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Molecular Cancer Research
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A Mechanism for Asymmetric Cell Division Resulting in Proliferative Asynchronicity

Ipsita Dey-Guha, Cleidson P. Alves, Albert C. Yeh, Salony, Xavier Sole, Revati Darp and Sridhar Ramaswamy
Ipsita Dey-Guha
1Massachusetts General Hospital Cancer Center, Boston, Massachusetts.
2Harvard Medical School, Boston, Massachusetts.
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Cleidson P. Alves
1Massachusetts General Hospital Cancer Center, Boston, Massachusetts.
2Harvard Medical School, Boston, Massachusetts.
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Albert C. Yeh
2Harvard Medical School, Boston, Massachusetts.
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Salony
1Massachusetts General Hospital Cancer Center, Boston, Massachusetts.
2Harvard Medical School, Boston, Massachusetts.
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Xavier Sole
1Massachusetts General Hospital Cancer Center, Boston, Massachusetts.
2Harvard Medical School, Boston, Massachusetts.
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Revati Darp
1Massachusetts General Hospital Cancer Center, Boston, Massachusetts.
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Sridhar Ramaswamy
1Massachusetts General Hospital Cancer Center, Boston, Massachusetts.
2Harvard Medical School, Boston, Massachusetts.
3Broad Institute of Harvard and MIT, Cambridge, Massachusetts.
4Harvard Stem Cell Institute, Cambridge, Massachusetts.
5Harvard-Ludwig Center for Cancer Research, Boston, Massachusetts.
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  • For correspondence: sridhar@mgh.harvard.edu
DOI: 10.1158/1541-7786.MCR-14-0474 Published February 2015
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Abstract

All cancers contain an admixture of rapidly and slowly proliferating cancer cells. This proliferative heterogeneity complicates the diagnosis and treatment of patients with cancer because slow proliferators are hard to eradicate, can be difficult to detect, and may cause disease relapse sometimes years after apparently curative treatment. While clonal selection theory explains the presence and evolution of rapid proliferators within cancer cell populations, the circumstances and molecular details of how slow proliferators are produced is not well understood. Here, a β1-integrin/FAK/mTORC2/AKT1–associated signaling pathway is discovered that can be triggered for rapidly proliferating cancer cells to undergo asymmetric cell division and produce slowly proliferating AKT1low daughter cells. In addition, evidence indicates that the proliferative output of this signaling cascade involves a proteasome-dependent degradation process mediated by the E3 ubiquitin ligase TTC3. These findings reveal that proliferative heterogeneity within cancer cell populations, in part, is produced through a targetable signaling mechanism, with potential implications for understanding cancer progression, dormancy, and therapeutic resistance.

Implications: These findings provide a deeper understanding of the proliferative heterogeneity that exists in the tumor environment and highlight the importance of designing future therapies against multiple proliferative contexts.

Visual Overview. A proposed mechanism for producing slowly proliferating cancer cells. http://mcr.aacrjournals.org/content/early/2015/01/09/1541-7786.MCR-14-0474/F1.large.jpg.

Mol Cancer Res; 13(2); 223–30. ©2015 AACR.

This article is featured in Highlights of This Issue, p. 209

  • Received August 25, 2014.
  • Revision received November 5, 2014.
  • Accepted November 17, 2014.
  • ©2015 American Association for Cancer Research.

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Molecular Cancer Research: 13 (2)
February 2015
Volume 13, Issue 2
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A Mechanism for Asymmetric Cell Division Resulting in Proliferative Asynchronicity
Ipsita Dey-Guha, Cleidson P. Alves, Albert C. Yeh, Salony, Xavier Sole, Revati Darp and Sridhar Ramaswamy
Mol Cancer Res February 1 2015 (13) (2) 223-230; DOI: 10.1158/1541-7786.MCR-14-0474

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A Mechanism for Asymmetric Cell Division Resulting in Proliferative Asynchronicity
Ipsita Dey-Guha, Cleidson P. Alves, Albert C. Yeh, Salony, Xavier Sole, Revati Darp and Sridhar Ramaswamy
Mol Cancer Res February 1 2015 (13) (2) 223-230; DOI: 10.1158/1541-7786.MCR-14-0474
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