Int J Biol Sci 2019; 15(6):1187-1199. doi:10.7150/ijbs.33496 This issue
1. Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Xiangya Hospital, Central South University, 87 Xiangya Road, Changsha, Hunan, 410008 China
2. Cancer Research Institute, Key Laboratory of Carcinogenesis, Ministry of Health, School of Basic Medicine, Central South University, 110 Xiangya Road, Changsha, Hunan, 410078 China
3. Department of Thoracic Surgery, Second Xiangya Hospital, Central South University, Changsha, China
4. Institute of Medical Sciences, Xiangya Hospital, Central South University, 87 Xiangya Road, Changsha, Hunan, 410008 China
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+ and THF. Their contents and functions in tumour cells and normal cells are significantly different. And the possible regulatory mechanisms that lead to these differences are proposed carefully. It is hoped that the key enzymes in these regulatory pathways could be used as new targets for tumour therapy.
Keywords: acetyl-CoA, SAM, FAD, NAD+, THF, cancer