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Research Paper|Volume 7, Issue 4|pp 233—240

Caloric restriction induces heat shock response and inhibits B16F10 cell tumorigenesis both in vitro and in vivo

Marta G. Novelle1,3, Ashley Davis1, Nathan L. Price1, Ahmed Ali1, Stefanie Fürer-Galvan1, Yongqing Zhang2, Kevin Becker2, Michel Bernier1, Rafael de Cabo1
  • 1Translational Gerontology Branch, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA
  • 2Gene Expression and Genomics Unit, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA
  • 3Department of Physiology, CIMUS, University of Santiago de Compostela-Instituto de Investigación Sanitaria, 15782 Santiago de Compostela, Spain; CIBER Fisiopatología de la Obesidad y Nutrición (CIBERobn), 15706 Santiago de Compostela, Spain
Received: December 1, 2014Accepted: March 24, 2015Published: April 5, 2015
https://doi.org/10.18632/aging.100732

Copyright: © 2015 Novelle et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Caloric restriction (CR) without malnutrition is one of the most consistent strategies for increasing mean and maximal lifespan and delaying the onset of age-associated diseases. Stress resistance is a common trait of many long-lived mutants and life-extending interventions, including CR. Indeed, better protection against heat shock and other genotoxic insults have helped explain the pro-survival properties of CR. In this study, both in vitro and in vivo responses to heat shock were investigated using two different models of CR. Murine B16F10 melanoma cells treated with serum from CR-fed rats showed lower proliferation, increased tolerance to heat shock and enhanced HSP-70 expression, compared to serum from ad libitum-fed animals. Similar effects were observed in B16F10 cells implanted subcutaneously in male C57BL/6 mice subjected to CR. Microarray analysis identified a number of genes and pathways whose expression profile were similar in both models. These results suggest that the use of an in vitro model could be a good alternative to study the mechanisms by which CR exerts its anti-tumorigenic effects.