High expression of USP18 is associated with the growth of colorectal carcinoma

xlomafota13 shared this article with you from Inoreader High expression of USP18 is associated with the growth of colorectal carcinoma Via Cellular and Molecular Biology Histol Histopathol. 2021 May 27:18346. doi: 10.14670/HH-18-346. Online ahead of print. ABSTRACT AIM: To investigate whether USP18 can be used as a predictive marker for the diagnosis and development of colorectal cancer. METHODS: The Gene Expression Omnibus (GEO) Dataset and the Cancer Genome Atlas (TCGA) database were used to select differential proteins for the ubiquitin-specific peptidases (USPs). The extensive target prediction and network analysis methods were used to assess the association with the USP18 interacting proteins, as well as the statistical correlation between USP18 and the clinical pathology parameters. The effects of USP18 on the proliferation of colorectal cancer were examined using CCK8. The effects of USP18 on the migration of colorectal cancer were examined using wound healing assays. Immunohistochemistry (IHC) was performed on the tissue microarray. RESULTS: The results showed that the expression of USP18 was related to age (P=0.014). The positive rates of the USP18 protein in T1, T2, T3, and T4 were 0.00%, 22.92%, 78.38%, and 95.35%, respectively (P<0.00). The positive rates of the USP18 protein in I, II, III, and IV were 47.43%, 83.12%, 66.67%, and 100.00%, respectively (P<0.00). The Western blot assay showed that the expression of USP18 in colorectal cancer tissues was significantly higher than that in matched paracancerous tissues (P<0.05). The CCK8 experiments suggested that USP18 promoted the migration of CRC cells. Wound healing assays suggested that USP18 promoted the proliferation of CRC cells. CONCLUSION: This study showed that USP18 can promote the proliferation of colorectal cancer cells and might be a potential biomarker for the diagnosis of CRC. PMID:34042164 | DOI:10.14670/HH-18-346 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.