The role of aldo‐keto reductase family 1 member B1 (AKR1B1) in cancer is not totally clear but growing evidence is suggesting to have a great impact on cancer progression. AKR1B1 could participate in a complicated network of signalling pathways, proteins and miRNAs such as mir‐21 mediating mechanisms like inflammatory responses, cell cycle, epithelial to mesenchymal transition, cell survival and apoptosis. AKR1B1 has been shown to be mostly overexpressed in cancer. This overexpression has been associated with inflammatory mediators including nuclear factor kappa‐light‐chain‐enhancer of activated B cells (NFκB), cell cycle mediators such as cyclins and cyclin‐dependent kinases (CDKs), survival proteins and pathways like mammalian target of rapamycin (mTOR) and protein kinase B (PKB) or AKT, and other regulatory factors in response to reactive oxygen species (ROS) and prostaglandin synthesis. In addition, inhibition of AKR1B1 has been shown to mostly have anti‐cancer effects. Several studies have also suggested that AKR1B1 inhibition as an adjuvant therapy could render tumour cells more sensitive to anti‐cancer therapy or alleviate the adverse effects of therapy. AKR1B1 could also be considered as a potential cancer diagnostic biomarker since its promoter has shown high levels of methylation. Although pre‐clinical investigations on the role of AKR1B1 in cancer and the application of its inhibitors have shown promising results, the lack of clinical studies on AKR1B1 inhibitors has hampered the use of these drugs to treat cancer. Thus, there is a need to conduct more clinical studies on the application of AKR1B1 inhibitors as adjuvant therapy on different cancers.

中文翻译：

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醛糖酮还原酶家族1成员B1（AKR1B1）在癌症过程中的作用及其治疗潜力。

醛基酮还原酶家族1成员B1（AKR1B1）在癌症中的作用尚不完全清楚，但越来越多的证据表明对癌症的进展有很大影响。AKR1B1可能参与信号通路，蛋白质和miRNA的复杂网络，例如mir-21介导的机制，例如炎症反应，细胞周期，上皮向间质转化，细胞存活和凋亡。AKR1B1已被证明在癌症中大多数过表达。这种过表达与炎症介质有关，包括活化的B细胞的核因子κ轻链增强子（NFκB），细胞周期介质，如细胞周期蛋白和细胞周期蛋白依赖性激酶（CDK），存活蛋白以及诸如雷帕霉素哺乳动物靶标的途径（mTOR）和蛋白激酶B（PKB）或AKT，以及其他对活性氧（ROS）和前列腺素合成的调节因子。此外，已显示抑制AKR1B1主要具有抗癌作用。多项研究还表明，抑制AKR1B1作为辅助治疗可能会使肿瘤细胞对抗癌治疗更加敏感或减轻治疗的不良反应。AKR1B1由于其启动子已经显示出高水平的甲基化，因此也可以被认为是潜在的癌症诊断生物标志物。尽管对AKR1B1在癌症中的作用及其抑制剂的临床前研究已显示出令人鼓舞的结果，但缺乏对AKR1B1抑制剂的临床研究阻碍了这些药物在癌症治疗中的应用。因此，需要进行更多的临床研究，以研究AKR1B1抑制剂作为不同癌症的辅助治疗方法。