Circ-METTL15 stimulates the aggressive behaviors of papillary thyroid cancer cells by coordinating the miR-200c-3p/XIAP axis

Author:

HUANG YUHAO,ZENG XINYU,CAI YANLING,YANG YAN,ZHANG YUJIE,MA YIQI,LI SUPING

Abstract

Background and objective: Thyroid cancer is the most common malignant tumor in the endocrine system. Papillary thyroid carcinoma (PTC) accounts for the vast majority of cases in this cancer. Recently, the vital role of circular RNA (circRNA) has been acknowledged in various cancers. However, to date, few studies have examined the roles of circRNAs in PTC. Therefore, this research aimed at exploring the function and mechanism of circ-methyltransferase-like 15 (METTL15) in PTC cells.Methods: First, quantitative measurements of circ-METTL15, miR-200c-3p, and X-linked inhibitor of apoptosis protein (XIAP) in PTC cells were completed with reverse transcription-quantitative polymerase chain reaction or Western blot analysis. After the intervention of circ-METTL15, miR-200c-3p, or XIAP expression, cell counting kit-8 and colony formation assays were used to examine cell proliferation, flow cytometry was used to examine apoptosis, and Transwell assays were used to examine migration and invasion. The targeted binding sites between miR-200c-3p and circ-METTL15 or XIAP were predicted by starBase and then verified by dual luciferase reporter assay.Results: circ-METTL15 and XIAP were upregulated in the PTC cells, while miR-200c-3p was downregulated. Downregulating circ-METTL15 or upregulating miR-200c-3p prevented the PTC cells from proliferating, migrating, and invading, and stimulated cell apoptosis. miR-200c-3p was the downstream molecule of circ-METTL15, and XIAP was the direct target of miR-200c-3p. Forcing XIAP expression obstructed circ-METTL15 silencing to inhibit PTC cell activity.Conclusion: Circ-METTL15 stimulates the aggressive behaviors of papillary thyroid cancer cells by coordinating the miR-200c-3p/XIAP axis.

Publisher

The Scientific and Technological Research Council of Turkey (TUBITAK-ULAKBIM) - DIGITAL COMMONS JOURNALS

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