Differential regulation of the Oct-3/4 gene in cell culture model systems that parallel different stages of mammalian development

2008 ◽  
Vol 75 (8) ◽  
pp. 1247-1257 ◽  
Author(s):  
Sunil Kumar Mallanna ◽  
Brian Boer ◽  
Michelle Desler ◽  
Angie Rizzino
2013 ◽  
Vol 94 (7) ◽  
pp. 1373-1379 ◽  
Author(s):  
Aoife L McCarthy ◽  
Yvonne C O'Callaghan ◽  
Alan Connolly ◽  
Charles O Piggott ◽  
Richard J FitzGerald ◽  
...  

2017 ◽  
Author(s):  
Pamela S. Shaw ◽  
Rick Nicoletti ◽  
Naghmeh Salimi ◽  
Helen L. Yang ◽  
Abigail E. Witt ◽  
...  

2021 ◽  
Vol 8 (7) ◽  
pp. 97
Author(s):  
Jennifer Rosendahl ◽  
Andreas Svanström ◽  
Mattias Berglin ◽  
Sarunas Petronis ◽  
Yalda Bogestål ◽  
...  

Current conventional cancer drug screening models based on two-dimensional (2D) cell culture have several flaws and there is a large need of more in vivo mimicking preclinical drug screening platforms. The microenvironment is crucial for the cells to adapt relevant in vivo characteristics and here we introduce a new cell culture system based on three-dimensional (3D) printed scaffolds using cellulose nanofibrils (CNF) pre-treated with 2,2,6,6-tetramethylpyperidine-1-oxyl (TEMPO) as the structural material component. Breast cancer cell lines, MCF7 and MDA-MB-231, were cultured in 3D TEMPO-CNF scaffolds and were shown by scanning electron microscopy (SEM) and histochemistry to grow in multiple layers as a heterogenous cell population with different morphologies, contrasting 2D cultured mono-layered cells with a morphologically homogenous cell population. Gene expression analysis demonstrated that 3D TEMPO-CNF scaffolds induced elevation of the stemness marker CD44 and the migration markers VIM and SNAI1 in MCF7 cells relative to 2D control. T47D cells confirmed the increased level of the stemness marker CD44 and migration marker VIM which was further supported by increased capacity of holoclone formation for 3D cultured cells. Therefore, TEMPO-CNF was shown to represent a promising material for 3D cell culture model systems for cancer cell applications such as drug screening.


2014 ◽  
Vol 122 (10) ◽  
pp. 575-581 ◽  
Author(s):  
Z. Molnár ◽  
R. Pálföldi ◽  
A. László ◽  
M. Radács ◽  
M. László ◽  
...  

2021 ◽  
Vol 122 ◽  
pp. 111914
Author(s):  
Alejandro Herreros-Pomares ◽  
Xuan Zhou ◽  
Silvia Calabuig-Fariñas ◽  
Se-Jun Lee ◽  
Susana Torres ◽  
...  

2007 ◽  
Vol 292 (4) ◽  
pp. E1149-E1156 ◽  
Author(s):  
David P. Sparling ◽  
Beth A. Griesel ◽  
Ann Louise Olson

GLUT4 promoter activity is regulated by hormonal, metabolic, and tissue-specific controls. This complicates the study of GLUT4 gene transcription, as no cell culture model adequately recapitulates these extracellular regulators. While investigating cultured primary adipocytes as a model system for GLUT4 transcription, we observed that GLUT4 mRNA was specifically and rapidly downregulated upon tissue dispersal. Downregulation of GLUT4 mRNA was mediated in part by loss of regulatory control by the trans-acting factors that control GLUT4 transcriptional activity [the myocyte enhancer factor 2 (MEF2) transcription factor family and the GLUT4 enhancer factor] and their cognate DNA binding sites in transgenic mice. The differences in GLUT4 transcription when whole adipose tissue and cell culture model systems are compared can be correlated to a posttranslational phosphorylation of the transcription factor MEF2A. The difference in the MEF2A phosphorylation state in whole tissue vs. isolated cells may provide a further basis for the development of an in vitro system that could recapitulate fully regulated GLUT4 promoter activity. Development of an in vitro system to reconstitute GLUT4 transcriptional regulation will further efforts to discern the molecular mechanisms that underlie GLUT4 expression.


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