Aldo–keto reductase family one, member B10 (AKR1B10) has been reported to be involved in the tumorigenesis of various cancers. It has been reported that colorectal cancer is closely associated with chronic inflammation, but the underlying molecular mechanisms are still elusive. In our study, we evaluated the relationship between AKR1B10 expression and clinicopathological characteristics of colon cancer and showed that AKR1B10 expression was significantly correlated with the T stage and clinical stage of colon cancer. Knockdown of AKR1B10 significantly decreased the expression of the inflammatory cytokines IL1α and IL6 induced by lipopolysaccharide by inhibiting the NF-κB signaling pathway. Furthermore, AKR1B10 depends on its reductase activity to affect the NF-κB signaling pathway and subsequently affect the production of inflammatory cytokines. In addition, knockdown of AKR1B10 effectively reduced cell proliferation and clonogenic growth, indicating the biological role of AKR1B10 in colon cancer. Together, our findings provide important insights into a previously unrecognized role of AKR1B10 in colon cancer.

据报道，醛酮还原酶家族一成员 B10 (AKR1B10) 参与各种癌症的肿瘤发生。据报道，结直肠癌与慢性炎症密切相关，但其潜在的分子机制仍然难以捉摸。在我们的研究中，我们评估了 AKR1B10 表达与结肠癌临床病理特征之间的关系，发现 AKR1B10 表达与结肠癌的 T 分期和临床分期显着相关。敲除AKR1B10通过抑制NF-κB信号通路显着降低脂多糖诱导的炎性细胞因子IL1α和IL6的表达。此外，AKR1B10 依赖于其还原酶活性来影响 NF-κB 信号通路并随后影响炎性细胞因子的产生。此外，AKR1B10 的敲低有效地降低了细胞增殖和克隆形成，表明 AKR1B10 在结肠癌中的生物学作用。总之，我们的研究结果为 AKR1B10 在结肠癌中以前未被认识的作用提供了重要的见解。