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.