Name: enhancement of apoptotic and autophagic induction by a novel synthetic c-1 analogue of 7-deoxypancratistatin in human breast adenocarcinoma and neuroblastoma cells with tamoxifen
Uploaded: 2012-05-30T12:00:00
Description: Watch this Scientific Journal Video about Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma

Este trabalho foi apoiado pelos Cavaleiros de Colombo Capítulo 9671 (Windsor, Ontário), e um CIHR Frederick Banting e Best Charles Canadá Bolsa de Pós-Graduação concedido a Dennis Ma. Obrigado a Robert Hodge e Elizabeth Fidalgo da Silva por sua ajuda com a microscopia de lapso de tempo. Obrigado a Katie Facecchia para editar os vídeos de lapso de tempo de microscopia. Gostaríamos também de agradecer Sudipa junho Chatterjee e Phillip Tremblay, pela revisão crítica deste manuscrito. Este trabalho é dedicado em memória de Kevin Couvillon que perdeu a batalha contra o câncer em 2010.

Introdução A apoptose, ou do tipo I morte celular programada, é um processo fisiológico que pode operar extrinsecamente, via ligação de um ligando de morte a um receptor de morte, ou intrinsecamente. A via intrínseca da apoptose é iniciada pelo stress intracelular, tais como danos no ADN e disfunção mitocondrial, o que conduz finalmente ao permeabilização da dissipação, mitocôndrias do potencial da membrana mitocondrial (MMP), a libertação de factores apoptogénica a partir do ...

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Os compostos de PST e semelhantes têm sido demonstrado que têm propriedades anti-cancro 11-15,21. Nós apresentamos previamente PST natural para desestabilizar a mitocôndria seletivamente nas células cancerosas, que assim induz a apoptose pela liberação de fatores de apoptogénica 12,14. É mais provável que JCTH-4 actua através do mesmo mecanismo; JCTH-4 Fig. causada colapso MMP em células MCF7 como visto com coloração TMRM (Fig. 5a), e aumentou geraç?...

<table border="1"><tbody><tr><td> Nome do material </td><td> Companhia </td><td> Número de catálogo </td></tr><tr><td> SH-SY5Y linha celular </td><td> ATCC </td><td> CRL-2266 </td></tr><tr><td> Modificação de Dulbecco Eagles Médio F-12 de HAM </td><td> Sigma-Aldrich </td><td> 51448C </td></tr><tr><td> Soro fetal de bovino </td><td> Gibco BRL </td><td> 16000-044 </td></tr><tr><td> MCF7 linha celular </td><td> ATCC </td><td> HTB-22 </td></tr><tr><td> Meio RPMI-1640 </td><td> Sigma-Aldrich </td><td> R 0883 </td></tr><tr><td> Aparentemente normal, linha celular humana fetal fibroblastos (NFF) </td><td> Coriell Institute for Medical Research </td><td> AG04431B </td></tr><tr><td> Meio Dulbecco modificado por Eagle, médio de glucose elevada </td><td> Thermo Scientific </td><td> SH30022.01 </td></tr><tr><td> Tamoxifen sal citrato </td><td> Sigma-Aldrich </td><td> T9262 </td&gt; </tr><tr><td> 35 mm de vidro de cultura pratos de fundo </td><td> MatTek </td><td> P35G-014-C </td></tr><tr><td> Leica DMI6000 microscópio invertido B </td><td> Leica Microsystems </td><td> N / A </td></tr><tr><td> Hoechst 33342 corante </td><td> Molecular Probes </td><td> H3570 </td></tr><tr><td> Leica DM IRB invertidos microscópio de fluorescência </td><td> Leica Microsystems </td><td> N / A </td></tr><tr><td> A anexina V-488 AlexaFluor </td><td> Invitrogen </td><td> A13201 </td></tr><tr><td> Trypan solução azul </td><td> Sigma-Aldrich </td><td> T8154-20ML </td></tr><tr><td> Hemocitómetro </td><td> Fisher Scientific </td><td> 267110 </td></tr><tr><td> WST-1 reagente </td><td> Roche Applied Science </td><td> 11644807001 </td></tr><tr><td> Wallac Victor 3 1420 Multilabel Contador </td><td> PerkinElmer </td><td> 1420-011 </td></tr><tr><td> Tetrametilrodamina metil éster (TMRM) </td><td> Gibco BRL </td><td> T-668 </td></tr><tr><td> Moedor de tecido de vidro </td><td> Fisher Scientific </td><td> K8885300-0002 </td></tr><tr><td> BioRad ensaio de proteína </td><td> Bio-Rad Laboratories </td><td> 500-0001Bottom da Forma </td></tr><tr><td> Amplex Vermelho </td><td> Invitrogen </td><td> A12222 </td></tr><tr><td> Peroxidase de rábano (HRP) </td><td> Sigma-Aldrich </td><td> P8125 </td></tr><tr><td> Spectramax Gêmeos XPS </td><td> Molecular Devices </td><td> 3126666 </td></tr><tr><td> Anti-LC3 anticorpo criado em coelhos </td><td> Novus Biologicals </td><td> NB100-2220 </td></tr><tr><td> Anticorpo anti-rato conjugado com HRP secundária </td><td> Abcam </td><td> ab6728 </td></tr><tr><td> Anticorpo anti-coelho conjugado com HRP secundária </td><td> Abcam </td><td> ab6802 </td></tr><tr><td> Substrato de peroxidase de quimioluminescência </td><td> Sigma-Aldrich </td><td> CPS160 </td></tr><tr><td> Monodansylcadaverine </td><td> Sigma-Aldrich </td><td> 30432 </td></tr></tbody></table>

