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Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
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The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
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Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
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Spatio-Temporal Manipulation of Small GTPase Activity at Subcellular Level and on Timescale of Seconds in Living Cells
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Translational control of the antiapoptotic function of Ras.

V A Polunovsky1, A C Gingras, N Sonenberg

  • 1Department of Medicine, University of Minnesota Medical School, Minneapolis, Minnesota 55455, USA.

The Journal of Biological Chemistry
|May 16, 2000
PubMed
Summary

Oncogenic Ras promotes cell survival by activating cap-dependent translation, preventing apoptosis. Inhibiting this process sensitizes Ras-transformed cells to cell death, highlighting a new therapeutic target.

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Area of Science:

  • Molecular Biology
  • Cell Biology
  • Oncology

Background:

  • Activated Ras signaling pathways are known to inhibit apoptosis.
  • The role of translational control in Ras-mediated survival signaling was previously unexplored.

Purpose of the Study:

  • To investigate the relationship between cap-dependent translation and Ras-induced apoptosis.
  • To determine if translational control mechanisms are essential for Ras-mediated cell survival.

Main Methods:

  • Utilized rapamycin and cycloheximide to modulate protein synthesis in Ras-transformed fibroblasts.
  • Examined the effects of eukaryotic translation initiation factor (eIF) 4E-binding protein (4E-BP1) expression on apoptosis.
  • Assessed the impact of 4E-BP1 on Ras-transformed cells in vivo using immunodeficient mice.

Main Results:

  • Inhibition of cap-dependent translation with rapamycin increased apoptosis in Ras-transformed cells.
  • Suppression of global protein synthesis with cycloheximide prevented apoptosis.
  • Ectopic expression of 4E-BP1 sensitized cells to apoptosis and reduced tumor formation in vivo.

Conclusions:

  • eIF4E-dependent protein synthesis is critical for the survival of Ras-bearing fibroblasts.
  • Targeting cap-dependent translation represents a potential strategy to overcome Ras-driven oncogenesis.