Expression profiles of tRNA-derived small RNA and their potential roles in oral submucous fibrosis.

BACKGROUND: Although transfer RNA (tRNA) has been found to be the main source of a rich class of noncoding RNA, the tRNA-derived small RNA (tsRNA) has been proved to play an irreplaceable role in the human body, and its dynamic imbalance could affect the progress of the disease. However, the research on tsRNA in oral submucous fibrosis (OSF) is still scarce. METHODS: We sequenced the OSF and validated it by PCR. We found that there were significant differences in their expression levels in OSF. Furthermore, bioinformatic analysis was performed to explore the roles of these fragments in oral submucous fibrosis. RESULTS: Of 126 tsRNAs in OSF were dysregulated, including 73 upregulated tsRNAs and 53 downregulated tsRNAs. The downregulated tiRNA-Val-CAC-002, tRF-Asn-GTT-005, tRF-Trp-CCA-007 and upregulated tRF-Gly-TCC-016, tRF-Pro-TGG-009 showed significant differences by qRT-PCR validation, which were consistent with the results of RNA sequencing. Gene ontology and pathway analysis revealed that tRF-Gly-TCC-016 would possibly promote the formation and progress of OSF through cytokine-cytokine receptor interaction and cAMP signal pathway, while tiRNA-Val-CAC-002 could be primarily concerned with the transition from OSF to oral squamous cell carcinoma (OSCC). CONCLUSION: tRNA-derived fragments are dysregulated and could be involved in the pathogenesis of oral submucous fibrosis. tRF-Gly-TCC-016 and tiRNA-Val-CAC-002 may be new regulatory molecules that could affect the process of OSF by regulating signal pathways through interacting with multiple genes.

Role of autophagy induced by arecoline in angiogenesis of oral submucous fibrosis.

OBJECTIVES: To detect the expression of protein light chain 3 (LC3) and p62-SQSTM1 (p62) in the lamina propria of oral submucous fibrosis (OSF) and to determine the association of autophagy with OSF. To investigate the role of autophagy in angiogenesis of human umbilical vein endothelial cells (HUVECs) and to assess whether this effect was induced by arecoline. METHODS: LC3 and p62 expression was detected in OSF tissue through immunohistochemistry (IHC). Transmission electron microscopy (TEM) and Western blot were used to investigate the expression of autophagy in HUVECs. The role of autophagy in angiogenesis in HUVECs was investigated using the Matrigel assay. RESULTS: 1: LC3 expression was upregulated in OSF samples. In contrast, p62 was downregulated in early and intermediate stages but upregulated in advanced stages of OSF. 2: HUVECs treated with arecoline exhibited increased autophagosomes, LC3 expression and reduced p62 expression, when co-treated with chloroquine (CQ), which is a specific autophagy inhibitor, revealed the opposite trend. 3: Autophagy inhibited angiogenesis in HUVECs. CONCLUSIONS: Our findings suggest that arecoline induces autophagy in HUVECs. The high level of autophagy could reduce cell viability and inhibit angiogenesis in HUVECs, potentially promoting the development of OSF.