enhancement of apoptotic and autophagic induction by a novel synthetic c-1 analogue of 7-deoxypancratistatin in human breast adenocarcinoma and neuroblastoma cells with tamoxifen

O câncer de mama é um dos cânceres mais comuns entre as mulheres na América do Norte. Muitos dos atuais tratamentos anti-câncer, incluindo a radiação ionizante, através de induzir a apoptose danos ao DNA. Infelizmente, tais tratamentos são não-selectivos para as células cancerosas e produzir toxicidade semelhante em células normais. Relatamos indução selectiva da apoptose em células cancerosas pela pancratistatin composto natural (PST). Recentemente, um novo análogo de PST, um derivado de C-1 acetoximetil de 7-deoxypancratistatin (JCTH-4), foi produzido por síntese de novo e exibe actividade indutora comparável selectiva apoptose em diversas linhagens de células cancerosas. Recentemente, autofagia tem sido implicado em doenças malignas como tanto pró-sobrevivência e os mecanismos de pró-morte em resposta à quimioterapia. O tamoxifeno (TAM) tem demonstrado, invariavelmente, a indução de pró-sobrevivência autofagia em inúmeros cânceres. Neste estudo, a eficácia da JCTH-4 isoladamente e em combinação com a TAM para induzir a morte celular em significância da mama humanor (MCF7) e neuroblastoma (SH-SY5Y) células foi avaliada. TAM sozinho induzida autofagia, mas a morte de células insignificante enquanto JCTH-4 sozinho causou indução significativa da apoptose com alguma indução de autofagia. Curiosamente, o tratamento combinatória produziu um aumento drástico na indução de apoptose e autofágica. Foram monitoradas a dependentes do tempo alterações morfológicas em células MCF7 submetidos a TAM induzida por autofagia, JCTH-4-induzida apoptose e autofagia e morte celular acelerada com o tratamento combinatório usando microscopia de lapso de tempo. Nós demonstramos que estes compostos para induzir a apoptose / autofagia por direccionamento mitocondrial nestas células cancerosas. É importante ressaltar que estes tratamentos não afetaram a sobrevivência dos não cancerosos fibroblastos humanos. Assim, estes resultados indicam que JCTH-4 em combinação com a TAM poderia ser utilizado como uma forma segura e muito potente terapia anti-cancro contra o cancro da mama e células de neuroblastoma.

Watch this Scientific Journal Video about Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma 

Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen

Temos sintetizado um análogo romance de pancratistatin com atividade anti-câncer comparável como pancratistatin nativa; curiosamente, o tratamento com tamoxifeno combinatória rendeu uma drástica melhoria na indução de apoptose e autofagia por mitocôndria com efeito mínimo sobre os fibroblastos não cancerosos. Assim, JCTH-4 em combinação com o tamoxifen poderia proporcionar uma terapia anti-cancro segura.

Melhoramento de Indução apoptose e autofagia por um sintético C-1 Novel Analogue, de 7 de deoxypancratistatin em adenocarcinoma de mama humano e células de neuroblastoma com tamoxifeno

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