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Glutaminolysis is the series of biochemical reactions by which glutamine is catabolized into downstream metabolites, e. Via the TCA cycle, alpha-KG undergoes catabolism to malate, which is transported into the cytoplasm and converted to pyruvate, and then ultimately to lactate [ 22 ].

SIRT4 is a mitochondrial-localized member of the sirtuin family of NAD-dependent enzymes that play fundamental roles in metabolism, stress response and longevity [ 58 ].

In regard to glutaminolysis, SIRT4 is a critical negative regulator for glutamine metabolism in mitochondria [ 58 ], which is down-regulated at the transcriptional level when the mTOR signaling pathway is activated [ 57 ]. As mentioned above, tumor tissue consists of a cellular population that is heterogeneous in terms of dependency on the Warburg effect and mitochondrial metabolism.

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Relative to slow-cycling CSCs, proliferative cancer cells tend to take up a great deal of glutamine, as well as glucose, for the generation of metabolites [ 54 ]. Both aerobic glycolysis and glutaminolysis are frequently simultaneously activated in malignant cancer cells [ 36 , 59 ]. Seemingly paradoxically, however, some cancer cell lines cannot survive and proliferate in the absence of glutamine, despite the fact that glutamine is a non-essential amino acids that can be synthesized from glucose [ 60 ].

Glutamine is a primary substrate for the TCA cycle and is required to maintain the redox state via the production of nicotinamide adenine dinucleotide phosphate NADPH. NADPH is a required electron donor for reductive steps in lipid synthesis, nucleotide metabolism, and maintenance of reduced GSH [ 21 ]. In this way, metabolic reprogramming of glutaminolysis enables cancer cells to regulate redox state. Oncogenic c-Myc mediates elevation of glutaminolysis in cancer cells. Drug repositioning DR , screening for anti-cancer therapeutic effects of conventionally administered medications for non-malignant disorders, has attracted a great deal of attention because the safety and frequency of side effects of these medicines have been already proven [ 64 ].

PPIs have exert synergistic effects on chemotherapy [ 66 ] by modulating the acidic microenvironment [ 67 ] or down-regulating microRNAs involved in chemotherapy resistance [ 68 ]. To address their anti-tumor therapeutic effects in clinical settings, all of those drugs are being tested in clinical trials or xenograft experiments. Here, we will describe in detail the potential effects of metformin as an anti-cancer drug. DR has revealed, for example, that metformin, an oral drug widely used to treat type 2 diabetes mellitus DM [ 76 ], prevents tumor growth and development.

Tumor angiogenesis: past, present and the near future | Carcinogenesis | Oxford Academic

A large number of retrospective clinical studies also show that metformin prevents carcinogenesis and improves clinical prognosis [ 77 — 79 ]. In particular, leucine uptake via LAT1 activates the mTOR signal pathway [ 81 , 82 ] leading to poor prognosis [ 83 , 84 ].

Therefore, the LKB1-AMPK-mTOR axis is orchestrated by amino-acid concentration in the tumor microenvironment, and this axis promotes metabolic reprogramming of cancer cells in response to the microenvironment. Consequently, metformin can inhibit the generation of the subpopulation of cancer cells that express high levels of ABCG2, an ATP-binding cassette ABC transporter responsible for active drug efflux.

In addition, metformin induces microRNAb-mediated suppression of ENPP1, which reduces chemoresistance and tumor seeding potential [ 86 ]. ENPP1 is widely accepted as a cause of insulin resistance in type 2 DM [ 88 ], emphasizing the significance of drug repositioning. Collectively, these observations indicate that this anti-DM agent is a promising means to attenuate the malignant behavior of cancer cells, much like other drugs conventionally administered for non-cancerous diseases. To facilitate development of novel therapeutic strategies, the synergistic effects of repositioned drugs with conventional anti-cancer agents should be evaluated in clinical trials in the near future.

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‘Cancer cure’ doubted as Israeli team claims it can’t afford to publish findings

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J Clin Oncol. GLUT1 gene is a potential hypoxic marker in colorectal cancer patients. Genotyping analysis and 1 8 FDG uptake in breast cancer patients: a preliminary research.

GLUT-1 expression is largely unrelated to both hypoxia and the Warburg phenotype in squamous cell carcinomas of the vulva. Glycolysis inhibition for anticancer treatment. The tumor suppressor folliculin regulates AMPK-dependent metabolic transformation. AMPK is a negative regulator of the Warburg effect and suppresses tumor growth in vivo. Cell Metab.

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