Background This study aimed to identify altered exosome circular RNA (circRNA) in the serum of patients with papillary thyroid carcinoma using high-throughput sequencing. Material/Methods Serum was collected from three patients with papillary thyroid carcinoma and three patients with a benign thyroid goiter. Exosomes were isolated using an exosome isolation kit and confirmed by transmission electron microscopy. Exosome circRNAs were analyzed by high-throughput sequencing using the HiSeq 4000 sequencer. The differentially expressed circRNAs were confirmed by fluorescence quantitative real-time polymerase chain reaction (qRT-PCR). Results Twenty-two differentially expressed circRNAs were screened, which included three that were upregulated and 19 that were down-regulated in serum from patients with papillary thyroid carcinoma compared with controls. Gene Ontology (GO) enrichment analysis showed that these differentially expressed circRNAs were associated with 16 signaling pathways, including the thyroid hormone signaling pathway, the PI3K-Akt signaling pathway, and the AMPK signaling pathway. Three differentially regulated circRNAs included hsacirc_007293, hsacirc_031752, and hsacirc_020135 were confirmed by qRT-PCR. The expression trends were consistent between the high-throughput sequencing technique and qRT-PCR. Conclusions The findings from this study have shown that gene regulation can be studied from exosomes obtained from serum samples in patients with papillary thyroid carcinoma, and supports the need for further studies on the role of exosome circRNAs in thyroid cancer.

Background: Oral tongue squamous carcinoma(OTSC) is an extremely malignant tumor specifically characterized by CDK2-mediated cell cycle perturbation.However,the underlying mechanism is poorly understood. HuR,an ubiquitously expressed member of the embryonic lethal abnormal vision family, participated in various malignent cancer. Therefore, this study aimed to explore the relationship of HuR and CDK2 in OTSC. Materials and methods: SCC25 cell line was sellected in vitro assay for the impact of HuR knockdown on tumor proliferation or CDK2 expression. IHC or mRNA levels of HuR and CDK2 expression were evaluated in malignent or benign lession tissue. Student’s t-test is used for two-group comparisons, and the one-way ANOVA for multiple group comparisons.Results:HuR knockdown reduced SCC25 proliferation, led to cell cycle arrest and dampened the colony formation. Mechanismly, HuR promoted CDK2 translation through binding to 3’untranslated regions. The luciferase activity assay futher authenticated the ARE-mediated HuR regulation on CDK2. Moreover, IHC results indicated that HuR expression exhibited progessive increase in the cases of pathological grade, accompanied by more cytoplasm distribution.Clinal datas demonstrated that the higher expression of HuR and CDK2 indicated poor prognosis and both had positive correlation. Conclutions: our study provides a compelling role of HuR in controlling the progression of OTSC by regulating CDK2 dependent cell cycle. These findings may provide a new therapeutic target for OTSC.

Background: Oral tongue squamous carcinoma(OTSC) is an extremely malignant tumor specifically characterized by CDK2-mediated cell cycle perturbation.However,the underlying mechanism is poorly understood. HuR,an ubiquitously expressed member of the embryonic lethal abnormal vision family, participated in various malignent cancer. Therefore, this study aimed to explore the relationship of HuR and CDK2 in OTSC.Materials and methods: SCC25 cell line was sellected in vitro assay for the impact of HuR knockdown on tumor proliferation or CDK2 expression. IHC or mRNA levels of HuR and CDK2 expression were evaluated in malignent or benign lession tissue. Student’s t-test is used for two-group comparisons, and the one-way ANOVA for multiple group comparisons.Results:HuR knockdown reduced SCC25 proliferation, led to cell cycle arrest and dampened the colony formation. Mechanismly, HuR promoted CDK2 translation through binding to 3’untranslated regions. The luciferase activity assay futher authenticated the ARE-mediated HuR regulation on CDK2. Moreover, IHC results indicated that HuR expression exhibited progessive increase in the cases of pathological grade, accompanied by more cytoplasm distribution.Clinal datas demonstrated that the higher expression of HuR and CDK2 indicated poor prognosis and both had positive correlation.Conclusions: our study provides a compelling role of HuR in controlling the progression of OTSC by regulating CDK2 dependent cell cycle. These findings may provide a new therapeutic target for OTSC.