ArticleExperimental and therapeutic medicine2021
Thymosin β10 mediates the effects of microRNA-184 in the proliferation and epithelial-mesenchymal transition of BCPAP cells.
Article in Experimental and therapeutic medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed, 2 citations in OpenAlex.
- Pan-cancer analysis identifies the correlations of Thymosin Beta 10 with predicting prognosis and immunotherapy response.Frontiers in immunology · 2023Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Thyroid cancer is the most common malignant tumor of the endocrine system. It has been reported that thymosin β10 (TMSB10) serves a vital role in tumor invasion and metastasis, and further understanding the role of TMSB10 in thyroid cancer may provide new insights into the development of novel targeted drugs. Bioinformatics analysis suggested that there might exist a regulatory relationship between miR-184 and TMSB10. Therefore, the expression of microRNA (miR)-184 was investigated in the TPC-1 and BCPAP thyroid cancer cell lines and the Nthy-ori 3-1 thyroid epithelial cell line via reverse transcription-quantitative PCR. The effect of miR-184 on BCPAP cell proliferation was evaluated using MTT and colony formation assays. In addition, the expression levels of epithelial-mesenchymal transition (EMT)-associated proteins were examined via western blot analysis and immunofluorescence staining. Furthermore, the targeting association between miR-184 and TMSB10 was verified using a dual-luciferase reporter assay. Notably, miR-184 overexpression attenuated BCPAP cell proliferation, increased the expression level of the epithelial marker E-cadherin, and decreased that of the mesenchymal marker vimentin. These effects were reversed in BCPAP cells following TMSB10 overexpression. The present study revealed that TMSB10 may be considered as a key mediator in promoting papillary thyroid carcinoma (PTC) cell proliferation and EMT, which were negatively regulated by miR-184. Therefore, the findings of the present study may provide a novel potential therapeutic target for attenuating PTC cell proliferation.
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