结直肠癌
促炎细胞因子
基因敲除
癌变
癌症研究
克隆形成试验
癌症
信号转导
炎症
生物
医学
内科学
细胞
细胞生物学
基因
生物化学
作者
Cong Liu,Lei Shi,Wanyun Li,Zilan Huang,Shengyu Wang,Peilan Xu,Tingting Li,Zhenyu Li,Fanghong Luo,Wengang Li,Jianghua Yan,Ting Wu
标识
DOI:10.1007/s10735-022-10093-7
摘要
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.
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