Background. Over the past decades, lots of advance have occurred in the prevention, diagnosis, and treatment of head and neck cancer (HNC). However, the contemporaneous incidence and survival trends, on the basis of population-based registry, have not been reported. Methods. The HNC cancer cases were accessed from the Surveillance, Epidemiology, and End Results (SEER) database. The incidence trend was analyzed by joinpoint analysis, with the survival trend being analyzed by period analysis of relative survival rate (RSR) and Kaplan-Meier analyses. Cox regression analysis was performed to identify the prognostic factors for overall survival. Results. The general incidence trend of HNC increases slightly, with an average annual percentage change of 0.6%, along with five fluctuating segments. The improvement of net survival over the past decades was showed by increasing 60-month RSR, from 54.1% to 56.0% to 60.9% to 66.8%, which was further confirmed by Kaplan-Meier analyses. Moreover, disparities in incidence and survival patterns can be observed in different subgroups. Conclusion. A fluctuating incidence pattern and an ever-improving survival were observed in HNC over time.
Dysregulation of microRNAs frequently contributes to the occurrence and progression of human diseases, including hepatocellular carcinoma (HCC). In this study, the role of miR‐450b‐3p in HCC was investigated. Gene Expression Omnibus database and HCC specimens were used to evaluate the expression level of miR‐450b‐3p and the patient's prognosis. Cell functional analyses and tumor xenograft model were used to assess the role of miR‐450b‐3p in HCC. Bioinformatics was used to predict the downstream target gene of miR‐450b‐3p, which was verified by dual‐luciferase reporter assay. MiR‐450b‐3p was found to be downregulated in HCC cell lines and tissues, compared with nontransformed immortal hepatic cells and adjacent normal liver tissues, respectively. Lower expression of miR‐450b‐3p was associated with poor overall survival and disease‐free survival in patients with HCC. Ectopic expression of miR‐450b‐3p inhibited HCC cell viability, colony formation, and cell‐cycle progression in vitro, and suppressed the growth of HCC xenograft tumors in vivo. Interestingly, a negative correlation between miR‐450b‐3p and phosphoglycerate kinase 1 (PGK1) protein was observed among HCC specimens. Additionally, miR‐450b‐3p inhibited PGK1 expression and phosphorylation of protein kinase B in HCC cell lines. Further experiments confirmed that PGK1 was a direct target of miR‐450b‐3p. Moreover, restoration of PGK1 abrogated the inhibitory effect of miR‐450b‐3p on HCC proliferation and cell division. In conclusion, miR‐450b‐3p is downregulated in human HCC and exerts tumor suppressive effects at least in part by inhibiting PGK1.
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