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Dual oxidase 2 (DUOX2) is an important regulatory protein in the organic process of thyroid hormone iodine. Mounting evidence suggests that  DUOX2  plays a crucial role in the occurrence and development of cancers. However, the function and mechanism of  DUOX2  in colorectal cancer (CRC) have not been fully clarified. In the present study, the relationship between the expression of  DUOX2  and the clinicopathological features and prognosis of CRC patients was analyzed. Furthermore, the effects of  DUOX2  on proliferation and invasion  in vitro  and  in vivo  were examined. DUOX2-associated proteins were identified by immunoprecipitation (IP). Next-generation sequencing detection was performed to illustrate the mechanism of  DUOX2  in CRC cells. It was found that the expression levels of  DUOX2  in metastatic sites were significantly higher than those in primary tumor tissues, and this was demonstrated to be associated with poor prognosis. The knockdown of  DUOX2  inhibited the invasion and migration of CRC cells. Furthermore, DUOX2 regulated the stability of ribosomal protein uL3 (RPL3) by affecting the ubiquitination status of RPL3, and the invasion and migration ability of  DUOX2  can be reversed by the overexpression of  RPL3 . The downregulation of  DUOX2  can affect the expression level of a large number of genes, and a number of these are enriched in the PI3K–AKT pathway. Some of the changes caused by  DUOX2  can be reversed by  RPL3 . In summary, DUOX2 exhibits a significantly higher expression in CRC tumor samples, and facilitates the invasion and metastasis ability of CRC cells by interacting with RPL3.

DUOX2 promotes the progression of colorectal cancer cells by regulating the AKT pathway and interacting with RPL3