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p53 and rapamycin are additive.

Barbara Christy1,2,3, Marco Demaria4, Judith Campisi4

  • 1Departments of Molecular Medicine and Institute of Biotechnology, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA.

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|July 10, 2015
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Summary
This summary is machine-generated.

The tumor suppressor p53 enhances rapamycin

Keywords:
SASPlongevitymTORp53rapamycin

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Area of Science:

  • Oncology
  • Molecular Biology
  • Gerontology

Background:

  • Mechanistic target of rapamycin (mTOR) is a kinase regulating cell growth and macromolecular synthesis, implicated in cancer.
  • mTOR complex 1 (mTORC1) is inhibited by the rapamycin-FK506 binding protein 12 (FKBP12) complex.
  • The tumor suppressor p53 inhibits mTORC1 via distinct stress-response pathways involving cell signaling and amino acid sensing.

Purpose of the Study:

  • To investigate the potential additive effects of p53 and rapamycin on mTORC1 inhibition.
  • To evaluate the combined impact of p53 and rapamycin on lifespan, radiation-induced senescence, and cellular metabolism.

Main Methods:

  • Utilized mouse models to assess lifespan extension.
  • Analyzed ionizing radiation (IR)-induced senescence-associated secretory phenotype (SASP) in cells.
  • Quantified amino acid and citric acid levels in mouse embryonic stem (ES) cells.

Main Results:

  • p53 significantly improved rapamycin's efficacy in extending mouse lifespan.
  • Combined p53 and rapamycin suppressed IR-induced SASP.
  • The combination therapy increased amino acid and citric acid levels in mouse ES cells.

Conclusions:

  • p53 and rapamycin exhibit additive anti-oncogenic effects through distinct mTORC1 inhibition pathways.
  • The synergistic action of p53 and rapamycin holds promise for cancer treatment strategies.
  • This study highlights the therapeutic potential of targeting both p53 and mTORC1 pathways.