Inflammaging and Cancer: A Challenge for the Mediterranean Diet

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Abstract

Aging is considered the major risk factor for cancer, one of the most important mortality causes in the western world. Inflammaging, a state of chronic, low-level systemic inflammation, is a pervasive feature of human aging. Chronic inflammation increases cancer risk and affects all cancer stages, triggering the initial genetic mutation or epigenetic mechanism, promoting cancer initiation, progression and metastatic diffusion. Thus, inflammaging is a strong candidate to connect age and cancer. A corollary of this hypothesis is that interventions aiming to decrease inflammaging should protect against cancer, as well as most/all age-related diseases. Epidemiological data are concordant in suggesting that the Mediterranean Diet (MD) decreases the risk of a variety of cancers but the underpinning mechanism(s) is (are) still unclear. Here we review data indicating that the MD (as a whole diet or single bioactive nutrients typical of the MD) modulates multiple interconnected processes involved in carcinogenesis and inflammatory response such as free radical production, NF-κB activation and expression of inflammatory mediators, and the eicosanoids pathway. Particular attention is devoted to the capability of MD to affect the balance between pro- and anti-inflammaging as well as to emerging topics such as maintenance of gut microbiota (GM) homeostasis and epigenetic modulation of oncogenesis through specific microRNAs.

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Inflamm-aging. An evolutionary perspective on immunosenescence.

C Franceschi, M BonaFe, S Valensin … (2000)

In this paper we extend the "network theory of aging," and we argue that a global reduction in the capacity to cope with a variety of stressors and a concomitant progressive increase in proinflammatory status are major characteristics of the aging process. This phenomenon, which we will refer to as "inflamm-aging," is provoked by a continuous antigenic load and stress. On the basis of evolutionary studies, we also argue that the immune and the stress responses are equivalent and that antigens are nothing other than particular types of stressors. We also propose to return macrophage to its rightful place as central actor not only in the inflammatory response and immunity, but also in the stress response. The rate of reaching the threshold of proinflammatory status over which diseases/disabilities ensue and the individual capacity to cope with and adapt to stressors are assumed to be complex traits with a genetic component. Finally, we argue that the persistence of inflammatory stimuli over time represents the biologic background (first hit) favoring the susceptibility to age-related diseases/disabilities. A second hit (absence of robust gene variants and/or presence of frail gene variants) is likely necessary to develop overt organ-specific age-related diseases having an inflammatory pathogenesis, such as atherosclerosis, Alzheimer's disease, osteoporosis, and diabetes. Following this perspective, several paradoxes of healthy centenarians (increase of plasma levels of inflammatory cytokines, acute phase proteins, and coagulation factors) are illustrated and explained. In conclusion, the beneficial effects of inflammation devoted to the neutralization of dangerous/harmful agents early in life and in adulthood become detrimental late in life in a period largely not foreseen by evolution, according to the antagonistic pleiotropy theory of aging.

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Metabolomic profiles delineate potential role for sarcosine in prostate cancer progression.

Arun Sreekumar, Laila Poisson, Thekkelnaycke M Rajendiran … (2009)

Multiple, complex molecular events characterize cancer development and progression. Deciphering the molecular networks that distinguish organ-confined disease from metastatic disease may lead to the identification of critical biomarkers for cancer invasion and disease aggressiveness. Although gene and protein expression have been extensively profiled in human tumours, little is known about the global metabolomic alterations that characterize neoplastic progression. Using a combination of high-throughput liquid-and-gas-chromatography-based mass spectrometry, we profiled more than 1,126 metabolites across 262 clinical samples related to prostate cancer (42 tissues and 110 each of urine and plasma). These unbiased metabolomic profiles were able to distinguish benign prostate, clinically localized prostate cancer and metastatic disease. Sarcosine, an N-methyl derivative of the amino acid glycine, was identified as a differential metabolite that was highly increased during prostate cancer progression to metastasis and can be detected non-invasively in urine. Sarcosine levels were also increased in invasive prostate cancer cell lines relative to benign prostate epithelial cells. Knockdown of glycine-N-methyl transferase, the enzyme that generates sarcosine from glycine, attenuated prostate cancer invasion. Addition of exogenous sarcosine or knockdown of the enzyme that leads to sarcosine degradation, sarcosine dehydrogenase, induced an invasive phenotype in benign prostate epithelial cells. Androgen receptor and the ERG gene fusion product coordinately regulate components of the sarcosine pathway. Here, by profiling the metabolomic alterations of prostate cancer progression, we reveal sarcosine as a potentially important metabolic intermediary of cancer cell invasion and aggressivity.

