E-GEOD-54713 - Cell state transitions regulated by Slug are critical for tissue regeneration and tumor initiation [Agilent microarray samples]

Released on 23 June 2014, last updated on 30 June 2014
Homo sapiens
Samples (36)
Array (1)
Protocols (5)
Alterations that perturb differentiation and cell state transitions can lead to defects in development, function and the genesis of cancer. Studying cellular plasticity at high resolution and in real time has proven difficult using existing methods. Here, we use a quantitative approach to gain insights into cell state dynamics of normal mammary epithelial cells (MECs) and validate the model's predictions in vivo. In the absence of Slug/SNAI2, basal mammary progenitor cells transition into a luminal differentiation state, while luminal progenitor cells proliferate and expand; these changes result in abnormal mammary architecture and defects in tissue function. Loss of Slug also disrupts cellular plasticity leading to defects in tissue regeneration and the initiation of cancer. Mechanistically, Slug promotes cellular plasticity by recruiting the chromatin modifier, LSD1 (lysine specific demethylase 1), to promoters of lineage specific genes to represses transcription. Together, these finding demonstrate that Slug is necessary for cellular adaptation during tissue development and regeneration, and that transitioning back into a more primitive stem-like state is a prerequisite for tumor initiation. reference x sample
Experiment type
transcription profiling by array 
Charles Perou <cperou@med.unc.edu>, Aleix Prat, Charles M Perou
Cell-State Transitions Regulated by SLUG Are Critical for Tissue Regeneration and Tumor Initiation. Phillips S, Prat A, Sedic M, Proia T, Wronski A, Mazumdar S, Skibinski A, Shirley SH, Perou CM, Gill G, Gupta PB, Kuperwasser C. , Europe PMC 24936451
Investigation descriptionE-GEOD-54713.idf.txt
Sample and data relationshipE-GEOD-54713.sdrf.txt
Processed data (1)E-GEOD-54713.processed.1.zip
Array designA-GEOD-10481.adf.txt