Metabolism of Amino Acids in Cancer

Wei, Zhen; Liu, Xiaoyi; Cheng, Chunming; Yu, Wei; Yi, Ping

doi:10.3389/fcell.2020.603837

Cited by 241 publications

(221 citation statements)

References 337 publications

(273 reference statements)

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“…While outside of the scope of this review, there are several fuel sources aside from NEAA not considered here that contribute to metabolic vulnerabilities, including glucose, essential amino acids, fatty acids, lactate, and acetate (8)(9)(10)(11). Furthermore, additional factors, including the expression of amino acid transporters (231)(232)(233)(234)(235)(236) and the effect of stromal cells on the microenvironment, can contribute to cancer metabolism and proliferation (8). It is also clear that optimal treatment strategies will consider mechanisms of cell adaptation to nutrient stress.…”

Section: Conclusion and Future Perspectivesmentioning

confidence: 99%

Amino Acid Metabolic Vulnerabilities in Acute and Chronic Myeloid Leukemias

et al. 2021

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Amino acid (AA) metabolism plays an important role in many cellular processes including energy production, immune function, and purine and pyrimidine synthesis. Cancer cells therefore require increased AA uptake and undergo metabolic reprogramming to satisfy the energy demand associated with their rapid proliferation. Like many other cancers, myeloid leukemias are vulnerable to specific therapeutic strategies targeting metabolic dependencies. Herein, our review provides a comprehensive overview and TCGA data analysis of biosynthetic enzymes required for non-essential AA synthesis and their dysregulation in myeloid leukemias. Furthermore, we discuss the role of the general control nonderepressible 2 (GCN2) and-mammalian target of rapamycin (mTOR) pathways of AA sensing on metabolic vulnerability and drug resistance.

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Section: Conclusion and Future Perspectivesmentioning

confidence: 99%

Amino Acid Metabolic Vulnerabilities in Acute and Chronic Myeloid Leukemias

et al. 2021

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“…Of those, amino acid metabolism was the greatest changed, with the largest number of metabolites identified and further validated by metabolic pathway analysis. The metabolic networks of all amino acids are complicated and highly interconnected with other pathways such as epigenetic modification as intracellular redox status (17,18). DNA methylation refers to the transfer of the methyl groups supplied by SAM to the 5-position carbon atom of cytosine to form 5-methylcytosine (12).…”

Section: Discussionmentioning

confidence: 99%

Intrauterine Hyperglycemia Alters the Metabolomic Profile in Fetal Mouse Pancreas in a Gender-Specific Manner

et al. 2021

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Mounting evidence has shown that intrauterine hyperglycemia exposure during critical stages of development may be contributing to the increasing prevalence of diabetes. However, little is known about the mechanisms responsible for offspring metabolic disorder. In this present study, we explored intrauterine hyperglycemia exposure on fetal pancreatic metabolome, and its potential link to impaired glucose tolerance in adult offspring. Here, using a GDM mouse model, we found the metabolome profiling of pancreas from male and female fetus showing altered metabolites in several important pathways, including 5-methylcytosine, α-KG, branched-chain amino acids, and cystine, which are associated with epigenetic modification, insulin secretion, and intracellular redox status, respectively. This finding suggests that intrauterine exposure to hyperglycemia could cause altered metabolome in pancreas, which might be a metabolism-mediated mechanism for GDM-induced intergenerational diabetes predisposition.

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“…Amino acids promote the survival and proliferation of cancer cells under genotoxicity, oxidative stress, and nutritional stress. Thus, targeting amino acid metabolism is a potential cancer treatment strategy ( Wei et al, 2020 ). Amino acid metabolites and metabolic enzymes also affect cisplatin resistance.…”

Section: Amino Acid Metabolism and Cisplatin Resistancementioning

confidence: 99%

The Role of Tumour Metabolism in Cisplatin Resistance

Wang

Zhao

et al. 2021

Front. Mol. Biosci.

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Cisplatin is a chemotherapy drug commonly used in cancer treatment. Tumour cells are more sensitive to cisplatin than normal cells. Cisplatin exerts an antitumour effect by interfering with DNA replication and transcription processes. However, the drug-resistance properties of tumour cells often cause loss of cisplatin efficacy and failure of chemotherapy, leading to tumour progression. Owing to the large amounts of energy and compounds required by tumour cells, metabolic reprogramming plays an important part in the occurrence and development of tumours. The interplay between DNA damage repair and metabolism also has an effect on cisplatin resistance; the molecular changes to glucose metabolism, amino acid metabolism, lipid metabolism, and other metabolic pathways affect the cisplatin resistance of tumour cells. Here, we review the mechanism of action of cisplatin, the mechanism of resistance to cisplatin, the role of metabolic remodelling in tumorigenesis and development, and the effects of common metabolic pathways on cisplatin resistance.

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Metabolism of Amino Acids in Cancer

Cited by 241 publications

References 337 publications

Amino Acid Metabolic Vulnerabilities in Acute and Chronic Myeloid Leukemias

Amino Acid Metabolic Vulnerabilities in Acute and Chronic Myeloid Leukemias

Intrauterine Hyperglycemia Alters the Metabolomic Profile in Fetal Mouse Pancreas in a Gender-Specific Manner

The Role of Tumour Metabolism in Cisplatin Resistance

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