Proliferating cells reduce their oxidative metabolism and rely more on glycolysis, even in the presence of O₂ (Warburg effect). This shift in metabolism reduces citrate biosynthesis and diminishes intracellular acidity, both of which promote glycolysis sustaining tumor growth. Because citrate is the donor of acetyl-CoA, its reduced production favors a deacetylation state of proteins favoring resistance to apoptosis and epigenetic changes, both processes contributing to tumor aggressiveness. Citrate levels could be monitored as an indicator of cancer aggressiveness (as already shown in human prostate cancer) and/or could serve as a biomarker for response to therapy. Strategies aiming to increase cytosolic citrate should be developed and tested in humans, knowing that experimental studies have shown that administration of citrate and/or inhibition of ACLY arrest tumor growth, inhibit the expression of the key anti-apoptotic factor Mcl-1, reverse cell dedifferentiation and increase sensibility to cisplatin.

增殖细胞会降低其氧化代谢，甚至在存在O ₂的情况下也更多地依赖于糖酵解（Warburg效应）。这种新陈代谢的转变减少了柠檬酸盐的生物合成并降低了细胞内的酸度，这两者都促进了糖酵解，维持了肿瘤的生长。因为柠檬酸盐是乙酰辅酶A的供体，其降低的产量有利于蛋白质的脱乙酰化状态，从而有利于抗凋亡和表观遗传变化，这两个过程均有助于肿瘤的侵袭性。柠檬酸盐水平可以被监测为癌症侵袭性的指标（如在人类前列腺癌中已经显示的）和/或可以用作对治疗反应的生物标志物。已知实验研究表明，柠檬酸盐的给药和/或抑制ACLY可阻止肿瘤生长，抑制关键的抗凋亡因子Mcl-1的表达，因此应在人体中制定和测试旨在提高胞浆柠檬酸水平的策略。