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癌症中的代谢异质性。

Metabolic heterogeneity in cancer.

机构信息

Laboratory of Cellular Metabolism and Metabolic Regulation, VIB-KU Leuven Center for Cancer Biology, Leuven, Belgium.

Laboratory of Cellular Metabolism and Metabolic Regulation, Department of Oncology, KU Leuven and Leuven Cancer Institute (LKI), Leuven, Belgium.

出版信息

Nat Metab. 2024 Jan;6(1):18-38. doi: 10.1038/s42255-023-00963-z. Epub 2024 Jan 24.

DOI:10.1038/s42255-023-00963-z
PMID:38267631
Abstract

Cancer cells rewire their metabolism to survive during cancer progression. In this context, tumour metabolic heterogeneity arises and develops in response to diverse environmental factors. This metabolic heterogeneity contributes to cancer aggressiveness and impacts therapeutic opportunities. In recent years, technical advances allowed direct characterisation of metabolic heterogeneity in tumours. In addition to the metabolic heterogeneity observed in primary tumours, metabolic heterogeneity temporally evolves along with tumour progression. In this Review, we summarize the mechanisms of environment-induced metabolic heterogeneity. In addition, we discuss how cancer metabolism and the key metabolites and enzymes temporally and functionally evolve during the metastatic cascade and treatment.

摘要

癌细胞在癌症进展过程中重新布线其代谢以存活。在这种情况下，肿瘤代谢异质性会因不同的环境因素而出现并发展。这种代谢异质性有助于癌症的侵袭性，并影响治疗机会。近年来，技术的进步使得能够直接描述肿瘤中的代谢异质性。除了在原发肿瘤中观察到的代谢异质性外，代谢异质性还会随着肿瘤的进展而随时间变化。在这篇综述中，我们总结了环境诱导的代谢异质性的机制。此外，我们还讨论了癌症代谢以及关键代谢物和酶在转移级联和治疗过程中如何随时间和功能演变。

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[3]
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[4]
Exploring Intratumoral Heterogeneity in Mixed Neuroendocrine-Nonneuroendocrine Neoplasms with Spatial Transcriptomics: Even More Diverse Than Anticipated.

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[5]
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[6]
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[7]
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[10]
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本文引用的文献

[1]
Spatial metabolomics principles and application to cancer research.

Curr Opin Chem Biol. 2023-10

[2]
Tumour extracellular vesicles and particles induce liver metabolic dysfunction.

Nature. 2023-6

[3]
Elevated serum β-hydroxybutyrate, a circulating ketone metabolite, accelerates colorectal cancer proliferation and metastasis via ACAT1.

Oncogene. 2023-6

[4]
Spatially resolved multi-omics highlights cell-specific metabolic remodeling and interactions in gastric cancer.

Nat Commun. 2023-5-10

[5]
Breast cancer cells that preferentially metastasize to lung or bone are more glycolytic, synthesize serine at greater rates, and consume less ATP and NADPH than parent MDA-MB-231 cells.

Cancer Metab. 2023-2-20

[6]
PHGDH-mediated endothelial metabolism drives glioblastoma resistance to chimeric antigen receptor T cell immunotherapy.

Cell Metab. 2023-3-7

[7]
ROS-lowering doses of vitamins C and A accelerate malignant melanoma metastasis.

Redox Biol. 2023-4

[8]
Slow TCA flux and ATP production in primary solid tumours but not metastases.

Nature. 2023-2

[9]
Immunoediting instructs tumor metabolic reprogramming to support immune evasion.

Cell Metab. 2023-1-3

[10]
CPT1A promotes anoikis resistance in esophageal squamous cell carcinoma via redox homeostasis.

Redox Biol. 2022-12

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