Colon cancer is one of the most common malignant tumors in the world; however, the mechanism underlying the progression of colon cancer remains unclear. In the present study, the expression of ubiquitin-specific peptidase 22 (USP22) in paraffin sections of human colon cancer tissues and normal colon tissues were examined using immunohistochemistry. The human colon cancer cell lines HCT116 and HT29 were used for USP22 knockdown experiments, and functional assays were performed. The results demonstrated that compared with normal colon tissues, human colon cancer tissues exhibited upregulated expression of USP22 and this was associated with tumor lymph node metastasis and tumor stage in colon cancer tissues. In addition, upregulated expression of USP22 was significantly correlated with both lower relapse-free survival and lower overall survival rates in patients with colon cancer. When USP22 was silenced in colon cancer cell lines, this resulted in a decrease in cell proliferation and metastatic behaviors. Furthermore, Bmi-1 and Cyclin D2 were found to be positively regulated by USP22, which may have mediated the tumorigenic effects of USP22 in human colon cancer. The results of the present study may have significant implications for examining the underlying mechanisms of cancer development and the potential development of cancer therapeutics.
Keywords: colon cancer; metastasis; oncogene; proliferation; ubiquitin-specific peptidase 22.
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