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E-GEOD-30465 - Asymmetric cancer cell division regulated by AKT, Reactive Oxygen Species (ROS) high versus ROS low mRNA

Released on 14 July 2011, last updated on 2 August 2011
Homo sapiens
Samples (12)
Array (1)
Protocols (8)
Human tumors often contain slowly proliferating cancer cells that resist treatment but we do not know precisely how these cells arise. We show that rapidly proliferating cancer cells can divide asymmetrically to produce slowly proliferating “G0-like” progeny that are enriched following chemotherapy in breast cancer patients. Asymmetric cancer cell division results from asymmetric suppression of AKT/PKB kinase signaling in one daughter cell during telophase of mitosis. Moreover, inhibition of AKT signaling with small molecule drugs can induce asymmetric cancer cell division and the production of slow proliferators. Cancer cells therefore appear to continuously flux between symmetric and asymmetric division depending on the precise state of their AKT signaling network. This model may have significant implications for understanding how tumors grow, evade treatment, and recur. 3 replicates each of MCF7 Reactive Oxygen Species (ROS) high, HCT116 ROS high, MCF7 ROS low, and HCT116 ROS low.
Experiment type
transcription profiling by array 
Ben S. Wittner <>, Albert C Yeh, Anita Wolfer, Ben S Wittner, Eduardo Leon, Emanuel F Petricoin, Ipsita Dey-Guha, John G Albeck, Julia D Wulfkuhle, Revati Darp, Sridhar Ramaswamy
Asymmetric cancer cell division regulated by AKT. Dey-Guha I, Wolfer A, Yeh AC, Albeck JG, Darp R, Leon E, Wulfkuhle J, Petricoin EF 3rd, Wittner BS, Ramaswamy S. , PMID:21757645
Investigation descriptionE-GEOD-30465.idf.txt
Sample and data relationshipE-GEOD-30465.sdrf.txt
Raw data (1)
Processed data (1)
Array designA-GEOD-9987.adf.txt
R ExpressionSetE-GEOD-30465.eSet.r