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miR-34b inhibits nasopharyngeal carcinoma cell proliferation by targeting ubiquitin-specific peptidase 22

Authors Xiao J, Li Y, Zhang W, Jiang Y, Du B, Tan Y

Received 15 October 2015

Accepted for publication 28 January 2016

Published 16 March 2016 Volume 2016:9 Pages 1525—1534


Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Chang Liu

Peer reviewer comments 2

Editor who approved publication: Dr Faris Farassati

Jianyong Xiao,1 Yingying Li,2 Wenyin Zhang,1 Yanni Jiang,1 Biaoyan Du,3 Yuhui Tan1

1Department of Biochemistry, Guangzhou University of Chinese Medicine, 2Department of Internal Medicine, Guangzhou Eighth People’s Hospital, 3Department of Pathology, Guangzhou University of Chinese Medicine, Guangzhou, People’s Republic of China

Objectives: This study aimed to investigate the precise role of miR-34b in nasopharyngeal carcinoma (NPC).
Materials and methods: The expression of miR-34b and transcription of ubiquitin-specific peptidase 22 (USP22) were examined using quantitative reverse transcription-polymerase chain reaction. Western blot analysis was used to measure the protein expression of USP22. A dual-luciferase assay was used to investigate the interaction between miR-34b and USP22. Cell viability was determined by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide assay. The cell cycle was analyzed by propidium iodide staining followed by flow cytometry analysis.
Results: miR-34b was significantly downregulated in NPC tissues and NPC cell lines. Overexpression of miR-34b in NPC SUNE-6-10B cells inhibited cell viability and proliferation. USP22 was highly expressed in NPC cells and promoted cell viability and proliferation. Restoration of USP22 expression could reverse the effect of miR-34b on NPC cell viability and proliferation.
Conclusion: miR-34b acts as a tumor suppressor in NPC, which is mediated via repression of the oncogene USP22.

Keywords: cell proliferation, miR-34b, nasopharyngeal carcinoma, overexpression, USP22

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