revealed that LSC represent a unique cell entity as their gene expression profile is different from luminal and basal/stem cells, but shares markers of each. Their intrinsic androgen signalling is markedly decreased, explaining why LSC tolerate androgen deprivation. This also illuminates why Pten tumours are castration-resistant since LSC represent the most prevalent cell type in this model. We validated CK4 as a specific marker for LSC on sorted cells and prostate tissues by immunostaining, allowing for the detection of LSC in various mouse prostate specimens. In castrated Pten prostates, there was significant proliferation of CK4 cells, further demonstrating their key role in castration-resistant prostate cancer progression. Taken together, this study identifies LSC as a probable source of prostate cancer relapse after androgen deprivation and as a new therapeutic target for the prevention of castrate-resistant prostate cancer. Copyright © 2017 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/deficiência
Proliferação Celular
Células-Tronco Neoplásicas/enzimologia
PTEN Fosfo-Hidrolase/deficiência
Neoplasias de Próstata Resistentes à Castração/enzimologia
[Mh] Termos MeSH secundário: Antagonistas de Androgênios/farmacologia
Animais
Antineoplásicos Hormonais/farmacologia
Ataxina-1/metabolismo
Biomarcadores Tumorais/genética
Linhagem da Célula
Proliferação Celular/efeitos dos fármacos
Resistência a Medicamentos Antineoplásicos
Perfilação da Expressão Gênica/métodos
Regulação Neoplásica da Expressão Gênica
Predisposição Genética para Doença
Integrina alfa6/metabolismo
Queratina-4/metabolismo
Masculino
Camundongos Endogâmicos C57BL
Camundongos Knockout
Recidiva Local de Neoplasia
Células-Tronco Neoplásicas/efeitos dos fármacos
Células-Tronco Neoplásicas/patologia
Células-Tronco Neoplásicas/transplante
Análise de Sequência com Séries de Oligonucleotídeos
PTEN Fosfo-Hidrolase/genética
Fenótipo
Neoplasias de Próstata Resistentes à Castração/tratamento farmacológico
Neoplasias de Próstata Resistentes à Castração/genética
Neoplasias de Próstata Resistentes à Castração/patologia
Receptores Androgênicos/efeitos dos fármacos
Receptores Androgênicos/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (AR protein, mouse); 0 (Androgen Antagonists); 0 (Antineoplastic Agents, Hormonal); 0 (Ataxin-1); 0 (Atxn1 protein, mouse); 0 (Biomarkers, Tumor); 0 (Integrin alpha6); 0 (Keratin-4); 0 (Receptors, Androgen); EC 3.1.3.67 (PTEN Phosphohydrolase); EC 3.1.3.67 (Pten protein, mouse)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170613
[St] Status:MEDLINE
[do] DOI:10.1002/path.4924


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[PMID]:28372578
[Au] Autor:Domínguez-Catzín V; Reveles-Espinoza AM; Sánchez-Ramos J; Cruz-Cadena R; Lemus-Hernández D; Garrido E
[Ad] Endereço:Laboratory of Research in Cancer Molecular and Cell Biology, Department of Genetics and Molecular Biology, CINVESTAV-IPN, Av. Instituto Politécnico Nacional 2508, Col. San Pedro Zacatenco, C.P. 07360, México D.F., Mexico.
[Ti] Título:HPV16-E2 protein modifies self-renewal and differentiation rate in progenitor cells of human immortalized keratinocytes.
[So] Source:Virol J;14(1):65, 2017 Apr 03.
