Abstract
The effects of miR-144-5p and paclitaxel (PTX) on thyroid carcinoma were less explored. Thus, we investigated the effects of miR-144-5p and PTX on thyroid carcinoma. The expression and target gene of miR-144-5p in thyroid carcinoma were analyzed by bioinformatics, y qRT-PCR and dual-luciferase reporter assay. After the transfection mediated by ultrasound-targeted microbubble destruction (UTMD) or liposome, or the treatment of PTX, the viability, proliferation, migration, and invasion of thyroid carcinoma cells were detected by MTT, colony formation, wound-healing, and transwell assays. The expressions of miR-144-5p, STON2, MMP-9, E-cadherin, and N-cadherin in cells were calculated via qRT-PCR or Western blotting. After a subcutaneous-xenotransplant tumor model was established using BALB/c nude mice and further treated with PTX and UTMD-mediated miR-144-5p, the volume, weight, and Ki67 level of tumor were recorded or evaluated by immunohistochemical assays. MiR-144-5p, which was low-expressed in thyroid carcinoma, directly down-regulated STON2 level. MiR-144-5p overexpression and PTX inhibited the viability, proliferation, migration, and invasion of thyroid carcinoma cells, while miR-144-5p silencing caused the opposite results. MiR-144-5p overexpression and PTX further up-regulated E-cadherin level and down-regulated those of MMP-9 and N-cadherin in thyroid carcinoma cells. STON2 overexpression reversed the effects of miR-144-5p overexpression.. MiR-144-5p overexpression enhanced the inhibiting effect of PTX on tumor volume, weight, and Ki67 level of xenotransplant tumor, and the effects of UTMD-mediated miR-144-5p overexpression were stronger than those mediated by liposome. Collectively, UTMD-mediated miR-144-5p overexpression enhanced the anti-tumor effect of PTX on thyroid carcinoma by targeting STON2.