Cancer cells constantly face a fluctuating nutrient supply and interference with adaptive responses might be an effective therapeutic approach. It has been discovered that in the absence of glucose, cancer cells can synthesize crucial metabolites by expressing phosphoenolpyruvate carboxykinase (PEPCK, PCK1 or PCK2) using abbreviated forms of gluconeogenesis. Gluconeogenesis, which in essence is the reverse pathway of glycolysis, uses lactate or amino acids to feed biosynthetic pathways branching from glycolysis. PCK1 and PCK2 have been shown to be critical for the growth of certain cancers. In contrast, fructose-1,6-bisphosphatase 1 (FBP1), a downstream gluconeogenesis enzyme, inhibits glycolysis and tumor growth, partly by non-enzymatic mechanisms. This review sheds light on the current knowledge of cancer cell gluconeogenesis and its role in metabolic reprogramming, cancer cell plasticity, and tumor growth.

癌细胞不断面临营养供应的波动，干扰适应性反应可能是一种有效的治疗方法。已经发现，在不存在葡萄糖的情况下，癌细胞可以通过使用糖异生的缩写形式表达磷酸烯醇丙酮酸羧激酶（PEPCK，PCK1或PCK2）来合成关键的代谢产物。糖原异生本质上是糖酵解的反向途径，它利用乳酸或氨基酸来补充从糖酵解分支出来的生物合成途径。PCK1和PCK2已被证明对于某些癌症的生长至关重要。相反，果糖-1,6-双磷酸酶1（FBP1）是一种下游糖异生酶，部分通过非酶促机制抑制糖酵解和肿瘤生长。