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The mitochondrial translation machinery as a therapeutic target in Myc-driven lymphomas

Aleco D'Andrea1, Ilaria Gritti1,2, Paola Nicoli1

  • 1Department of Experimental Oncology, European Institute of Oncology, Milan, Italy.

Oncotarget
|September 17, 2016
PubMed

Insights

Myc drives cancer by activating mitochondrial processes. Inhibiting mitochondrial translation with Tigecycline shows synthetic lethality with Myc, offering a new therapeutic strategy for Myc-driven tumors.

Area of Science:

  • Oncology
  • Molecular Biology
  • Metabolic Pathways

Background:

  • The transcription factor Myc is crucial for various cancer progressions.
  • Targeting Myc or its downstream pathways is a key strategy in cancer therapy.

Purpose of the Study:

  • To identify novel therapeutic targets in Myc-driven tumors.
  • To investigate the role of Myc-activated genes in tumor maintenance.

Main Methods:

  • An in vivo reverse-genetic screen of 241 Myc-activated mRNAs in mouse B-cell lymphomas.
  • Inhibition of mitochondrial translation using the antibiotic Tigecycline.
  • Assessment of tumor cell survival, respiratory activity, and lifespan in vivo.

Main Results:

  • A critical role for mitochondrial ribosomal protein (MRP) Ptcd3 in Myc-induced lymphoma maintenance was identified.
  • Coordinate activation of mitochondrial translation machinery was observed in Myc-driven lymphomas.
  • Tigecycline exhibited synthetic lethality with Myc activation, impaired tumor cell respiration and survival, and extended lifespan in mice.

Conclusions:

  • Myc-overexpressing tumors exhibit a metabolic dependency on mitochondrial translation.
  • Targeting mitochondrial translation with antibiotics like Tigecycline presents a promising therapeutic avenue for Myc-driven cancers.
Keywords:
MycTigecyclinelymphomamitochondriamitochondrial translation

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