MicroRNA-16 functions as a tumor-suppressor gene in oral squamous cell carcinoma by targeting AKT3 and BCL2L2.

Abstract:

:Aberrant expressions of microRNAs have been reported to be strongly associated with the progression and prognosis of various tumors, including oral squamous cell carcinoma (OSCC). Recent studies on miRNA expression profiling have suggested that microRNA-16 (miR-16) may be dysregulated in OSCC. However, the tumorigenic roles and mechanisms of miR-16 in OSCC are still largely unknown. In this study, we demonstrated that miR-16 was specifically downregulated in both OSCC patients and cancer cell lines. In addition, functional roles of miR-16 in vitro suggested that the miR-16 mimic inhibited cell proliferation and induced apoptosis, whereas miR-16 inhibitor displayed the opposite effects. Luciferase reporter assay and correlation analysis showed that AKT3 and BCL2L2 were directly targeted by miR-16 and were inversely expressed with miR-16 in OSCC. Moreover, restoration of AKT3 and BCL2L2 expression could partially reverse the cell proliferation inhibition and apoptosis induction caused by miR-16. In xenograft nude mice, miR-16 mimics decreased the expression of AKT3 and BCL2L2 and reduced the tumors volumes and weights, whereas the miR-16 inhibitor exhibited adverse effects in the derived xenografts. In conclusion, the findings suggested that miR-16 functions as a tumor suppressor miRNA to inhibit cell proliferation and induce apoptosis in OSCC through decreasing the oncogenes AKT3 and BCL2L2 and that miR-16 could be a potential therapeutic target for OSCC.

journal_name

J Cell Physiol

authors

Wang X,Li GH

doi

10.1002/jcp.26833

subject

Has Abstract

pub_date

2018-12-01 00:00:00

pages

9447-9457

issue

12

eissn

0021-9541

issn

1097-4652

journal_volume

233

pub_type

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