ArticleCell cycle (Georgetown, Tex.)2022
Ultrasound-targeted microbubble destruction-mediated miR-144-5p overexpression enhances the anti-tumor effect of paclitaxel on thyroid carcinoma by targeting STON2.
Article in Cell cycle (Georgetown, Tex.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- Ultrasound-targeted delivery of miR-513a-5p inhibits ferroptosis and restores vascular function in preeclampsia.Journal of molecular histology · 2026Article
- Targeting miR-144-5p/ACSM1 Axis Alleviates Doxorubicin-Induced Heart Failure by Inhibiting Lipid Peroxidation.Current medical science · 2025Article
- Advances and innovations in ultrasound-based tumor management: current applications and emerging directions.The ultrasound journal · 2025Review
- Annexin A1-FPR1 Interaction in dendritic cells promotes immune microenvironment modulation in Thyroid Cancer.Cell biology and toxicology · 2025Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
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