Expression data from menadione, PERK inhibitor, or control-treated HMLE-shGFP and HMLE-Twist human mammary epithelial cells

ABSTRACT: Malignant carcinomas that recur following therapy are typically de-differentiated and multi-drug resistant (MDR). De-differentiated cancer cells acquire MDR by upregulating reactive oxygen species (ROS)-scavenging enzymes and drug efflux pumps, but how these genes are upregulated in response to de-differentiation is not known. Here, we examine this question by using global transcriptional profiling to identify ROS-induced genes that are already upregulated in de-differentiated cells, even in the absence of oxidative damage. Using this approach, we found that the Nrf2 transcription factor, which is the master regulator of cellular response to oxidative stress, is pre-activated in de-differentiated cells. In de-differentiated cells, Nrf2 is not activated by oxidation but rather through a non

ORGANISM(S): Homo sapiens

SUBMITTER: Catherine Del Vecchio 

PROVIDER: E-GEOD-59780 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress