Publisher Correction: Methionine is a metabolic dependency of tumor-initiating cells

Wang, Zhenxun; Yip, Lian Yee; Lee, Jia Hui Jane; Wu, Zhengwei; Chew, Hui Yi; Chong, Pooi Kiat William; Teo, Chin Chye; Ang, Heather Yin-Kuan; Peh, Kai Lay Esther; Yuan, Ju; Ma, Siming; Choo, Li Shi Kimberly; Basri, Nurhidayah; Jiang, Xia; Yu, Qiang; Hillmer, Axel M.; Lim, Wan Teck; Lim, Tony Kiat Hon; Takano, Angela; Tan, Eng Huat; Tan, Daniel S.W.; Ho, Ying Swan; Lim, Bing; Tam, Wai Leong

doi:10.1038/s41591-019-0486-3

Cited by 3 publications

(2 citation statements)

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“…Likewise, tumor-initiating cells (also called CSCs) derived from resected primary NSCLC adenocarcinoma samples and grown as non-adherent tumor spheres display increased methionine cycle metabolites, including SAM, and dependency on exogenous methionine. The small molecule MAT2A inhibitor FIDAS-5, which perturbs the methionine metabolic cycle, potently reduces intracellular levels of SAM and SAH and the tumorigenic potential of tumor-initiating cells by altering the methylation status of histones [ 48 ].…”

Section: Methioninementioning

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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Section: Methioninementioning

confidence: 99%

Amino Acid Metabolism in Cancer Drug Resistance

Yoo

Han

2022

Cells

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“…Similarly, tumor-initiating cells (TICs) derived from resected primary NSCLC display an elevated methionine cycle activity, thus becoming addicted to exogenous methionine. Therefore, methionine depletion impacts TICs tumorigenic capability by imposing epigenetic alterations [75]. In patient-derived lung adenocarcinoma cells and xenograft models, mitochondrial methylenetethrahydrofolate dehydrogenase 2 (MTHFD2) is essential to confer stem-like properties through the β-catenin pathway and ensure TKi-gefitinib resistance by modulating purine metabolism.…”

Section: Amino Acid Metabolic Regulation Of Cancer Stem Cells Supports Cancer Aggressivenessmentioning

confidence: 99%

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

et al. 2021

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Overcoming anticancer drug resistance is a major challenge in cancer therapy, requiring innovative strategies that consider the great tumor heterogeneity and adaptability. Here we provide recent evidence highlighting the key role of amino acid (AA) metabolic reprogramming in cancer cells and the supportive microenvironment in driving resistance to anticancer therapies. AAs sustain the acquisition of anticancer resistance by providing essential building blocks for biosynthetic pathways and for maintaining a balanced redox status, and modulating the epigenetic profile of both malignant and non-malignant cells. Besides, AAs also support the reduced intrinsic susceptibility of cancer stem cells to antineoplastic therapies. These findings shed new light on the possibility of targeting non-responding tumors by modulating AAs availability, through pharmacological approaches or dietary interventions.

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Dissecting the impact of metabolic environment on three common cancer cell phenotypes

Kochanowski

Sander

Link

et al. 2020

Preprint

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8The impact of different metabolic environments on cancer cell behavior is poorly understood. Here, we 9 systematically altered nutrient composition of cell culture media and examined the impact on three 10 phenotypes-drug-treatment survival, cell migration, and lactate overflow-that are frequently studied 11 in cancer cells. These perturbations across diverse metabolic environments revealed simple relationships 12 between cell growth rate and drug-treatment survival or migration. In contrast, lactate overflow was 13 highly sensitive to changes in sugar availability but largely insensitive to changes in amino acid availability, 14regardless of the growth rate. Further investigation suggested that the degree of lactate overflow across 15 metabolic environments is largely determined by the cells' ability to maintain high rates of sugar uptake. 16This study enabled us to elucidate quantitative relationships between metabolic environment and cancer 17 cell phenotypes, which echo empirical growth laws discovered to govern analogous phenotypes in 18 microbes. 19

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Publisher Correction: Methionine is a metabolic dependency of tumor-initiating cells

Abstract: In the version of this article originally published, the graph in Extended Data Fig. 2c was a duplication of Extended Data Fig. 2b. The correct version of Extended Data Fig. 2c is now available online.

Cited by 3 publications

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Amino Acid Metabolism in Cancer Drug Resistance

Amino Acid Metabolism in Cancer Drug Resistance

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

Dissecting the impact of metabolic environment on three common cancer cell phenotypes

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