Punnasseril Jilsy M J, Auwal Abdul, Gopalan Vinod, Lam Alfred King-Yin, Islam Farhadul
School of Medicine & Dentistry, Griffith University, Gold Coast Campus, Southport, Queensland, Australia.
Department of Biochemistry & Molecular Biology, Rajshahi University, Rajshahi, Bangladesh.
Cancer Med. 2025 Sep;14(18):e71244. doi: 10.1002/cam4.71244.
Cancer metabolism is a field focused on the unique alterations in metabolic pathways that occur in cancer cells, distinguishing them from the metabolic processes in normal cells.
An extensive review of the current literature on the metabolic adaptation of cancer cells was carried out in the current study.
The rapidly proliferating cells require high levels of molecules, such as glucose, amino acids, lipids, and nucleotides, along with increased energy demand (ATP). These requirements are met through alterations in the processes involving glucose, amino acid, lipid, and nucleotide metabolism. Modifications in glucose metabolism in cancer cells involve changes in glucose uptake, glycolysis, the pentose phosphate pathway, and the tricarboxylic acid cycle. Similarly, alterations in amino acid metabolism in cancer cells relate to upregulated amino acid transport and glutaminolysis. Cancer cells also have increased lipid intake from the extracellular microenvironment, upregulated lipogenesis, and enhanced lipid storage and mobilization from intracellular lipid droplets. These rapidly proliferating cells also achieve their increased demand for nucleotides by changing the expression of enzymes in the salvage and de novo nucleotide pathways. Consequently, these metabolic processes are targets for developing cancer therapeutics. However, it is important to note that the metabolic changes in cancer cells can also contribute to resistance against various cancer therapies.
This review will explore the various ways in which cancer cells reprogram metabolic processes to sustain rapid proliferation and survival. The information presented in this report could help in the therapeutics designed to target them, and the challenges of cancer drug resistance arising from these metabolic adaptations.
癌症代谢是一个专注于癌细胞中发生的代谢途径独特改变的领域，这些改变将癌细胞与正常细胞的代谢过程区分开来。
本研究对当前关于癌细胞代谢适应的文献进行了广泛综述。
快速增殖的细胞需要高水平的分子，如葡萄糖、氨基酸、脂质和核苷酸，同时能量需求（ATP）增加。这些需求通过涉及葡萄糖、氨基酸、脂质和核苷酸代谢过程的改变来满足。癌细胞中葡萄糖代谢的改变涉及葡萄糖摄取、糖酵解、磷酸戊糖途径和三羧酸循环的变化。同样，癌细胞中氨基酸代谢的改变与氨基酸转运上调和谷氨酰胺分解有关。癌细胞还从细胞外微环境中增加脂质摄取，上调脂肪生成，并增强细胞内脂质滴的脂质储存和动员。这些快速增殖的细胞还通过改变补救和从头合成核苷酸途径中酶的表达来满足其对核苷酸增加的需求。因此，这些代谢过程是开发癌症治疗方法的靶点。然而，需要注意的是，癌细胞中的代谢变化也可能导致对各种癌症治疗的耐药性。
本综述将探讨癌细胞重新编程代谢过程以维持快速增殖和存活的各种方式。本报告中提供的信息有助于设计针对它们的治疗方法，以及应对这些代谢适应引起的癌症耐药性挑战。
