IL‐1β maintains the redox balance by regulating glutaredoxin 1 expression during oral carcinogenesis

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Interleukin‐1 beta (IL‐1β) is a pleiotropic cancer–inflammation‐linked cytokine which has been reported upregulated in breast, colon, lung, and esophageal cancers 1. In our previous study, IL‐1β was found to be one of the key node genes during oral malignant transformation, and targeting IL‐1β could interrupt oral carcinogenesis by reprogramming the tumor microenvironment 2. One of the interesting findings from this study is that glutaredoxin 1 (Grx1) was identified as one of downstream genes of IL‐1β through bioinformatics analysis and subsequent verification.
Grx1 is ubiquitous oxidoreductase belonging to the thioredoxin (Trx) superfamily, which are necessary for scavenging the reactive oxygen species (ROS) and the maintenance of intracellular redox balance 3. The role of antioxidants in tumorigenesis has been controversial for years. Recently, there has been a resurgence of evidence indicating that antioxidants contribute to tumorigenesis by preventing ROS accumulation and subsequent oxidative stress in cancer cells 4. ROS have been viewed as detrimental stress‐inducing molecules that promote cancer initiation, but new evidence indicates that oxidative stress can be beneficial 5. Low concentration of ROS is necessary for maintaining normal cell function, while moderate or high ROS concentration could lead to carcinogenesis 6.
Considering the significant roles of IL‐1β and ROS in carcinogenesis, based on our previous finding on the regulatory role of IL‐1β on Grx1 expression, we hypothesize that IL‐1β may play a pivotal role in maintaining the redox balance by regulating Grx1 expression during oral malignant transformation. In this study, we have evaluated the role of IL‐1β in production and scavenging systems of ROS in oral carcinogenesis, as well as the possible involvement of Grx1 in this procedure in vivo and in vitro. Our results suggested that IL‐1β finely orchestrated the redox balance during carcinogenesis by modulating Grx1 expression, which was involved in the invasion and migration of OSCC cells.
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