果糖代谢已成为癌细胞增殖的重要因素，但癌细胞果糖的潜在机制和来源仍不完全清楚。在这项研究中，我们证明癌细胞可以通过 AKR1B1 介导的多元醇途径将葡萄糖转化为果糖。通过 AKR1B1 缺失抑制内源果糖的产生，可显着抑制糖酵解，从而减少癌细胞迁移、抑制生长，并诱导细胞凋亡和细胞周期停滞。相反，通过 AKR1B1 过度表达加速内源性果糖已被证明可显着增强癌细胞增殖和迁移，并增加 S 细胞周期进程。我们的研究结果强调了内源性果糖在癌细胞恶性肿瘤中的关键作用，并支持进一步研究 AKR1B1 作为潜在癌症治疗靶点的必要性。© 2024。作者。

Fructose metabolism has emerged as a significant contributor to cancer cell proliferation, yet the underlying mechanisms and sources of fructose for cancer cells remain incompletely understood. In this study, we demonstrate that cancer cells can convert glucose into fructose through a process called the AKR1B1-mediated polyol pathway. Inhibiting the endogenous production of fructose through AKR1B1 deletion dramatically suppressed glycolysis, resulting in reduced cancer cell migration, inhibited growth, and the induction of apoptosis and cell cycle arrest. Conversely, the acceleration of endogenous fructose through AKR1B1 overexpression has been shown to significantly enhance cancer cell proliferation and migration with increased S cell cycle progression. Our findings highlight the crucial role of endogenous fructose in cancer cell malignancy and support the need for further investigation into AKR1B1 as a potential cancer therapeutic target.© 2024. The Author(s).