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Suppression of miR-886-3p mediated by arecoline (ARE) contributes to the progression of oral squamous cell carcinoma
  1. Yanbo Zhang,
  2. Xuefeng Wang,
  3. Shangzhi Han,
  4. Yangyang Wang,
  5. Rui Liu,
  6. Fanli Meng,
  7. Zhejun Su,
  8. Feng Huo
  1. Department of Stomatology, Chengde Medical University Affiliated Hospital, Chengde, Hebei, China
  1. Correspondence to Dr Feng Huo, Chengde Medical University Affiliated Hospital, Chengde, Hebei, China; huofeng412{at}126.com

Abstract

Previous studies have reported that as the main extract of areca nut, arecoline (ARE) causes DNA damage and in turn contributes to the carcinogenesis of oral epithelial cells. It has been reported that ARE can inhibit the expression of miR-886-3p. In the current study, we aimed to explore the expression and biological functions of miR-886-3p in oral squamous cell carcinoma (OSCC). Herein, we demonstrated that in OSCC cells treated with ARE, the expression level of miR-886-3p was negatively correlated with the concentration of ARE. Compared with adjacent tissue, the expression level of miR-886-3p in OSCC tissue was remarkably downregulated. Transfection of miR-886-3p mimics markedly decreased viability, migration and invasion of OSCC cells. These experimental data implied that miR-886-3p suppression mediated by ARE took part in the proliferation and metastasis of OSCC. This study can help elucidate the mechanism by which areca nut chewing contributes to the malignant transformation of oral epithelial cells.

  • precancerous conditions

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Footnotes

  • Contributors YW, RL, ZS and FH designed this research. FM and YW carried out the experiments. RL, XW and SH analyzed the data. YZ, YW and RL drew the figures and drafted this manuscript. ZS helped check the manuscript and figures. YZ and FH performed the revision. All authors read and approved the final manuscript.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests None declared.

  • Patient consent for publication Not required.

  • Ethics approval Our study was approved by the Ethics Review Board of the Affiliated Hospital of Chengde Medical University (No. 201703024).

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Data availability statement The data used to support the findings of this study are available from the corresponding author on reasonable request.

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