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miR-96-5p Suppresses the Progression of Nasopharyngeal Carcinoma by Targeting CDK1

Authors Luo X, He X, Liu X, Zhong L, Hu W

Received 4 February 2020

Accepted for publication 2 July 2020

Published 30 July 2020 Volume 2020:13 Pages 7467—7477


Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 3

Editor who approved publication: Dr Cho

Xiaoqin Luo,1 Xian He,1 Xing Liu,2 Lunkun Zhong,1 Wenjian Hu1

1Department of Otolaryngology, Affiliated Traditional Chinese Medicine Hospital of Southwest Medical University, Luzhou, Sichuan 646699, People’s Republic of China; 2Department of Urology, Affiliated Traditional Chinese Medicine Hospital of Southwest Medical University, Luzhou, Sichuan 646699, People’s Republic of China

Correspondence: Wenjian Hu Department of Otolaryngology
Affiliated Traditional Chinese Medicine Hospital of Southwest Medical University, Luzhou City, Sichuan Province 646699, People’s Republic of China
Tel +86 13980247707

Background: Nasopharyngeal carcinoma (NPC) is a malignant tumor that occurs in the nasopharyngeal mucosa. Clinically, radiotherapy is the preferred treatment for NPC, and cervical lymph node metastasis is easy to emerge in the early stage. Therefore, this study aimed to investigate the role and potential molecular mechanisms of miR-96-5p in NPC cells to develop new therapeutic horizons.
Methods: The expression of miR-96-5p and CDK1 was measured by RT-qPCR or Western blot. The target relationship between miR-96-5p and CDK1 was confirmed by luciferase reporter assay. CCK-8, sphere formation, flow cytometry and colony formation assay were employed to examine cell viability, stem-like property, apoptosis and cycle, respectively. Male BALB/c nude mice model (6– 8 weeks, weigh 18– 20 g) was used to evaluate the effect of miR-96-5p on tumor growth in vivo.
Results: miR-96-5p was lowly expressed and CDK1 was highly expressed in NPC tissues and cell lines. CDK1 was identified as a direct target of miR-96-5p, and its expression was negatively regulated by miR-96-5p. By targeting CDK1, miR-96-5p overexpression significantly inhibited tumor sphere formation, promoted apoptosis and cell cycle arrest in CNE-2Z cells. Importantly, CCK-8 and colony formation assay demonstrated that elevated miR-96-5p enhanced the radiotherapy and chemotherapy sensitivity of CNE-2Z cells. Animal experiments showed that the overexpression of miR-96-5p reduced tumor weight and size in tumor-bearing mice and inhibited the expression of stem-like marker proteins and apoptosis-related proteins.
Conclusion: These results, together, suggested that miR-96-5p induced cell cycle arrest and apoptosis, inhibited stem-like property, and enhanced the radiochemical sensitivity of NPC by targeting CDK1. In short, miR-96-5p may be a diagnostic and therapeutic target for NPC.

Keywords: nasopharyngeal carcinoma, miR-96-5p, CDK1, stem-like property, radio-chemosensitivity

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