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癌症中的代谢重编程：结直肠癌治疗中的小分子抑制剂。

Metabolic Rewiring in Cancer: Small Molecule Inhibitors in Colorectal Cancer Therapy.

机构信息

Department of Basic Biotechnological Sciences, Intensivological and Perioperative Clinics, Catholic University of the Sacred Heart, Largo Francesco Vito 1, 00168 Rome, Italy.

Laboratory Affiliated to Istituto Pasteur Italia-Fondazione Cenci Bolognetti, Department of Drug Chemistry and Technologies, Sapienza University of Rome, Piazzale Aldo Moro 5, 00185 Rome, Italy.

出版信息

Molecules. 2024 May 2;29(9):2110. doi: 10.3390/molecules29092110.

DOI:10.3390/molecules29092110
PMID:38731601
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11085455/
Abstract

Alterations in cellular metabolism, such as dysregulation in glycolysis, lipid metabolism, and glutaminolysis in response to hypoxic and low-nutrient conditions within the tumor microenvironment, are well-recognized hallmarks of cancer. Therefore, understanding the interplay between aerobic glycolysis, lipid metabolism, and glutaminolysis is crucial for developing effective metabolism-based therapies for cancer, particularly in the context of colorectal cancer (CRC). In this regard, the present review explores the complex field of metabolic reprogramming in tumorigenesis and progression, providing insights into the current landscape of small molecule inhibitors targeting tumorigenic metabolic pathways and their implications for CRC treatment.

摘要

细胞代谢的改变，如肿瘤微环境中缺氧和低营养条件下糖酵解、脂质代谢和谷氨酰胺分解的失调，是癌症的公认特征。因此，了解有氧糖酵解、脂质代谢和谷氨酰胺分解之间的相互作用对于开发基于代谢的癌症有效疗法至关重要，特别是在结直肠癌（CRC）的背景下。在这方面，本综述探讨了肿瘤发生和进展中代谢重编程的复杂领域，深入了解了针对致癌代谢途径的小分子抑制剂的现状及其对 CRC 治疗的意义。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdc/11085455/032777387b6d/molecules-29-02110-g014.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdc/11085455/28110d4fed23/molecules-29-02110-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdc/11085455/167abef46e03/molecules-29-02110-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdc/11085455/3e18b69a01e5/molecules-29-02110-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdc/11085455/1c4544cbe3e4/molecules-29-02110-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdc/11085455/14042d0a626c/molecules-29-02110-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdc/11085455/845eeb4662e7/molecules-29-02110-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdc/11085455/1071228a86da/molecules-29-02110-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdc/11085455/cfd3fc6d76f2/molecules-29-02110-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdc/11085455/867599cf25e1/molecules-29-02110-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdc/11085455/e9b009821634/molecules-29-02110-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdc/11085455/85094081b03d/molecules-29-02110-g011.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdc/11085455/d47d95708528/molecules-29-02110-g012.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdc/11085455/b6f4c9706b35/molecules-29-02110-g013.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdc/11085455/032777387b6d/molecules-29-02110-g014.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdc/11085455/28110d4fed23/molecules-29-02110-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdc/11085455/167abef46e03/molecules-29-02110-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdc/11085455/3e18b69a01e5/molecules-29-02110-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdc/11085455/1c4544cbe3e4/molecules-29-02110-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdc/11085455/14042d0a626c/molecules-29-02110-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdc/11085455/845eeb4662e7/molecules-29-02110-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdc/11085455/1071228a86da/molecules-29-02110-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdc/11085455/cfd3fc6d76f2/molecules-29-02110-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdc/11085455/867599cf25e1/molecules-29-02110-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdc/11085455/e9b009821634/molecules-29-02110-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdc/11085455/85094081b03d/molecules-29-02110-g011.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdc/11085455/d47d95708528/molecules-29-02110-g012.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdc/11085455/b6f4c9706b35/molecules-29-02110-g013.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdc/11085455/032777387b6d/molecules-29-02110-g014.jpg

相似文献

[1]
Metabolic Rewiring in Cancer: Small Molecule Inhibitors in Colorectal Cancer Therapy.

