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SNORD93 suppresses colorectal cancer progression by inducing G0/G1 arrest and apoptosis
Yingzhi Xu1, Mingzhen Cai1, Jiaming Li1
1Department of Clinical Laboratory, Quanzhou First Hospital Affiliated to Fujian Medical University, Quanzhou, China.
Background:
Colorectal cancer (CRC) is one of the most common malignant tumors in the world. Dysregulated small nucleolar RNAs (snoRNAs) have recently been demonstrated to participate in cancer activity through their influence on cellular transformation and carcinogenesis. Specifically, SNORD93 exhibits consistent dysregulation across multiple malignancies and demonstrates significant correlation with adverse clinical outcomes, but it remains unclear how SNORD93 is involved in the development of CRC. In this study, we examined the role of SNORD93 in CRC pathogenesis in order to provide novel diagnostic and treatment targets for CRC.
Methods:
The expression levels of SNORD93 were quantified in CRC tissue samples (n=13) and paired adjacent normal tissue samples (n=13) from the same patients, as well as in human CRC cell lines (HT-29, SW480, and HCT-15) and the normal human intestinal epithelial crypt cell (HIEC) line via quantitative real-time polymerase chain reaction (qRT-PCR). The biological significance of SNORD93 in the proliferation, migration, cell cycle progression, and cell apoptosis was examined through gain-of-function analyses via Cell Counting Kit-8 (CCK-8) assay, colony formation assay, wound healing assay, and flow cytometry. Additionally, the expression of related proteins was quantified through Western blotting (WB).
Results:
A significant downregulation of SNORD93 was identified in CRC tissues and cells. Moreover, downregulation of SNORD93 was significantly associated with the poor survival of patients with CRC. In contrast, the overexpression of SNORD93 suppressed the growth of CRC cells in vitro but did not affect CRC cell migration. In terms of mechanism, SNORD93 inhibited cellular proliferation by arresting cells at the G1/S transition phase, while simultaneously inducing apoptosis. Moreover, SNORD93 overexpression correlated with elevated phosphorylation of both receptor-interacting protein (RIP) and mixed lineage kinase domain-like protein (MLKL), suggesting potential involvement of necroptosis pathways.
Conclusions:
Collectively, these results establish SNORD93 as a functionally significant tumor-suppressive snoRNA in CRC.
Insights
SNORD93 acts as a tumor suppressor in colorectal cancer (CRC). Its downregulation is linked to poor survival, while its overexpression inhibits CRC cell growth and induces apoptosis, suggesting it as a potential therapeutic target.
Area of Science:
- Oncology
- Molecular Biology
- Epigenetics
Background:
- Colorectal cancer (CRC) is a leading cause of cancer mortality worldwide.
- Small nucleolar RNAs (snoRNAs) are increasingly implicated in carcinogenesis.
- SNORD93, a specific snoRNA, shows dysregulation in various cancers, but its role in CRC remains unclear.
Purpose of the Study:
- To investigate the role of SNORD93 in the pathogenesis of colorectal cancer.
- To explore SNORD93 as a potential diagnostic and therapeutic target for CRC.
Main Methods:
- Quantitative real-time polymerase chain reaction (qRT-PCR) to measure SNORD93 expression in CRC tissues and cell lines.
- Gain-of-function experiments (Cell Counting Kit-8, colony formation, wound healing, flow cytometry) to assess SNORD93's impact on CRC cell proliferation, migration, cell cycle, and apoptosis.
- Western blotting (WB) to analyze related protein expression.
Main Results:
- SNORD93 was significantly downregulated in CRC tissues and cell lines.
- Lower SNORD93 expression correlated with poorer patient survival.
- Overexpression of SNORD93 inhibited CRC cell proliferation by inducing G1/S cell cycle arrest and apoptosis.
- SNORD93 overexpression was associated with increased RIP and MLKL phosphorylation, suggesting involvement of necroptosis pathways.
Conclusions:
- SNORD93 functions as a tumor suppressor in colorectal cancer.
- SNORD93 holds promise as a novel biomarker and therapeutic target for CRC.
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