Cancer Cell Metabolic Reprogramming: Dietary, Pharmacological Strategies and Clinical Perspectives
7 affiliations
- 1Global Business School for Health, University College London, London WC1E 6BT, UK
- 2Third Department of Internal Medicine, Sotiria General Hospital for Chest Diseases, National and Kapodistrian University of Athens, 11527 Athens, Greece
- 3Department of Basic and Clinical Sciences, Medical School, University of Nicosia, UNIC Athens, 16777 Athens, Greece
- 4Department of Pathology and Surgery, Hygeia Hospital, 15123 Athens, Greece
- 5Division of Biotechnology, Biomedical Research Foundation of the Academy of Athens, 11527 Athens, Greece
- 6Department of Digital Systems, University of Piraeus, 18534 Piraeus, Greece
- 7First Department of Neurology, Aeginition Hospital, National and Kapodistrian University of Athens, 11528 Athens, Greece
Abstract
Metabolic reprogramming, a key feature of cancer progression that enables tumor adaptation to stress and therapy, represents an emerging target in anticancer research through dietary and pharmacological modulation. Dietary strategies such as caloric restriction (CR), intermittent fasting, and nutrient-specific modifications are emerging approaches to target oncogenic metabolism. Preclinical studies show that CR reduces tumor burden and inhibits IGF-1/mTOR signaling, while restoring immune pathways. Complementary preclinical evidence confirms that pharmacological inhibitors of the IGF-1R and mTOR pathways independently expose metabolic vulnerabilities, while concurrent autophagy blockade alongside mTOR inhibition can further reduce cancer cell viability by preventing stress adaptation. Multi-omics analyses facilitate the identification of how dietary restriction and pharmacological interventions remodel the tumor microenvironment by altering immune infiltration and stromal interactions, and uncover metabolic dependencies, that represent actionable therapeutic vulnerabilities. These findings suggest that dietary and pharmacological metabolic modulation represents an innovative approach in anticancer research. Preclinical models demonstrate the capability of these interventions to suppress tumor growth and enhance therapeutic responses, while early-phase clinical trials currently establish their safety and biological feasibility. In this review, we aim to summarize findings from in vitro models, in vivo animal studies, clinical observations, and multi-omics analyses to assess the potential of diet and pharmacological mimetics in influencing tumor metabolism and the tumor microenvironment.
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BibTeX
@article{xydas2026cancer,
title = {{Cancer Cell Metabolic Reprogramming: Dietary, Pharmacological Strategies and Clinical Perspectives}},
author = {Nikolaos Xydas and Emmanouil Panagiotou and Vasileios Kassos and Athina Maria Gkirmpa and Paraskevi Kassou and Ioannis Voyiatzis and Paoula Prenti and George Manias and Aigli Vakrakou and Athanasios K. Anagnostopoulos},
journal = {Cancers},
year = {2026},
month = oct,
doi = {10.3390/cancers18203372},
url = {https://www.mdpi.com/2072-6694/18/20/3372},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Cancer Cell Metabolic Reprogramming: Dietary, Pharmacological Strategies and Clinical Perspectives
AU - Nikolaos Xydas
AU - Emmanouil Panagiotou
AU - Vasileios Kassos
AU - Athina Maria Gkirmpa
AU - Paraskevi Kassou
AU - Ioannis Voyiatzis
AU - Paoula Prenti
AU - George Manias
AU - Aigli Vakrakou
AU - Athanasios K. Anagnostopoulos
PY - 2026
DA - 2026/10/01
JO - Cancers
DO - 10.3390/cancers18203372
UR - https://www.mdpi.com/2072-6694/18/20/3372
AB - Metabolic reprogramming, a key feature of cancer progression that enables tumor adaptation to stress and therapy, represents an emerging target in anticancer research through dietary and pharmacological modulation. Dietary strategies such as caloric restriction (CR), intermittent fasting, and nutrient-specific modifications are emerging approaches to target oncogenic metabolism. Preclinical studies show that CR reduces tumor burden and inhibits IGF-1/mTOR signaling, while restoring immune pathways. Complementary preclinical evidence confirms that pharmacological inhibitors of the IGF-1R and mTOR pathways independently expose metabolic vulnerabilities, while concurrent autophagy blockade alongside mTOR inhibition can further reduce cancer cell viability by preventing stress adaptation. Multi-omics analyses facilitate the identification of how dietary restriction and pharmacological interventions remodel the tumor microenvironment by altering immune infiltration and stromal interactions, and uncover metabolic dependencies, that represent actionable therapeutic vulnerabilities. These findings suggest that dietary and pharmacological metabolic modulation represents an innovative approach in anticancer research. Preclinical models demonstrate the capability of these interventions to suppress tumor growth and enhance therapeutic responses, while early-phase clinical trials currently establish their safety and biological feasibility. In this review, we aim to summarize findings from in vitro models, in vivo animal studies, clinical observations, and multi-omics analyses to assess the potential of diet and pharmacological mimetics in influencing tumor metabolism and the tumor microenvironment.
SN - 2072-6694
ER -