MicroRNA-7 regulates cell growth, migration and invasion via direct targeting of PAK1 in thyroid cancer.

Abstract

The expression and function of microRNA-7 (miR-7) has been studied in a variety of different cancer types. However, to date, no studies have investigated the expression of miR‑7 in human thyroid cancer. In the present study, the expression levels and biological function of miR‑7 were investigated in human thyroid cancer, with the aim of evaluating whether it may serve as a therapeutic biomarker. The expression levels of miR‑7 in human thyroid cancer tissues, matched, adjacent normal tissues, normal thyroid tissues and human thyroid cancer cell lines were determined using RT‑qPCR and western blot analysis. To explore the functional role of miR‑7 in human thyroid cancer cell lines, MTT assays, cell migration and invasion assays were employed. TargetScan software identified p21 activated kinase‑1 (PAK1) as a putative interacting partner of miR‑7. Therefore, functional assays were performed to explore the effects of endogenous PAK1 in thyroid cancer. In the present study, miR‑7 was significantly downregulated in thyroid cancer tissues and cells compared with normal thyroid tissue samples. A correlation between miR‑7 expression and thyroid tumor stage was also observed. Ectopic expression of miR‑7 was found to suppress the proliferation, migra-tion and invasion of thyroid cancer cells invitro. Dual-luciferase reporter assays demonstrated that PAK1 was a direct target of miR-7 invitro. RT-qPCR and western blot analysis demonstrated that miR‑7 negatively regulates PAK1 protein expression but has no effect on PAK1 mRNA expression. Knockdown of PAK1 expression markedly suppressed thyroid cancer cell proliferation, migration and invasion. These results suggest that miR‑7 functions as a tumor suppressor by targeting PAK1 directly and may therefore present a novel therapeutic target for the treatment of thyroid cancer.