flavin-adenine-dinucleotide and Carcinogenesis

Traditional antitumor drugs inhibit the proliferation and metastasis of tumour cells by restraining the replication and expression of DNA. These drugs are usually highly cytotoxic. They kill tumour cells while also cause damage to normal cells at the same time, especially the hematopoietic cells that divide vigorously. Patients are exposed to other serious situations such as a severe infection caused by a decrease in the number of white blood cells. Energy metabolism is an essential process for the survival of all cells, but differs greatly between normal cells and tumour cells in metabolic pathways and metabolic intermediates. Whether this difference could be used as new therapeutic target while reducing damage to normal tissues is the topic of this paper. In this paper, we introduce five major metabolic intermediates in detail, including acetyl-CoA, SAM, FAD, NAD

Topics: Acetyl Coenzyme A; Antineoplastic Agents; Carcinogenesis; Cell Proliferation; Disease Progression; Flavin-Adenine Dinucleotide; Humans; NAD; Neoplasm Invasiveness; Neoplasms; S-Adenosylmethionine; Tetrahydrofolates