Molecules. 2024-5-2

[2]
New strategies for targeting glucose metabolism-mediated acidosis for colorectal cancer therapy.

J Cell Physiol. 2018-8-1

[3]
Altered metabolism in cancer: insights into energy pathways and therapeutic targets.

Mol Cancer. 2024-9-18

[4]
Involvement of tumor immune microenvironment metabolic reprogramming in colorectal cancer progression, immune escape, and response to immunotherapy.

Front Immunol. 2024

[5]
Targeting Strategies for Glucose Metabolic Pathways and T Cells in Colorectal Cancer.

Curr Cancer Drug Targets. 2019

[6]
The Circadian Clock Regulates Metabolic Phenotype Rewiring Via HKDC1 and Modulates Tumor Progression and Drug Response in Colorectal Cancer.

EBioMedicine. 2018-7-10

[7]
Metabolic Reprogramming of Colorectal Cancer Cells and the Microenvironment: Implication for Therapy.

Int J Mol Sci. 2021-6-10

[8]
The dichotomous role of the glycolytic metabolism pathway in cancer metastasis: Interplay with the complex tumor microenvironment and novel therapeutic strategies.

Semin Cancer Biol. 2019-8-21

[9]
Lipidome in colorectal cancer.

Oncotarget. 2016-5-31

[10]
Tumor suppressor NDRG2 inhibits glycolysis and glutaminolysis in colorectal cancer cells by repressing c-Myc expression.

Oncotarget. 2015-9-22

引用本文的文献

[1]
Migrasome-Related Prognostic Genes in Gastric Cancer: A Transcriptomic and Immunotherapeutic Analysis.

Onco Targets Ther. 2025-8-13

[2]
Clinical application prospects of traditional Chinese medicine as adjuvant therapy for metabolic reprogramming in colorectal cancer.

Front Immunol. 2025-7-15

[3]
Lipid metabolic reprogramming in colorectal cancer: mechanisms and therapeutic strategies.

Front Immunol. 2025-7-11

[4]
Alcoholic Extract Targets Warburg Effect, Apoptosis and Cell Cycle Progression in Colorectal Cancer Cell Lines.

Int J Mol Sci. 2025-2-28

[5]
Plant-derived terpenoids modulating cancer cell metabolism and cross-linked signaling pathways: an updated reviews.

Naunyn Schmiedebergs Arch Pharmacol. 2025-2-28

[6]
Identification of EARS2 as a Potential Biomarker with Diagnostic, Prognostic, and Therapeutic Implications in Colorectal Cancer.

Immunotargets Ther. 2025-1-30

本文引用的文献

[1]
Recent advance of ATP citrate lyase inhibitors for the treatment of cancer and related diseases.

Bioorg Chem. 2024-1

[2]
Signaling pathways in cancer metabolism: mechanisms and therapeutic targets.

Signal Transduct Target Ther. 2023-5-10

[3]
Emerging Direct Targeting β-Catenin Agents.

Molecules. 2022-11-10

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Induction of Ferroptosis in Glioblastoma and Ovarian Cancers by a New Pyrrole Tubulin Assembly Inhibitor.

J Med Chem. 2022-12-8

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Nat Rev Clin Oncol. 2022-12

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Discovery of novel human lactate dehydrogenase inhibitors: Structure-based virtual screening studies and biological assessment.

Eur J Med Chem. 2022-10-5

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The Glutaminase Inhibitor Compound 968 Exhibits Potent and Anti-tumor Effects in Endometrial Cancer.

Anticancer Agents Med Chem. 2023

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Reconsidering Otto Warburg's glycolytic shift: pyrimidine derivatives are effective for the treatment of tumors exerting aerobic glycolysis.

Panminerva Med. 2022-12

[9]
Galloflavin Relieves the Malignant Behavior of Colorectal Cancer Cells in the Inflammatory Tumor Microenvironment.

Front Pharmacol. 2021-12-10

[10]
Metabolic Reprogramming of Colorectal Cancer Cells and the Microenvironment: Implication for Therapy.

Int J Mol Sci. 2021-6-10

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