Circ_0000144 facilitates the progression of thyroid cancer via the miR‐217/AKT3 pathway.

Background: Thyroid carcinoma (TC) is the most common malignancy of the endocrine system. Circular RNA (circRNA) is vital in the regulation of tumor progression. Circ_0000144 serves as a novel oncogenic circRNA, and miR‐217 is reported to inhibit the malignant phenotypes of cancer cells by targeting AKT3 in TC. The present study aimed to explore the regulatory mechanism of circ_0000144 and miR‐217 in the progression of TC. Methods: Circ_0000144 expression in 32 pairs of TC tissues and different TC cell lines (including BCPAP, K1, H7H83, and TPC‐1) was detected by employing a quantitative real‐time polymerase chain reaction (qRT‐PCR). Circ_0000144 small interfering RNA was used to establish loss‐of‐function models. Cell counting kit‐8 (CCK‐8), BrdU (5‐bromo‐2'‐deoxyuridine) and transwell assays were utilized to verify the effects of circ_0000144 on TC cell proliferation, migration and invasion, respectively. Bioinformatics, western blotting, a luciferase reporter experiment and qRT‐PCR were employed to confirm the relationships among circ_0000144, miR‐217 and AKT3. Results: Circ_0000144 expression was remarkably elevated in TC tissues (p < 0.001) and TC cell lines. The elevation of circ_0000144 expression was markedly linked to tumor size (p = 0.015), TNM stage (p = 0.025) and lymph node metastasis (p = 0.017) of the patients. Functional studies showed that knocking down circ_0000144 repressed the malignancy of TC cells. Furthermore, miR‐217 was identified as a downstream target of circ_0000144; inhibition of miR‐217 could reverse the effects induced by circ_0000144 knockdown. Moreover, circ_0000144 could regulate AKT3 expression by suppressing miR‐217 expression. Conclusions: Circ_0000144 exerts a cancer‐promoting effect on TC cells via the miR‐217/AKT3 pathway. [ABSTRACT FROM AUTHOR]