Publication: Análisis de la expresión génica diferencial de células eritroleucémicas resistentes a la diferenciación: relevancia de las proteínas del citoesqueleto de actina
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2018-09-14
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Universidad Complutense de Madrid
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Abstract
Las células eritroleucémicas Friend (MEL) derivan de eritroblastostransformados con el SFFV (Spleen Focus Forming Virus) (Friend et al. 1966)integrado corriente arriba del locus PU.1 (Fernandez-Nestosa et al. 2013). Estascélulas permanecen en estado proliferativo y no se diferencian en presencia deeritropoyetina. Las células MEL-DS19 pueden superar el bloqueo y reiniciar elprograma de diferenciación celular cuando se exponen a compuestos químicoscomo el hexametilen-bis-acetamida (HMBA). Esta característica hace de las célulasMEL-DS19 un excelente modelo de estudio de la reprogramación de un tumor haciaun fenotipo normal. En un trabajo previo se estableció una línea celular derivada dela misma, MEL-R, que muestra resistencia a la diferenciación incluso en presenciadel agente inductor (Fernandez-Nestosa et al. 2008).La red de filamentos de actina proporciona soporte mecánico alcitoesqueleto. Se reconoce además, que contribuye a otros procesos celularescríticos. En los últimos años aumentan las evidencias que indican que elcitoesqueleto de actina participa en el control y regulación de rutas de señalización(Mattila et al. 2016). En este sentido, cambios en la regulación del citoesqueleto deactina podrían inducir un bloqueo del programa de diferenciación celular...
Friend murine erythroleukemia cells (MEL) derive from erythroblaststransformed with the Spleen Focus Forming Virus (SFFV) where integration occurredseveral kilobases upstream the PU.1 locus (Friend et al. 1966; Ruscetti 1999). Thesecells remain in proliferative state and do not differentiate in the presence oferythropoietin. MEL-DS19 cells may overcome the blockage, however, and reinitiatedifferentiation when exposed to a number of different chemical agents, such ashexamethylene-bis-acetamide (HMBA). This feature makes MEL-DS19 cells anextremely useful model to study reprogramming of tumor cells to a non-malignantphenotype and to analyze the mode of action of different chemotheraupeticscompounds. We previously reported the establishment of hexamethylene-bisacetamide(HMBA)-resistant cell lines (MEL-R) that are unable to differentiate, evenin the presence of the inducer (Fernandez-Nestosa et al. 2008).On the other hand, the network of actin filaments provides mechanicalsupport to the cell cytoskeleton, but it is increasingly acknowledged that it alsocontributes to other critical cellular processes. Emerging evidence points to a rolefor the actin cytoskeleton in controlling and regulating receptor signaling (Mattila etal. 2016). In this line, changes in the regulation of actin cytoskeleton could beimplicated in the blockade of the erythroid differentiation program...
Friend murine erythroleukemia cells (MEL) derive from erythroblaststransformed with the Spleen Focus Forming Virus (SFFV) where integration occurredseveral kilobases upstream the PU.1 locus (Friend et al. 1966; Ruscetti 1999). Thesecells remain in proliferative state and do not differentiate in the presence oferythropoietin. MEL-DS19 cells may overcome the blockage, however, and reinitiatedifferentiation when exposed to a number of different chemical agents, such ashexamethylene-bis-acetamide (HMBA). This feature makes MEL-DS19 cells anextremely useful model to study reprogramming of tumor cells to a non-malignantphenotype and to analyze the mode of action of different chemotheraupeticscompounds. We previously reported the establishment of hexamethylene-bisacetamide(HMBA)-resistant cell lines (MEL-R) that are unable to differentiate, evenin the presence of the inducer (Fernandez-Nestosa et al. 2008).On the other hand, the network of actin filaments provides mechanicalsupport to the cell cytoskeleton, but it is increasingly acknowledged that it alsocontributes to other critical cellular processes. Emerging evidence points to a rolefor the actin cytoskeleton in controlling and regulating receptor signaling (Mattila etal. 2016). In this line, changes in the regulation of actin cytoskeleton could beimplicated in the blockade of the erythroid differentiation program...
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Tesis inédita de la Universidad Complutense de Madrid, Facultad de Ciencias Biológicas, leída el 31-03-2017