Small Nucleolar RNA, C/D Box 16 (SNORD16) Acts as a Potential Prognostic Biomarker in Colon Cancer

Abstract

Colon cancer (CC) is considered one of the most common and lethal malignancies occurring both in male and female. Its widespread prevalence demonstrates the need for novel diagnostic and prognostic biomarkers for CC. Emerging evidence has shown that small nucleolar RNAs play critical roles in tumor development. In this study, we investigated the expression profile and functions of SNORD16 in CC. Our data showed that SNORD16, rather than its host gene (RPL4), was upregulated in CC cell lines. Compared to matched adjacent normal tissues, CC tissues showed higher SNORD16 expression levels, and no correlation was found between SNORD16 and RPL4. Patients with high SNORD16 expression levels had a worse prognosis, and multivariate analysis showed the high SNORD16 expression was an independent prognostic factor for CC. In vitro gain- and loss-of-function studies revealed that SNORD16 can promote cell growth, proliferation, migration, and invasion of CC cells by inhibiting apoptosis. These results suggested that SNORD16 has an oncogenic role in CC and might be a novel diagnostic and prognostic biomarker for CC.

Glioma glycolipid metabolism: MSI2–SNORD12B–FIP1L1–ZBTB4 feedback loop as a potential treatment target

“…15 In colon cancer, SNORD16 promotes tumorigenesis, and SNORD16 knockdown restrains the proliferated, migrated, and invaded ability of colon cancer cells and promotes apoptosis. 16 SNORD12B is formed from the splicing intron of the long noncoding RNA ZFAS1. SNORD12B expression is upregulated in colon cancer and is correlated with its metastasis.…”

Ribosome Biogenesis Alterations in Colorectal Cancer

“…The human nucleolar enzyme NSUN5 catalyzes the C 5 methylation of cytosine residue C 3782 of the 28S rRNA (18S-m 5 C3782) and is upregulated in CRC and associated with disease progression [153]. The C/D-Box small nucleolar RNA 16 (SNORD16) guides fibrillarin (FBL) to methylate the 2 O-ribose on the 18S-Am484 site and constitutes a molecular marker of CRC and a driver of colorectal tumorigenesis [154]. The ribosome biogenesis protein TSR3 induces the 1-methyl-3α-amino-α-carboxyl-propyl pseudouridine (m 1 acp 3 Ψ) modification on uridine U1248 of the 18S rRNA and is overexpressed in CRC and associated with colorectal tumorigenesis [155].…”

“…In human Hela cells, SNORD16 is the snoRNA which directly interacts with the 18S rRNA and guides FBL to methylate the 2 O-ribose on the 18S-Am484 site [167]. It was recently shown that SNORD16 is a molecular marker of human CRC and a driver of colorectal tumorigenesis [154]. SNORD16 overexpression is significantly correlated with age, cancer cell invasion, patient history of colon polyps, and is associated with a poor patient overall survival [154].…”

“…It was recently shown that SNORD16 is a molecular marker of human CRC and a driver of colorectal tumorigenesis [154]. SNORD16 overexpression is significantly correlated with age, cancer cell invasion, patient history of colon polyps, and is associated with a poor patient overall survival [154]. HCT-116 and SW-620 cells transduced with lentiviral-SNORD16 exhibited significant increases in cell proliferation, colony formation, and migratory and invasive capacities [154].…”

“…SNORD16 overexpression is significantly correlated with age, cancer cell invasion, patient history of colon polyps, and is associated with a poor patient overall survival [154]. HCT-116 and SW-620 cells transduced with lentiviral-SNORD16 exhibited significant increases in cell proliferation, colony formation, and migratory and invasive capacities [154]. Although not determined in this study, the impact of SNORD16 on colorectal tumorigenesis is likely to be mediated through altered rRNA 2 -O-ribose methylation profiles and a translational reprogramming which could provide new targets when developing CRC therapies.…”