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Trends Endocrinol Metab. 2018 Apr;29(4):271-280. doi: 10.1016/j.tem.2018.01.008. Epub 2018 Feb 17.

Starvation, Stress Resistance, and Cancer.

Author information

1
Longevity Institute, School of Gerontology, Department of Biological Sciences, University of Southern California, 3715 McClintock Avenue, Los Angeles, CA 90089-0191, USA; IFOM FIRC Institute of Molecular Oncology, Via Adamello 16, 20139 Milan, Italy.
2
Longevity Institute, School of Gerontology, Department of Biological Sciences, University of Southern California, 3715 McClintock Avenue, Los Angeles, CA 90089-0191, USA; IFOM FIRC Institute of Molecular Oncology, Via Adamello 16, 20139 Milan, Italy; Eli and Edythe Broad Center for Regenerative Medicine and Stem Cell Research at USC, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA. Electronic address: vlongo@usc.edu.

Abstract

Cancer cells are characterized by dysregulation in signal transduction and metabolic pathways leading to increased glucose uptake, altered mitochondrial function, and the evasion of antigrowth signals. Fasting and fasting-mimicking diets (FMDs) provide a particularly promising intervention to promote differential effects in normal and malignant cells. These effects are caused in part by the reduction in IGF-1, insulin, and glucose and the increase in IGFBP1 and ketone bodies, which generate conditions that force cancer cells to rely more on metabolites and factors that are limited in the blood, thus resulting in cell death. Here we discuss the cellular and animal experiments demonstrating the differential effects of fasting on normal and cancer cells and the mechanisms responsible for these effects.

KEYWORDS:

IGF-1; cancer; differential stress resistance; differential stress sensitization; fasting-mimicking diet; starvation

PMID:
29463451
DOI:
10.1016/j.tem.2018.01.008
[Indexed for MEDLINE]

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