miR‑122‑5p suppresses the oncogenesis of PTC by inhibiting DUSP4 expression
- Ning Hu
- Yanhua Tian
- Yanmei Song
- Leilei Zang
Affiliations: Department IV of General Surgery, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050005, P.R. China, Department II of Oncology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050005, P.R. China, Department of Infection Management/Public Health, Hebei People's Hospital, Shijiazhuang, Hebei 050057, P.R. China, Department V of General Surgery, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050005, P.R. China
- Published online on: March 16, 2021 https://doi.org/10.3892/mmr.2021.12007
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MicroRNAs (miRNAs or miRs) play an important role in regulating the occurrence and development of papillary thyroid carcinoma (PTC). miR‑122‑5p is widely considered a tumour inhibitor, which has not been fully explored in PTC. Bioinformatics analysis identified dual specificity phosphatase 4 (DUSP4), a tumour promoter gene for PTC, as a downstream target of miR‑122‑5p. The aim of the present study was to investigate the role and molecular mechanism of miR‑122‑5p in PTC oncogenesis. In this study, the expression pattern of miR‑122‑5p in PTC cancer tissues and PTC cell lines was investigated via reverse transcription‑quantitative PCR. Furthermore, the roles of miR‑122‑5p in PTC were explored using gain‑of‑function and loss‑of‑function assays. The results revealed that the expression of miR‑122‑5p was significantly lower in PTC cancer tissues, especially in cancer tissues with significant invasion or metastasis. Overexpression of miR‑122‑5p caused by miR‑122‑5p mimics inhibited the proliferation, invasion, and migration of the PTC cell line K1, while knockdown of miR‑122‑5p by miR‑122‑5p inhibitors exhibited the opposite effect. Furthermore, in vivo assays revealed that miR‑122‑5p overexpression inhibited tumour growth. In addition, miR‑122‑5p was negatively correlated with DUSP4 expression in PTC cancer tissues. miR‑122‑5p overexpression inhibited DUSP4 expression in K1 cells, while miR‑122‑5p downregulation produced the inverse effect. Specifically, a luciferase reporter assay confirmed the binding sites of miR‑122‑5p on the 3'‑UTR of DUSP4, demonstrating the targeting effect of miR‑122‑5p on DUSP4. miR‑122‑5p inhibited the oncogenesis of PTC by targeting DUSP4, revealing the potential application value of miR‑122‑5p in the diagnosis and treatment of PTC.