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Review
. 2024 Oct 17:15:1450441.
doi: 10.3389/fphar.2024.1450441. eCollection 2024.

Cancer metabolic reprogramming and precision medicine-current perspective

Affiliations
Review

Cancer metabolic reprogramming and precision medicine-current perspective

Tingting Gao et al. Front Pharmacol. .

Abstract

Despite the advanced technologies and global attention on cancer treatment strategies, cancer continues to claim lives and adversely affects socio-economic development. Although combination therapies were anticipated to eradicate this disease, the resilient and restorative nature of cancers allows them to proliferate at the expense of host immune cells energetically. This proliferation is driven by metabolic profiles specific to the cancer type and the patient. An emerging field is exploring the metabolic reprogramming (MR) of cancers to predict effective treatments. This mini-review discusses the recent advancements in cancer MR that have contributed to predictive, preventive, and precision medicine. Current perspectives on the mechanisms of various cancer types and prospects for MR and personalized cancer medicine are essential for optimizing metabolic outputs necessary for personalized treatments.

Keywords: immune cell; mechanism; metabolic reprogramming; precision medicine; treatment strategies.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

FIGURE 1
FIGURE 1
The main metabolic pathways and changes in cancer Abbreviation used: PM: plasma membrane; ROS: reactive oxygen species; TCA: tricarboxylic acid; OXPHOS: oxidative phosphorylation; ATP: adenosine triphosphate; MCT1: monocarboxylate transporter-1; TGF-β:Transforming growth factor-β; MCT4: monocarboxylate transporters 4; HIF-1α: hypoxia-inducible factor-1 α; NF-κB: nuclear factor κB; Cav1: Caveolin-1; PPP: pentose phosphate pathway; SHMT: serine hydroxy methyltransferase; THF: tetrahydrofolate; SAM: S-adenosylmethionine; α-KG: α-ketoglutarate; NADH: nicotinamide adenine dinucleotide; FA: fatty acid. FAD: flavin adenine dinucleotide; FADH2: reduced flavin adenine dinucleotide; I: NADH-coenzyme Q reductase; II: succinate coenzyme Q reductase; III: coenzyme Q cytochrome c reductase; IV: cytochrome c oxidase; V: ATP synthase.
FIGURE 2
FIGURE 2
Various genes across multiple cancer types are involved in metabolic reprogramming as potential targets for precision medicine.

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