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Growth controls connect: interactions between c-myc and the tuberous sclerosis complex-mTOR pathway

Emmett V Schmidt1, Michael J Ravitz, Li Chen

  • 1Cancer Research Center at Massachusetts General Hospital, and Harvard Medical School, Boston, MA 02114, USA. Schmidt@helix.mgh.harvard.edu

Cell Cycle (Georgetown, Tex.)
|April 4, 2009
PubMed

Insights

The target of rapamycin (TOR) pathway regulates cell growth via tuberous sclerosis complex (TSC) genes and c-myc. This review highlights Myc as a direct repressor of TSC2, forming a feed-forward loop that amplifies oncogenic effects.

Area of Science:

  • Molecular Biology
  • Cellular Biology
  • Oncology

Background:

  • Cell growth is tightly regulated by the target of rapamycin (TOR) pathway, involving tuberous sclerosis complex (TSC) genes and c-myc.
  • Myc and TSC1/2 exhibit opposing effects on cell growth and proliferation, yet their direct regulatory interactions are not fully understood.

Purpose of the Study:

  • To review evidence on the transcriptional regulation of TSC genes, specifically TSC2.
  • To elucidate the regulatory relationship between Myc and the TSC complex.

Main Methods:

  • Literature review focusing on transcriptional regulation.
  • Analysis of existing studies on Myc and TSC gene interactions.

Main Results:

  • Transcriptional controls are significant regulators of TSC2 expression.
  • Myc directly represses the expression of TSC2.
  • Loss of tuberin (TSC protein) leads to de-repression of Myc protein.

Conclusions:

  • A feed-forward loop exists between Myc and TSC, where Myc represses TSC2 and tuberin loss de-represses Myc.
  • This loop amplifies oncogenic signals from decreased tuberin or increased Myc.
  • Further research is needed to clarify mechanisms and the role in cancer development.

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