miR-103a-3p Suppresses Cell Proliferation and Invasion by Targeting Tumor Protein D52 in Prostate Cancer

Abstract

Growing evidence points at an association between microRNAs and tumor development. Although dysregulation of microRNA-103a-3p (miR-103a-3p) in multiple human cancers has been reported, its expression in prostate cancer (PCa) remains unknown and there is currently no research on the relationship between miR-103a-3p and tumor protein D52 (TPD52) in PCa. Our aim in this study was to explore the effect and potential mechanism of miR-103a-3p in PCa. qRT-PCR was performed to detected the level of miR-103a-3p in PCa tissues and cells, and in normal tissues. Colony, wound-healing, invasion, proliferation, and apoptosis assays were performed in search miR-103a-3p effect in PCa. TargetScan was used to predict potential targets of miR-103a-3p. Additionally, dual-luciferase reporter, western blot, and immunofluorescence assays were performed to detected the target gene of miR-103a-3p. Finally, we explore the differences in tumor xenograft experiments between nude mice injected with stably miR-103a-3p expressing cells and those expressing a miR-negative control. Low level of miR-103a-3p was detected in PCa tissues and cells, when compared with normal tissues. Enhancement of miR-103a-3p significantly inhibited migration and invasion of PCa cells, and negatively regulated expression of the oncogenic tumor protein D52 (TPD52) through direct binding to its 3’-UTR. Interestingly, overexpression of TPD52 significantly attenuated the effect of mir-103a-3p on PCa. Our study provides the first evidence that miR-103a-3p directly targets TPD52 and inhibits the proliferation and invasion of PCa. This finding helps clarify the role of mir-103a-3p-TPD52 axis in PCa and may provide new therapeutic targets for the disease.

Keywords:

• miR-103a-3p
• proliferation
• invasion
• tumor protein D52
• prostate cancer

Author contributions

JG, HG and CG conceived and designed the project, JG, WQ and HG acquired the data, JG, LM, NW and ZD analyzed and interpreted the data, and JG wrote the paper.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Abbreviations

miR-103a-3p, microRNA-103a-3p; TPD52, tumor protein D52; PCa, prostate cancer; 3′UTR, 3′untranslated region; NC, negative control; qRT-PCR, quantitative real-time PCR; GBD, Global Burden of Disease; CRPC, castration-resistant prostate cancer; PDCD10, programed cell death protein 10; CBZ, cabazitaxel.

Ethics approval

The study was conducted in accordance with the principles of the Declaration of Helsinki. The procedures related to tissue collection and the ensuing experiments were approved by the Ethics Committee of The Second Affiliated Hospital of Bengbu Medical College. The ethics committee of the Bengbu Medical College approved all animal experiments in accordance with the National Institutes of Health’s guidelines for the care and use of laboratory animals.

Additional information

Funding

This study was supported by grants from Science Foundation of Anhui Province [KJ2018A0214, KJ2018A0989], the First Affiliated Hospital of Bengbu Medical College Science Fund for Outstanding Young Scholars [2019BYYFYYQ09], Science Foundation of Bengbu Medical College [BYKY2019014ZD, BYKF18106], the First Affiliated Hospital of Bengbu Medical College Science Foundation [BYYFYKJ201805] and the Anhui Bengbu Medical College Postgraduate Research Innovation Project (Byycx1826). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.