MiR-32 functions as a tumor suppressor and directly targets EZH2 in human oral squamous cell carcinoma
Authors: Dafeng Zhang
Xingqiao Xu
Jin Xiao
Zhenyu Ni
Journal: Medical Science Monitor (2014)
Discipline: CLINICAL MEDICINE
Keywords: MicroRNA-32; oral squamous cell carcinoma; tumorigenesis; development; expression level
Affiliations: Department of Prosthodontics, School and Hospital of Stomatology, Wenzhou Medical University, Wenzhou, Zhejiang, China (mainland)., Department of Orthodontics, School and Hospital of Stomatology, Wenzhou Medical University, Wenzhou, Zhejiang, China (mainland)., Department of Oral and Maxillofacial Surgery, School and Hospital of Stomatology, Wenzhou Medical University, Wenzhou, Zhejiang, China (mainland).

Abstract:  Background: MicroRNA-32 (miR-32) is dysregulated in certain human malignancies and correlates with tumor progression. However, its expression and function in oral squamous cell carcinoma (OSCC) remain unclear. Thus, the aim of this study was to explore the effects of miR-32 expression on OSCC tumorigenesis and development. Material/methods: Real-time quantitative PCR was applied to evaluate the expression level of miR-32 in OSCC cell lines and primary tumor tissues. The association of miR-32 expression with clinicopathological factors and prognosis was also analyzed. In vitro cell proliferation, apoptosis, invasion, and migration assays were executed to elucidate biological effects of miR-32. Western blotting and luciferase assays were performed to confirm the regulation of EZH2 by miR-32. Results: Down-regulation of miR-32 was found in OSCC tissues compared with corresponding noncancerous tissues (P&lt;0.001). Decreased miR-32 expression was significantly associated with advanced T classifications, positive N classification, advanced TNM stage, and shorter overall survival (all P&lt;0.05). Multivariate regression analysis corroborated that low-level expression of miR-32 was an independent unfavorable prognostic factor for OSCC patients. In vitro functional assays showed that overexpression of miR-32 reduced OSCC cell proliferation, migration, and invasion, and promoted cell apoptosis. In contrast, miR-32 knock-down resulted in an increase in cell growth and invasiveness. Finally, we identified EZH2 as the functional downstream target of miR-32 by directly targeting the 3'-UTR of EZH2. Conclusions: These findings indicate that miR-32 may act as a tumor suppressor in OSCC and could serve as a novel therapeutic agent for miR-based therapy. 

Retracted: No

PubPeer comments:
 This is one of a large set of papers [flagged in 2016 by a Chinese science-integrity enthusiast] as possible outputs from a papermill. ![] The present Fig 3: ![file] For comparison, Figs 3 from [Tang et al (2016)] [**RETRACTED**] and [Lin et al (2014)] [**RETRACTED**]: ![] From Tang et al again, and from [Zhu et al (2014)] [**Expression of Concern**]: ![] Other journal editors seem more concerned about the overlaps than the present editors. Notably, the overlap with Lin et al (2014) led to that paper s retraction on [20 October 2016] :  The Editor-in-Chief and Publisher of OncoTargets and Therapy have been alerted to unacceptable levels of duplication with another published paper: Zhang D, Ni Z, Xu X, and Xiao J. MiR-32 Functions as a Tumor Suppressor and Directly Targets EZH2 in Human Oral Squamous Cell Carcinoma. Medical Science Monitor. 20:2527u20132535, 2014.  Accordingly, we retract Lin FO, Yao LJ, Xiao J, Liu DF, and Ni ZY. MiR-206 functions as a tumor suppressor and directly targets K-Ras in human oral squamous cell carcinoma. Onco-Targets and Therapy. 2014;7:1583u20131591. ,