Metabolic Reprogramming in Anticancer Drug Resistance: A Focus on Amino Acids

Pranzini, Erica; Pardella, Elisa; Paoli, Paolo De; Fendt, Sarah-Maria; Taddei, Maria Letizia

doi:10.1016/j.trecan.2021.02.004

Cited by 68 publications

(48 citation statements)

References 158 publications

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“…The presently observed high GSH levels indicate that GSH is not depleted by cisPt in cells with chronic cisPt exposure. Moreover, GSH is still provided in excess in cells a long time after suspension of chronic exposure reflecting cellular adaptation and metabolic reprogramming for maintaining the intracellular redox-balance [26]. In agreement with the current findings, significantly elevated GSH levels were recently reported in cisPt resistant ovarian A2780 cancer cells compared to the non-resistant parental cell line.…”

Section: Glutathione (Gsh)supporting

confidence: 91%

1H HR-MAS NMR Based Metabolic Profiling of Lung Cancer Cells with Induced and De-Induced Cisplatin Resistance to Reveal Metabolic Resistance Adaptations

et al. 2021

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Cisplatin (cisPt) is an important drug that is used against various cancers, including advanced lung cancer. However, drug resistance is still a major ongoing problem and its investigation is of paramount interest. Here, a high-resolution magic angle spinning (HR-MAS) NMR study is presented deciphering the metabolic profile of non-small cell lung cancer (NSCLC) cells and metabolic adaptations at different levels of induced cisPt-resistance, as well as in their de-induced counterparts (cells cultivated in absence of cisPt). In total, fifty-three metabolites were identified and quantified in the 1H-HR-MAS NMR cell spectra. Metabolic adaptations to cisPt-resistance were detected, which correlated with the degree of resistance. Importantly, de-induced cell lines demonstrated similar metabolic adaptations as the corresponding cisPt-resistant cell lines. Metabolites predominantly changed in cisPt resistant cells and their de-induced counterparts include glutathione and taurine. Characteristic metabolic patterns for cisPt resistance may become relevant as biomarkers in cancer medicine.

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Section: Glutathione (Gsh)supporting

confidence: 91%

1H HR-MAS NMR Based Metabolic Profiling of Lung Cancer Cells with Induced and De-Induced Cisplatin Resistance to Reveal Metabolic Resistance Adaptations

et al. 2021

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“…In addition, intercellular or subcellular transportation of amino acids and altered metabolism induced by overexpression of amino acid transporters support cancer cell metabolism overcoming drug-induced stress [ 7 , 8 ]. Growing evidence indicates that suppressing or enhancing amino acid metabolism and depletion or supplementation of amino acid availability is effective in abolishing drug resistance in cancer cells [ 9 , 10 ].…”

Section: Introductionmentioning

confidence: 99%

Amino Acid Metabolism in Cancer Drug Resistance

Yoo

Han

2022

Cells

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Despite the numerous investigations on resistance mechanisms, drug resistance in cancer therapies still limits favorable outcomes in cancer patients. The complexities of the inherent characteristics of tumors, such as tumor heterogeneity and the complicated interaction within the tumor microenvironment, still hinder efforts to overcome drug resistance in cancer cells, requiring innovative approaches. In this review, we describe recent studies offering evidence for the essential roles of amino acid metabolism in driving drug resistance in cancer cells. Amino acids support cancer cells in counteracting therapies by maintaining redox homeostasis, sustaining biosynthetic processes, regulating epigenetic modification, and providing metabolic intermediates for energy generation. In addition, amino acid metabolism impacts anticancer immune responses, creating an immunosuppressive or immunoeffective microenvironment. A comprehensive understanding of amino acid metabolism as it relates to therapeutic resistance mechanisms will improve anticancer therapeutic strategies.

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“…Cancer cells reprogram their amino acid metabolisms to sustain tumor progression, then carry out specific strategies of resistance to anticancer therapies. 32 In this study, the potential metabolic pathways related to chemoresistant status showed typical metabolic pathways including biosynthesis of phenylalanine, tyrosine and tryptophan, phenylalanine metabolism as well as purine metabolism were participated in the process of K562 chemoresistance.…”

Section: Discussionmentioning

confidence: 77%

Characterization of Drug Resistance in Chronic Myeloid Leukemia Cells Based on Laser Tweezers Raman Spectroscopy

Zhang

Wang

et al. 2021

Appl Spectrosc

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Multidrug resistance (MDR) is highly associated with poor prognosis of chronic myeloid leukemia (CML). This work aims to explore whether the laser tweezers Raman spectroscopy (LTRS) could be practical in separating adriamycin (ADR) resistance CML cells K562/ADR from its parental cells K562, and to explore the potential mechanisms. Detection of LTRS initially reflected the spectral differences caused by chemoresistance including bands assigned to carbohydrates, amino acid, protein, lipids and nucleic acid. In addition, principal components analysis (PCA) as well as the classification and regression trees (CRT) algorithms showed that the specificity and sensitivity were above 90%. Moreover, the band data-based CRT model and receiver operating characteristic (ROC) curve further determined some important bands and band intensity ratios to be reliable indexes in discriminating K562 chemoresistance status. Finally, we highlighted three metabolism pathways correlated with chemoresistance. This work demonstrates that the label-free LTRS analysis combined with multivariate statistical analyses have great potential to be a novel analytical strategy at the single-cell level for rapid evaluation the chemoresistance status of K562 cells.

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Metabolic Reprogramming in Anticancer Drug Resistance: A Focus on Amino Acids

Cited by 68 publications

References 158 publications

1H HR-MAS NMR Based Metabolic Profiling of Lung Cancer Cells with Induced and De-Induced Cisplatin Resistance to Reveal Metabolic Resistance Adaptations

1H HR-MAS NMR Based Metabolic Profiling of Lung Cancer Cells with Induced and De-Induced Cisplatin Resistance to Reveal Metabolic Resistance Adaptations

Amino Acid Metabolism in Cancer Drug Resistance

Characterization of Drug Resistance in Chronic Myeloid Leukemia Cells Based on Laser Tweezers Raman Spectroscopy

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