代谢重编程支持肿瘤形成，其特征是营养吸收、糖酵解和谷氨酰胺分解增加。 c-Myc 原癌基因是一种转录因子，在大多数癌症中表达上调，一些报告显示 c-Myc 在其他代谢途径（如葡萄糖、氨基酸和核苷酸代谢）中的作用。在这份简短的报告中，我们试图总结在不同癌症类型中进行的关于 c-Myc 以及脂质和丝氨酸代谢的研究的现有要点。在这里，我们报告 c-Myc 可以在肿瘤形成的背景下激活脂质和丝氨酸代谢，而阿司匹林和洛美他派等不同疗法则针对 c-Myc 和代谢之间的联系，以减缓肿瘤进展和侵袭。我们还报道了在不同癌症中影响 c-Myc 的多种上游调节因子，有趣的是，脂质代谢的成分（如脂质磷酸酶和瘦素）和丝氨酸代谢在某些情况下也可以作用于 c-Myc 的上游。最后，我们还总结了表观遗传途径和非编码RNA参与调节肿瘤细胞脂质和丝氨酸代谢以及c-Myc的现有知识。非编码因子和表观遗传机制的鉴定提供了一个有前途的研究途径，可以使研究人员能够针对 c-Myc 以及脂质和丝氨酸代谢途径进行新型抗癌治疗！版权所有 © 2024。由 Elsevier Inc. 出版。

Tumor formation is supported by metabolic reprogramming, characterized by increase nutrient uptake, glycolysis and glutaminolysis. The c-Myc proto-oncogene is a transcription factor, upregulated in most cancers and several reports showed the role of c-Myc in other metabolic pathways such as glucose, amino acid, and nucleotide metabolism. In this short report, we tried to summarize the existing takeaway points from studies conducted in different cancer types with respect to c-Myc and lipid and serine metabolism. Here, we report that c-Myc can activate both lipid and serine metabolism against the backdrop of tumor formation, and different therapies like aspirin and lomitapide target the links between c-Myc and metabolism to slow down tumor progression and invasion. We also report diverse upstream regulators that influence c-Myc in different cancers, and interestingly components of the lipid metabolism (like lipid phosphate phosphatase and leptin) and serine metabolism can also act upstream of c-Myc in certain occasions. Finally, we also summarize the existing knowledge on the involvement of epigenetic pathways and non-coding RNAs in regulating lipid and serine metabolism and c-Myc in tumor cells. Identification of non-coding factors and epigenetic mechanisms present a promising avenue of study that could empower researchers with novel anticancer treatment targeting c-Myc and lipid and serine metabolism pathways!Copyright © 2024. Published by Elsevier Inc.