Metabolic Reprogramming Induced by Aging Modifies the Tumor Microenvironment

Bibliographic Details
Title: Metabolic Reprogramming Induced by Aging Modifies the Tumor Microenvironment
Authors: Xingyu Chen, Zihan Wang, Bo Zhu, Min Deng, Jiayue Qiu, Yunwen Feng, Ning Ding, Chen Huang
Source: Cells, Vol 13, Iss 20, p 1721 (2024)
Publisher Information: MDPI AG, 2024.
Publication Year: 2024
Collection: LCC:Cytology
Subject Terms: metabolic reprogramming, aging, metabolic plasticity, tumor immune microenvironment, pan-cancer, glioma, Cytology, QH573-671
More Details: Aging is an important risk factor for tumorigenesis. Metabolic reprogramming is a hallmark of both aging and tumor initiation. However, the manner in which the crosstalk between aging and metabolic reprogramming affects the tumor microenvironment (TME) to promote tumorigenesis was poorly explored. We utilized a computational approach proposed by our previous work, MMP3C (Modeling Metabolic Plasticity by Pathway Pairwise Comparison), to characterize aging-related metabolic plasticity events using pan-cancer bulk RNA-seq data. Our analysis revealed a high degree of metabolically organized heterogeneity across 17 aging-related cancer types. In particular, a higher degree of several energy generation pathways, i.e., glycolysis and impaired oxidative phosphorylation, was observed in older patients. Similar phenomena were also found via single-cell RNA-seq analysis. Furthermore, those energy generation pathways were found to be weakened in activated T cells and macrophages, whereas they increased in exhausted T cells, immunosuppressive macrophages, and Tregs in older patients. It was suggested that aging-induced metabolic switches alter glucose utilization, thereby influencing immune function and resulting in the remodeling of the TME. This work offers new insights into the associations between tumor metabolism and the TME mediated by aging, linking with novel strategies for cancer therapy.
Document Type: article
File Description: electronic resource
Language: English
ISSN: 2073-4409
Relation: https://www.mdpi.com/2073-4409/13/20/1721; https://doaj.org/toc/2073-4409
DOI: 10.3390/cells13201721
Access URL: https://doaj.org/article/a01a4e029e34475e82dddcc53efe9376
Accession Number: edsdoj.01a4e029e34475e82dddcc53efe9376
Database: Directory of Open Access Journals
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More Details
ISSN:20734409
DOI:10.3390/cells13201721
Published in:Cells
Language:English