MicroRNA‑618 modulates cell growth via targeting PI3K/Akt pathway in human thyroid carcinomas.

ABSTRACT

OBJECTIVE: MicroRNAs (miRNAs) were popularly investigated in many cancers. The aim of this study was to evaluate the expression, role, and mechanism of microRNA‑618 (miR‑618) in human thyroid cancer (TC) cells. MATERIALS AND METHODS: Quantitative real‑time polymerase chain reaction was carried out to examine the expression level of miR‑618 in 20 TC tissues with 15 adjacent normal tissues. Synthesized mimics medicated miR‑618 overexpression model was done in TC TPC‑1 cell line. The effects of cell growth were determined by the 3‑(4,5‑dimethylthiazol‑2‑yl)‑2,5‑diphenyl‑tetrazoliumbromide method. In addition, PI staining followed by flow cytometry was performed to analyze cell cycle. Then, we performed Western blotting to analyze the impact of miR‑618 overexpression on the classical PI3K/Akt signaling pathway. RESULTS: We confirmed previous findings that miR‑618 was downregulated in TC. Functionally, we found that forced expression of miR‑618 suppressed cell proliferation and led to G2/M arrest in TPC‑1 cells. Mechanically, we showed that miR‑618 overexpression induced a significant inhibition of PI3K/Akt signaling pathway in TPC‑1 cells. Importantly, restoration of Akt reversed the growth inhibitory effects of miR‑618. CONCLUSION: Taken together, our results described a growth‑suppressive role of miR‑618 in TC cells partially targeting the PI3K/Akt signaling pathway.