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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
Summary
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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