Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 108, Issue 31, Pages 12845-12850Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1109632108
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Funding
- Massachusetts General Hospital Cancer Center
- National Cancer Institute [K08 CA100339, P50 CA89393, P50 CA127003]
- Department of Defense [W81XH-06-2-0033]
- Howard Hughes Medical Institute
- Sidney Kimmel Foundation
- Smith Family Foundation
- Swiss National Science Foundation
- Emma Muschamp Foundation
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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.
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