Thyroid cancer is derived from follicular or thyroid cells and has become the most prevalent malignant tumor of endocrine organs, with increased morbidity and mortality. Circular RNAs (circRNAs) are used as prognostic and predictive markers for different types of cancer. However, the role of circRNA_0000285 in thyroid cancer and its potential molecular mechanism remain unclear. The present study aimed to investigate the roles and underlying molecular mechanism of circRNA_0000285 in thyroid cancer to identify novel treatments for this disease. The target binding site of circRNA_0000285 and microRNA-654-3p (miR-654-3p) were predicted and confirmed via the dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. Thyroid cancer cell viability and apoptosis were determined via the MTT assay and flow cytometric analysis, respectively, whereas the expression levels of circRNA_0000285 and miR-654-3p were determined via reverse transcription-quantitative PCR analysis. In addition, the protein expression levels of the apoptosis-associated proteins, Bax and B-cell lymphoma 2 (Bcl-2), were detected via western blotting. The results of the dual-luciferase reporter and RIP assays demonstrated that miR-654-3p directly targeted circRNA_0000285. The expression levels of circRNA_0000285 and miR-654-3p in thyroid cancer cells (TPC-1 and FTC133) were upregulated and downregulated, respectively. Knockdown of circRNA_0000285 via small interfering (si)RNA inhibited circRNA_0000285 levels and increased miR-654-3p levels. In addition, miR-654-3p expression decreased following transfection with miR-654-3p inhibitor. Functional experiments demonstrated that circRNA_0000285-siRNA decreased thyroid cancer cell proliferation, promoted cell apoptosis, enhanced Bax expression and suppressed Bcl-2 expression. All these effects were reversed following transfection with miR-654-3p inhibitor. Taken together, the results of the present study suggest that circRNA_0000285 plays a vital role in thyroid cancer progression by regulating miR-654-3p, which provides a potential therapeutic target for this disease.

Papillary thyroid carcinoma (PTC) is the most common thyroid malignancy. Long non coding RNAs (lncRNAs) have been involved in regulating tumor progression including PTC. In the present study, we demonstrated that long non coding RNA LINC01186 was significantly downregulated in PTC tissue samples compared with adjacent normal tissue samples in patients. LINC01186 expression was also found to be higher in PTC cells. Lower LINC01186 expression was associated with lymph node metastasis of PTC patients. Functionally, LINC01186 overexpression significantly suppressed cell proliferation, cell colony formation and cell invasion ability in TPC-1 and IHH-4 cells. In addition, we demonstrated that LINC01186 overexpression inhibited large tumor suppressor kinase 1 (LATS1)/YY1 associated protein 1 (YAP) signaling by reducing YAP1 expression, while increasing LATS1 expression in TPC-1 and IHH-4 cells. Collectively, our data suggested that LINC01186 may serve as a potential target for therapy in thyroid carcinoma.

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