[Is] ISSN:1743-422X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Cervical cancer is the fourth cause of death worldwide by cancer in women and is a disease associated to persistent infection with human papillomavirus (HPV), particularly from two high-risk types HPV16 and 18. The virus initiates its replicative cycle infecting cells located in the basal layer of the epithelium, where a small population of epithelial stem cells is located performing important functions of renewal and maintenance of the tissue. Viral E2 gene is one of the first expressed after infection and plays relevant roles in the replicative cycle of the virus, modifying fundamental processes in the infected cells. Thus, the aim of the present study was to demonstrate the presence of hierarchic subpopulations in HaCaT cell line and evaluate the effect of HPV16-E2 expression, on their biological processes. METHODS: HaCaT-HPV16-E2 cells were generated by transduction of HaCaT cell line with a lentiviral vector. The α6-integrin-CD71 expression profile was established by immunostaining and flow cytometric analysis. After sorting, cell subpopulations were analyzed in biological assays for self-renewal, clonogenicity and expression of stemness factors (RT-qPCR). RESULTS: We identified in HaCaT cell line three different subpopulations that correspond to early differentiated cells (α6-integrin ), transitory amplifying cells (α6-integrin /CD71 ) and progenitor cells (α6-integrin /CD71 ). The last subpopulation showed stem cell characteristics, such as self-renewal ability, clonogenicity and expression of the well-known stem cell factors SOX2, OCT4 and NANOG, suggesting they are stem-like cells. Interestingly, the expression of HPV16-E2 in HaCaT cells changed its α6-integrin-CD71 immunophenotype modifying the relative abundance of the cell subpopulations, reducing significantly the percentage of α6-integrin /CD71 cells. Moreover, the expression of the stem cell markers was also modified, increasing the expression of SOX2 and NANOG, but decreasing notably the expression of OCT4. CONCLUSIONS: Our data demonstrated the presence of a small subpopulation with epithelial "progenitor cells" characteristics in the HaCaT cell line, and that HPV16-E2 expression on these cells induces early differentiation.
[Mh] Termos MeSH primário: Diferenciação Celular
Proteínas de Ligação a DNA/metabolismo
Interações Hospedeiro-Patógeno
Papillomavirus Humano 16/fisiologia
Queratinócitos/virologia
Proteínas Oncogênicas Virais/metabolismo
Células-Tronco/virologia
[Mh] Termos MeSH secundário: Antígenos CD/análise
Linhagem Celular
Citometria de Fluxo
Vetores Genéticos
Seres Humanos
Imuno-Histoquímica
Integrina alfa6/análise
Queratinócitos/fisiologia
Lentivirus/genética
Receptores da Transferrina/análise
Células-Tronco/fisiologia
Transdução Genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (CD71 antigen); 0 (DNA-Binding Proteins); 0 (E2 protein, Human papillomavirus type 16); 0 (Integrin alpha6); 0 (Oncogene Proteins, Viral); 0 (Receptors, Transferrin)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170828
[Lr] Data última revisão:
170828
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170405
[St] Status:MEDLINE
[do] DOI:10.1186/s12985-017-0736-2


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[PMID]:28134816
[Au] Autor:Metral E; Bechetoille N; Demarne F; Rachidi W; Damour O
[Ad] Endereço:Gattefossé, 36 chemin de Genas, F-69800 Saint-Priest, France. odile.damour@chu-lyon.fr.
[Ti] Título:α6 Integrin (α6 )/Transferrin Receptor (CD71) Keratinocyte Stem Cells Are More Potent for Generating Reconstructed Skin Epidermis Than Rapid Adherent Cells.
[So] Source:Int J Mol Sci;18(2), 2017 Jan 27.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:The epidermis basal layer is composed of two keratinocyte populations: Keratinocyte Stem cells (KSC) and Transitory Amplifying (TA) cells that arise from KSC division. Unfortunately, no specific marker exists to differ between KSC and TA cells. Here, we aimed at comparing two different methods that pretended to isolate these two populations: (i) the rapid adhesion method on coated substrate and (ii) the flow cytometry method, which is based on the difference in cell surface expressions of the α6 integrin and transferrin receptor (CD71). Then, we compared different parameters that are known to discriminate KSC and TA populations. Interestingly, we showed that both methods allow enrichment in stem cells. However, cell sorting by flow cytometry (α6 /CD71 ) phenotype leads to a better enrichment of KSC since the colony forming efficiency is five times increased versus total cell suspension, whereas it is only 1.4 times for the adhesion method. Moreover, α6 /CD71 cells give rise to a thicker pluristratified epithelium with lower seeding density and display a low Ki67 positive cells number, showing that they have reached the balance between proliferation and differentiation. We clearly demonstrated that cells isolated by a rapid adherent method are not the same population as KSC isolated by flow cytometry following α6 /CD71 phenotype.