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The complexity of NF-κB signaling in inflammation and cancer

Bastian Hoesel, Johannes A. Schmid (2013)

The NF-κB family of transcription factors has an essential role in inflammation and innate immunity. Furthermore, NF-κB is increasingly recognized as a crucial player in many steps of cancer initiation and progression. During these latter processes NF-κB cooperates with multiple other signaling molecules and pathways. Prominent nodes of crosstalk are mediated by other transcription factors such as STAT3 and p53 or the ETS related gene ERG. These transcription factors either directly interact with NF-κB subunits or affect NF-κB target genes. Crosstalk can also occur through different kinases, such as GSK3-β, p38, or PI3K, which modulate NF-κB transcriptional activity or affect upstream signaling pathways. Other classes of molecules that act as nodes of crosstalk are reactive oxygen species and miRNAs. In this review, we provide an overview of the most relevant modes of crosstalk and cooperativity between NF-κB and other signaling molecules during inflammation and cancer.

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Journal

Journal ID (nlm-ta): Nutrients

Journal ID (iso-abbrev): Nutrients

Journal ID (publisher-id): nutrients

Title: Nutrients

Publisher: MDPI

ISSN (Electronic): 2072-6643

Publication date (Electronic): 09 April 2015

Publication date Collection: April 2015

Volume: 7

Issue: 4

Pages: 2589-2621

Affiliations

[1 ]Department of Experimental, Diagnostic and Specialty Medicine (DIMES), University of Bologna, Via San Giacomo 12, 40126 Bologna, Italy; E-Mails: rita.ostan3@ 123456unibo.it (R.O.); catia.lanzarini2@ 123456unibo.it (C.L.); elisa.pini5@ 123456unibo.it (E.P.); maria.scurti@ 123456unibo.it (M.S.); dario.vianello@ 123456unibo.it (D.V.); claudia.bertarelli@ 123456unibo.it (C.B.); cristina.fabbri12@ 123456unibo.it (C.F.); morena.martucci3@ 123456unibo.it (M.M.); elena.bellavista2@ 123456unibo.it (E.B.); stefano.salvioli@ 123456unibo.it (S.S.); miriam.capri@ 123456unibo.it (M.C.); claudio.franceschi@ 123456unibo.it (C.F.)

[2 ]Interdepartmental Centre “L. Galvani” (CIG) University of Bologna, Via San Giacomo 12, 40126 Bologna, Italy; E-Mails: massimo.izzi@ 123456unibo.it (M.I.); mariagiustina.palmas@ 123456unibo.it (G.P.); fiammetta.biondi2@ 123456unibo.it (F.B.)

[3 ]IRCCS, Institute of Neurological Sciences, Via Altura 3, 40139 Bologna, Italy

[4 ]National Research Council of Italy, CNR, Institute for Organic Synthesis and Photoreactivity (ISOF), Via P. Gobetti 101, 40129 Bologna, Italy

Author notes

[* ]Author to whom correspondence should be addressed; E-Mail: aurelia.santoro@ 123456unibo.it ; Tel.: +39-051-2094-758; Fax: +39-051-2094-747.

Article

Publisher ID: nutrients-07-02589

DOI: 10.3390/nu7042589

PMC ID: 4425163

PubMed ID: 25859884

SO-VID: 3102b8a5-dbe0-40a5-b09c-a437ca280026

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This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license ( http://creativecommons.org/licenses/by/4.0/).

Inflammaging and Cancer: A Challenge for the Mediterranean Diet

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Karger: Nutrition and Dietetics

Most cited references 148

Inflamm-aging. An evolutionary perspective on immunosenescence.

Metabolomic profiles delineate potential role for sarcosine in prostate cancer progression.

The complexity of NF-κB signaling in inflammation and cancer

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