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Targeted cancer therapy: what if the driver is just a messenger?

Jonathan H Schatz1, Hans-Guido Wendel

  • 1Cancer Biology and Genetics Program, Memorial Sloan-Kettering Cancer Center, New York, NY, USA. schatzj@mskcc.org

Cell Cycle (Georgetown, Tex.)
|November 9, 2011
PubMed

Insights

Targeted cancer therapies face resistance due to signaling network redundancy. Blocking cap-dependent translation offers a novel strategy by inhibiting multiple oncogenic pathways simultaneously, showing promise for effective cancer treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Therapeutics

Background:

  • Targeted cancer therapies aim to inhibit specific signaling pathways.
  • Resistance to targeted inhibitors is a significant challenge, often due to signaling network redundancy.
  • Overcoming resistance requires alternative therapeutic strategies beyond single-target inhibition.

Purpose of the Study:

  • To explore the blockade of cap-dependent translation as a therapeutic strategy against cancer.
  • To investigate the convergence of oncogenic signaling pathways on translation.
  • To assess the sensitivity of cancer cells to reduced expression of key oncoproteins.

Main Methods:

  • Analysis of converging oncogenic signaling pathways (AKT, MAPK, PIM kinase).
  • Investigation of cap-dependent translation activation in cancer cells.
  • Evaluation of the impact of translational inhibition on oncoprotein expression.

Main Results:

  • Multiple oncogenic pathways converge on the activation of cap-dependent translation.
  • Aberrant translation activation promotes expression of oncoproteins like c-MYC, MCL1, CYCLIN D1, and PIM kinases.
  • Cancer cells exhibit heightened sensitivity to reductions in these critical proteins.

Conclusions:

  • Direct blockade of cap-dependent translation is a viable strategy to target multiple oncogenic signals.
  • Translational inhibitor therapy presents a promising approach to overcome resistance in cancer treatment.
  • Targeting translation offers a novel way to exploit cancer cell vulnerabilities.

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