Background
Circular RNAs (circRNAs) and long non-coding RNAs (lncRNAs) have been recently identified as new classes of non-coding RNAs which participate in carcinogenesis and tumor progression. However, the functions of these non-coding RNAs and gene expression patterns are largely unknown.
Conclusions
Our study was the first to describe the non-coding RNA profile of LC, and suggested that dysregulated non-coding RNAs could be involved in LC tumorigenesis. SNHG29 was demonstrated to play crucial roles in inhibiting the pathogenesis and progression of LC. Our findings provide a new approach for further analyses of pathogenetic mechanisms, the detection of novel transcripts, and the identification of valuable biomarkers for this tumor.
Methods
We carried out high-throughput sequencing to analyze the differential expression of RNAs in 5 coupled laryngeal cancer (LC) and corresponding adjacent noncancerous tissues. Bioinformatics analyses were performed to predict the functions of these non-coding RNAs via co-expression, competing endogenous RNA networks and pathway enrichment analysis. The differential expression of the selected RNAs were confirmed using RT-qPCR. The CCK8, EDU, Transwell, and wound healing assays were conducted to validate the biological functions of SNHG29 in LC. Western blot assay was performed to identify the effects of SNHG29 having on the epithelial to mesenchymal transition process. Kaplan-Meier analysis was used to investigate whether the expression level of SNHG29 correlated with survival in LC patients. One-way ANOVA was used to analyze the correlation between the expression of SNHG29 and clinicopathological parameters of the included patients.
Results
Compared to normal laryngeal tissues, 31,763 non-coding RNAs were upregulated and 11,557 non-coding RNAs were downregulated in cancer tissues. SNHG29 expression was low in the LC cell lines and tissues predicting a better clinical prognosis. SNHG29 was also found to inhibit the proliferation, migration, and invasion ability of LC, exerting a suppressive role in the epithelial to mesenchymal transition process as well. SNHG29 downregulation was significantly correlated with differentiation (P=0.026), T-stage (P=0.041), lymphatic metastasis (P=0.044), and clinical stage (P=0.037). We found that the biological functions of differentially expressed transcripts included cell adhesion, biological adhesion, and migration and invasion related to adherens junction pathways. Conclusions: Our study was the first to describe the non-coding RNA profile of LC, and suggested that dysregulated non-coding RNAs could be involved in LC tumorigenesis. SNHG29 was demonstrated to play crucial roles in inhibiting the pathogenesis and progression of LC. Our findings provide a new approach for further analyses of pathogenetic mechanisms, the detection of novel transcripts, and the identification of valuable biomarkers for this tumor.