Literature DB >> 35920984

AKR1B10 accelerates the production of proinflammatory cytokines via the NF-κB signaling pathway in colon cancer.

Cong Liu1, Lei Shi1, Wanyun Li1, Zilan Huang1, Shengyu Wang1, Peilan Xu1, Tingting Li1, Zhenyu Li1, Fanghong Luo2, Wengang Li3, Jianghua Yan4, Ting Wu5,6.   

Abstract

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.
© 2022. The Author(s), under exclusive licence to Springer Nature B.V.

Entities:  

Keywords:  AKR1B10; Cell proliferation; Clinicopathological features; Colon cancer; Inflammatory cytokine

Mesh:

Substances:

Year:  2022        PMID: 35920984     DOI: 10.1007/s10735-022-10093-7

Source DB:  PubMed          Journal:  J Mol Histol        ISSN: 1567-2379            Impact factor:   3.156


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