[Mh] Termos MeSH primário: Antígenos CD/metabolismo
Epiderme/citologia
Integrina alfa6/metabolismo
Queratinócitos/citologia
Receptores da Transferrina/metabolismo
Células-Tronco/metabolismo
[Mh] Termos MeSH secundário: Adesão Celular
Separação Celular
Células Clonais
Colágeno Tipo I/metabolismo
Ensaio de Unidades Formadoras de Colônias
Citometria de Fluxo
Seres Humanos
Fenótipo
Regeneração
Temperatura Ambiente
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (CD71 antigen); 0 (Collagen Type I); 0 (Integrin alpha6); 0 (Receptors, Transferrin)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170424
[Lr] Data última revisão:
170424
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170131
[St] Status:MEDLINE


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[PMID]:28131812
[Au] Autor:Villegas-Pineda JC; Toledo-Leyva A; Osorio-Trujillo JC; Hernández-Ramírez VI; Talamás-Rohana P
[Ad] Endereço:Departamento de Infectómica y Patogénesis Molecular, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional, Av. Instituto Politécnico Nacional 2508, Col. San Pedro Zacatenco, Delegación Gustavo A. Madero, Ciudad de México 07360, Mexico. Electronic address: jcvillegas@cin
[Ti] Título:The translational blocking of α5 and α6 integrin subunits affects migration and invasion, and increases sensitivity to carboplatin of SKOV-3 ovarian cancer cell line.
[So] Source:Exp Cell Res;351(2):127-134, 2017 Feb 15.
[Is] ISSN:1090-2422
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Epithelial ovarian cancer is the most lethal gynecologic malignancy. Integrins, overexpressed in cancer, are involved in various processes that favor the development of the disease. This study focused on determining the degree of involvement of α5, α6 and ß3 integrin subunits in the establishment/development of epithelial ovarian cancer (EOC), such as proliferation, migration, invasion, and response to carboplatin. The translation of the α5, α6 and ß3 integrins was blocked using morpholines, generating morphant cells for these proteins, which were corroborated by immunofluorescence assays. WST-1 proliferation assay showed that silencing of α5, α6, and ß3 integrins does not affect the survival of morphants. Wound healing and transwell chamber assays showed that blocking α5 and α6 integrins decrease, in lesser and greater level respectively, the migratory and the invasive capacity of SKOV-3 cells. Finally, blocking α5 and α6 integrins partially sensitized the cells response to carboplatin, while blocking integrin ß3 generated resistance to this drug. Statistical analyses were performed with the GraphPad Prism 5.0 software employing one way and two-way ANOVA tests; data are shown as average±SD. Results suggest that α5 and α6 integrins could become good candidates for chemotherapy targets in EOC.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Carboplatina/farmacologia
Regulação Neoplásica da Expressão Gênica
Integrina alfa5/genética
Integrina alfa6/genética
Morfolinas/farmacologia
Biossíntese de Proteínas/efeitos dos fármacos
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Movimento Celular/efeitos dos fármacos
Cultura em Câmaras de Difusão
Resistência a Medicamentos Antineoplásicos/efeitos dos fármacos
Resistência a Medicamentos Antineoplásicos/genética
Células Epiteliais/efeitos dos fármacos
Células Epiteliais/metabolismo
Células Epiteliais/patologia
Feminino
Seres Humanos
Integrina alfa5/metabolismo
Integrina alfa6/metabolismo
Integrina beta3/genética
Integrina beta3/metabolismo
Ovário/efeitos dos fármacos
Ovário/metabolismo
Ovário/patologia
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Integrin alpha5); 0 (Integrin alpha6); 0 (Integrin beta3); 0 (Morpholines); BG3F62OND5 (Carboplatin)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170518
[Lr] Data última revisão:
170518
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170130
[St] Status:MEDLINE



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