miR-424-5p has been widely identified to function as an oncomiR in multiple human
cancer types. However, the biological function of miR-424-5p in distant
metastasis of
thyroid cancer, as well as the underlying mechanism, remains not clarified yet. In the current study, miR-424-5p expression was elucidated in 10 paired fresh
thyroid cancer tissues and the
thyroid cancer dataset from The
Cancer Genome Atlas (TCGA). Lung
metastasis colonization models in vivo and functional assays in vitro were used to determine the role of miR-424-5p in
thyroid cancer. Bioinformatics analysis, western blot,
luciferase reporter, and immunofluorescence assays were applied to identify the potential targets and underlying mechanism involved in the functional role of miR-424-5p in lung
metastasis of
thyroid cancer. Here, we reported that miR-424-5p was upregulated in
thyroid cancer, and overexpression of miR-424-5p significantly correlated with distant
metastasis of
thyroid cancer. Upregulating miR-424-5p promoted, whereas silencing miR-424-5p inhibited, anoikis resistance in vitro and lung
metastasis in vivo. Mechanistic investigation further revealed that miR-424-5p promoted anoikis resistance and lung
metastasis by inactivating Hippo signaling via simultaneously targeting WWC1, SAV1, and LAST2. Therefore, our results support the idea that miR-424-5p may serve as a potential therapeutic target in lung
metastasis of
thyroid cancer.