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Molecular Pathways: Targeting MYC-induced metabolic reprogramming and oncogenic stress in cancer

Bo Li1, M Celeste Simon

  • 1Authors' Affiliations: Abramson Family Cancer Research Institute, Perelman School of Medicine at the University of Pennsylvania; and Howard Hughes Medical Institute, Philadelphia, Pennsylvania.

Clinical Cancer Research : an Official Journal of the American Association for Cancer Research
|July 31, 2013
PubMed

Insights

MYC transcription factor deregulation drives cancer by altering cell metabolism and stress. Targeting these MYC-driven metabolic and stress pathways offers promising therapeutic strategies for MYC-amplified tumors.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Metabolism

Background:

  • MYC is a key transcription factor frequently deregulated in human cancers.
  • MYC controls cell proliferation, metabolism, and stress responses, crucial for tumor progression.
  • Directly targeting MYC is challenging, necessitating focus on its downstream effects.

Purpose of the Study:

  • To explore targeting MYC-reprogrammed cancer cell metabolism as a therapeutic strategy.
  • To investigate the potential of targeting oncogenic stress in MYC-driven tumors.
  • To evaluate combined targeting of MYC-mediated pathways for cancer treatment.

Main Methods:

  • Analysis of MYC's role in cancer cell metabolism reprogramming.
  • Preclinical studies on targeting MYC-induced metabolic alterations.
  • Investigation of oncogenic stress pathways in MYC-amplified tumors.

Main Results:

  • MYC reprograms cancer metabolism, distinct from normal cells, with increased glucose/glutamine uptake and altered amino acid metabolism.
  • Targeting MYC-reprogrammed metabolism shows promise in preclinical models.
  • MYC-driven tumors exhibit increased biosynthetic demand and oncogenic stress, presenting therapeutic vulnerabilities.

Conclusions:

  • Targeting MYC-reprogrammed metabolism is a viable therapeutic approach for MYC-amplified cancers.
  • Exploiting oncogenic stress in these tumors offers additional therapeutic opportunities.
  • Combined targeting of MYC-mediated proliferation, metabolism, and stress pathways is the optimal strategy for treating MYC-amplified tumors.

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