Cancer Management and Research (Oct 2020)

MiRNA-128 and MiRNA-142 Regulate Tumorigenesis and EMT in Oral Squamous Cell Carcinoma Through HOXA10

  • Yao Y,
  • Xu Q,
  • Yan L,
  • Jiao Y,
  • Su Q,
  • Li X,
  • Liu C,
  • Zhao F

Journal volume & issue
Vol. Volume 12
pp. 9987 – 9997

Abstract

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Yao Yao,* Qian Xu,* Liyong Yan, Yan Jiao, Qingqi Su, Xiaoguang Li, Cong Liu, Feng Zhao Department of Stomatology, Central Hospital of Taian, Taian, Shandong, People’s Republic of China*These authors contributed equally to this workCorrespondence: Feng Zhao Tel +86-538-6298546Email [email protected]: Oral squamous cell carcinoma (OSCC) accounts for more than 90% of all oral cavity cancers, and the 5-year survival rate for OSCC patients remains unsatisfactory. MiRNA-128/miRNA-142 has been reported to work as a tumor suppressor in diverse tumors. However, the biological function of miR-128/miR-142 in OSCC is still unknown.Methods: The expression of miR-128/miR-142 and homeobox A10 (HOXA10) in OSCC tissues and cells was measured by quantitative real-time polymerase chain reaction (RT-qPCR). The effects of miR-128/miR-142 or HOXA10 on proliferation, migration, invasion and apoptosis were detected by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT), transwell and flow cytometry assays, respectively. The expression levels of epithelial–mesenchymal transition (EMT)-associated proteins (E-cadherin, N-cadherin and Vimentin), proliferation-associated protein ki-67 and HOXA10 were detected by Western blot assay. The interaction between HOXA10 and miR-128/miR-142 was predicted by TargetScan, and then confirmed by dual-luciferase reporter assay.Results: MiR-128/miR-142 was downregulated in OSCC tissues and cells. Overexpression of miR-128/miR-142 inhibited proliferation, migration, invasion and EMT and induced apoptosis in OSCC cells. HOXA10 as the target of miR-128/miR-142 was verified in OSCC cells. Knockdown of HOXA10 also repressed proliferation, migration, invasion and EMT and boosted apoptosis in OSCC cells. Upregulation of miR-128/miR-142 hindered the expression level of HOXA10, while introduction of HOXA10 weakened the effect.Conclusion: MiR-128/miR-142 suppressed OSCC tumorigenesis and metastasis by targeting HOXA10, providing a new promising therapeutic approach for OSCC patient diagnosis and treatment.Keywords: miR-128, miR-142, oral squamous cell carcinoma, HOXA10, tumorigenesis, EMT

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