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Sestrin1, a tumor suppressor that can be rescued
Maria C Donaldson1, Natalya Katanayeva1, Elisa Oricchio1
1Swiss Institute for Experimental Cancer Research (ISREC), School of Life Sciences, École Polytechnique Fédérale de Lausanne (EPFL), Lausanne, Switzerland.
Molecular & Cellular Oncology
|December 7, 2017
Summary
SESTRIN1 acts as a tumor suppressor in follicular lymphoma by regulating mTORC1. Inhibiting EZH2 reactivates SESTRIN1, restoring its tumor-suppressive function and offering a potential epigenetic therapy.
Area of Science:
- Oncology
- Molecular Biology
- Epigenetics
Background:
- SESTRIN1 functions as a tumor suppressor in follicular lymphoma.
- It regulates the activity of mTORC1, a key cellular pathway.
- Inactivation occurs via chromosomal deletions or epigenetic silencing by mutant EZH2 (Y641X).
Purpose of the Study:
- To investigate the role of SESTRIN1 in follicular lymphoma.
- To explore the potential of targeting EZH2 for SESTRIN1 re-expression.
- To assess the feasibility of epigenetically controlling mTORC1 activity.
Main Methods:
- Analysis of SESTRIN1 inactivation mechanisms in follicular lymphoma.
- Pharmacological inhibition of EZH2.
- Assessment of SESTRIN1 re-expression and tumor suppressive activity restoration.
Main Results:
- SESTRIN1 is inactivated by chromosomal deletions or EZH2 (Y641X) mutations.
- Pharmacological EZH2 inhibition leads to SESTRIN1 re-expression.
- Re-expressed SESTRIN1 restores its tumor suppressive activity.
Conclusions:
- SESTRIN1 is a crucial tumor suppressor in follicular lymphoma.
- Targeting EZH2 offers a strategy for epigenetic restoration of SESTRIN1.
- This approach may enable epigenetic control of mTORC1 activity in cancer therapy.
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