Cancer Management and Research (Aug 2020)

Silenced Myeloblastosis Protein Suppresses Oral Tongue Squamous Cell Carcinoma via the microRNA-130a/Cylindromatosis Axis

  • Yang R,
  • Shui Y,
  • Hu S,
  • Zhang K,
  • Wang Y,
  • Peng Y

Journal volume & issue
Vol. Volume 12
pp. 6935 – 6946

Abstract

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Ran Yang,1 Yusen Shui,2 Shoushan Hu,2 Kun Zhang,2 Yuru Wang,2 Yiran Peng1 1State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, Chengdu 610041, Sichuan, People’s Republic of China; 2Department of Pediatric Dentistry, West China Hospital of Stomatology, Sichuan University, Chengdu 610041, Sichuan, People’s Republic of ChinaCorrespondence: Yiran PengDepartment of Pediatric Dentistry, West China Hospital of Stomatology, Sichuan University, 14 Renmin South Road Third Section, Chengdu 610041, Sichuan, People’s Republic of ChinaTel/ Fax +86-28-85503527Email [email protected]: Oral tongue squamous cell carcinoma (OTSCC) represents oral epithelial cell damage. Myeloblastosis (MYB) is involved in OTSCC. This study tried to probe roles of MYB in OSCC with potential axis.Methods: Expression of MYB and miR-130a in OTSCC was detected. Western blot analysis was utilized to determine epithelial–mesenchymal transition-related protein levels. Dual-luciferase reporter gene assay certified the target relation between miR-130a and CYLD. Moreover, xenograft tumors in nude mice were applied to confirm the in vitro experiments.Results: Both MYB and miR-130a were highly expressed in OTSCC, which promoted cell growth. Meanwhile, silenced miR-130a discouraged cell development enhanced by overexpressed MYB. CYLD was poorly expressed in OTSCC and targeted by miR-130a. Additionally, MYB knockdown activated CYLD to suppress OTSCC by downregulating miR-130a.Conclusion: Our experiment supported that silenced MYB suppressed OTSCC malignancy by inhibiting miR-130a and activating CYLD. This investigation may provide novel insights for OTSCC treatment.Keywords: oral tongue squamous cell carcinoma, MYB, microRNA-130a, CYLD, epithelial–mesenchymal transition, proliferation

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