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Id: biblio-887236
Autor: Bautista, Wendy; Lipschitz, Jeremy; McKay, Andrew; Minuk, Gerald Y.
Título: Cancer Stem Cells are Depolarized Relative to Normal Stem Cells Derived from Human Livers
Fonte: Ann. hepatol;16(2):297-303, Mar.-Apr. 2017. tab, graf.
Idioma: en.
Resumo: ABSTRACT Introduction and aim. The inability to distinguish cancer (CSCs) from normal stem cells (NSCs) has hindered attempts to identify safer, more effective therapies for hepatocellular carcinoma (HCC). The aim of this study was to document and compare cell membrane potential differences (PDs) of CSCs and NSCs derived from human HCC and healthy livers respectively and determine whether altered GABAergic innervation could explain the differences. Material and methods. Epithelial cell adhesion molecule (EpCAM) positive stem cells were isolated from human liver tissues by magnetic bead separations. Cellular PDs were recorded by microelectrode impalement of freshly isolated cells. GABAA receptor subunit expression was documented by reverse transcriptase polymerase chain reaction (RT-PCR) and immunofluorescence. Results. CSCs were significantly depolarized (-7.0 ± 1.3 mV) relative to NSCs (-23.0 ± 1.4 mV, p < 0.01). The depolarized state was associated with different GABAA receptor subunit expression profiles wherein phasic transmission, represented by GAGAA α3 subunit expression, was prevalent in CSCs while tonic transmission, represented by GABAA α6 subunit expression, prevailed in NSCs. In addition, GABAA subunits α3, β3, γ3 and δ were strongly expressed in CSCs while GABAA π expression was dominant in NSCs. CSCs and NSCs responded similarly to GABAA receptor agonists (ΔPD: 12.5 ± 1.2 mV and 11.0 ± 3.5 mV respectively). Conclusion. The results of this study indicate that CSCs are significantly depolarized relative to NSCs and these differences are associated with differences in GABAA receptor subunit expression. Together they provide new insights into the pathogenesis and possible treatment of human HCC.
Descritores: Células-Tronco Neoplásicas/metabolismo
Receptores de GABA-A/metabolismo
Carcinoma Hepatocelular/genética
Carcinoma Hepatocelular/metabolismo
Agonistas de Receptores de GABA-A/farmacologia
Molécula de Adesão da Célula Epitelial/metabolismo
Fígado/citologia
Neoplasias Hepáticas/metabolismo
-Fenótipo
Células-Tronco/efeitos dos fármacos
Células-Tronco Neoplásicas/efeitos dos fármacos
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Biomarcadores/metabolismo
Imunofluorescência
Separação Imunomagnética
Receptores de GABA-A/efeitos dos fármacos
Receptores de GABA-A/genética
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Subunidades Proteicas
Neoplasias Hepáticas/genética
Potenciais da Membrana/efeitos dos fármacos
Limites: Humanos
Responsável: BR1.1 - BIREME



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