De novo nucleotide biosynthetic pathway and cancer

Chen, Jie; Yang, Siqi; Li, Yingge; Xu, Ziwen; Zhang, Pingfeng; Song, Qibin; Yao, Yi; Pei, Huadong

doi:10.1016/j.gendis.2022.04.018

Cited by 12 publications

(12 citation statements)

References 68 publications

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“… 45 Cells in proliferation require nutrients (glucose, glutamine and CO2) to generate energy that drives the anabolism of nucleic acids. 46 The de novo biosynthetic pathway remains the main pathway through which the cellular synthesis of nucleotides and their metabolites is carried out, although nucleotides participate in the salvage pathway. 46 Changed nucleotide metabolism accelerates cancer development and inhibits the normal immune response in the tumour microenvironment.…”

Section: Resultsmentioning

confidence: 99%

“… 46 The de novo biosynthetic pathway remains the main pathway through which the cellular synthesis of nucleotides and their metabolites is carried out, although nucleotides participate in the salvage pathway. 46 Changed nucleotide metabolism accelerates cancer development and inhibits the normal immune response in the tumour microenvironment. 43 , 45 Few studies on altered nucleotide metabolism exist.…”

Section: Resultsmentioning

confidence: 99%

“… 42 – 44 Nucleotide metabolism enzyme blockers include purine, pyrimidine and general inhibitors like mizoribine, merimepodib and mycophenolate mofetil. 42 , 46 Pemetrexed inhibits folate-dependent enzymes such as TS and GART. 42 MLN4924m, a structural analogue of AMP, inhibits carcinogenesis by blocking the proteasomal degradation pathway.…”

Section: Resultsmentioning

confidence: 99%

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Uncovering novel therapeutic targets in glucose, nucleotides and lipids metabolism during cancer and neurological diseases

Jovičić

2024

Int J Immunopathol Pharmacol

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Background Cell metabolism functions without a stop in normal and pathological cells. Different metabolic changes occur in the disease. Cell metabolism influences biochemical and metabolic processes, signaling pathways, and gene regulation. Knowledge regarding disease metabolism is limited. Objective The review examines the cell metabolism of glucose, nucleotides, and lipids during homeostatic and pathological conditions of neurotoxicity, neuroimmunological disease, Parkinson’s disease, thymoma in myasthenia gravis, and colorectal cancer. Methods Data collection includes electronic databases, the National Center for Biotechnology Information, and Google Scholar, with several inclusion criteria: cell metabolism, glucose metabolism, nucleotide metabolism, and lipid metabolism in health and disease patients suffering from neurotoxicity, neuroinflammation, Parkinson’s disease, thymoma in myasthenia gravis. The initial number of collected and analyzed papers is 250. The final analysis included 150 studies out of 94 selected papers. After the selection process, 62.67% remains useful. Results and Conclusion A literature search shows that signaling molecules are involved in metabolic changes in cells. Differences between cancer and neuroimmunological diseases are present in the result section. Our finding enables insight into novel therapeutic targets and the development of scientific approaches for cancer and neurological disease onset, outcome, progression, and treatment, highlighting the importance of metabolic dysregulation. Current understanding, emerging research technologies and potential therapeutic interventions in metabolic programming is disucussed and highlighted.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

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Uncovering novel therapeutic targets in glucose, nucleotides and lipids metabolism during cancer and neurological diseases

Jovičić

2024

Int J Immunopathol Pharmacol

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“…As described in [ 157 ] PRPS activity in erythrocytes and fibroblasts differs significantly, a situation which has the potential to be exploited for cancer therapy [ 139 , 140 ]. The signalling functions attributed to nucleotides, impinge on the homeostasis of cancer cell proliferation [ 223 ].…”

Section: Discussionmentioning

confidence: 99%

Contribution of Model Organisms to Investigating the Far-Reaching Consequences of PRPP Metabolism on Human Health and Well-Being

Ugbogu

Schweizer

2022

Cells

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Phosphoribosyl pyrophosphate synthetase (PRS EC 2.7.6.1) is a rate-limiting enzyme that irreversibly catalyzes the formation of phosphoribosyl pyrophosphate (PRPP) from ribose-5-phosphate and adenosine triphosphate (ATP). This key metabolite is required for the synthesis of purine and pyrimidine nucleotides, the two aromatic amino acids histidine and tryptophan, the cofactors nicotinamide adenine dinucleotide (NAD+) and nicotinamide adenine dinucleotide phosphate (NADP+), all of which are essential for various life processes. Despite its ubiquity and essential nature across the plant and animal kingdoms, PRPP synthetase displays species-specific characteristics regarding the number of gene copies and architecture permitting interaction with other areas of cellular metabolism. The impact of mutated PRS genes in the model eukaryote Saccharomyces cerevisiae on cell signalling and metabolism may be relevant to the human neuropathies associated with PRPS mutations. Human PRPS1 and PRPS2 gene products are implicated in drug resistance associated with recurrent acute lymphoblastic leukaemia and progression of colorectal cancer and hepatocellular carcinoma. The investigation of PRPP metabolism in accepted model organisms, e.g., yeast and zebrafish, has the potential to reveal novel drug targets for treating at least some of the diseases, often characterized by overlapping symptoms, such as Arts syndrome and respiratory infections, and uncover the significance and relevance of human PRPS in disease diagnosis, management, and treatment.

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“…De novo nucleotides biosynthesis is crucial for tumor cell growth and metabolism, serving as a building block for DNA and RNA synthesis and as a source of ATP to fulfill the energy demands of rapidly proliferating tumor cells ( 31 ). The presence of FOXK2-binding motifs (GTAAACA) in the promoter region of various nucleotide biosynthesis genes suggests that FOXK2 plays a pivotal role in regulating nucleotide biosynthesis directly ( 24 ).…”

Section: Biological Functions Of Foxk2mentioning

confidence: 99%

Emerging roles of FOXK2 in cancers and metabolic disorders

Xing,

Que,

Zheng

et al. 2024

Front. Oncol.

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FOXK2, a member of the Forkhead box K (FOXK) transcription factor family, is widely expressed in various tissues and organs throughout the body. FOXK2 plays crucial roles in cell proliferation, differentiation, autophagy, de novo nucleotide biosynthesis, DNA damage response, and aerobic glycolysis. Although FOXK2 is recognized as an oncogene in colorectal cancer and hepatocellular carcinoma, it acts as a tumor suppressor in breast cancer, cervical cancer, and non-small cell lung cancer (NSCLC). This review provides an overview of the recent progress in understanding the regulatory mechanisms of FOXK2 and its downstream targets, highlights the significant impact of FOXK2 dysregulation on cancer etiology, and discusses the potential of targeting FOXK2 for cancer treatment.

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De novo nucleotide biosynthetic pathway and cancer

Cited by 12 publications

References 68 publications

Uncovering novel therapeutic targets in glucose, nucleotides and lipids metabolism during cancer and neurological diseases

Uncovering novel therapeutic targets in glucose, nucleotides and lipids metabolism during cancer and neurological diseases

Contribution of Model Organisms to Investigating the Far-Reaching Consequences of PRPP Metabolism on Human Health and Well-Being

Emerging roles of FOXK2 in cancers and metabolic disorders

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