| Literature DB >> 30005868 |
Shanshan Wang1, Juekun Wu2, Jianwei Ren3, Alexander C Vlantis1, Ming-Yue Li3, Shirley Y W Liu3, Enders K W Ng3, Amy B W Chan4, Ding-Cun Luo5, Zhimin Liu6, Wei Guo7, Lingbin Xue1, Siu Kwan Ng1, C Andrew van Hasselt1, Michael C F Tong1, George G Chen8.
Abstract
Thyroid cancer is rapidly increasing in incidence worldwide. Although most thyroid cancer can be cured with surgery, radioactive iodine, and/or chemotherapy, thyroid cancers still recur and may become chemoresistant. Autophagy is a complex self-degradative process that plays a dual role in cancer development and progression. In this study, we found that miR-125b was downregulated in tissue samples of thyroid cancer as well as in thyroid cancer cell lines, and the expression of Foxp3 was upregulated. Further, we demonstrated that miR-125b could directly act on Foxp3 by binding to its 3' UTR and inhibit the expression of Foxp3. A negative relationship between miR-125b and Foxp3 was thus revealed. Overexpression of miR-125b markedly sensitized thyroid cancer cells to cisplatin treatment by inducing autophagy through an Atg7 pathway in vitro and in vivo. Taken together, our findings demonstrate a novel mechanism by which miR-125b has the potential to negatively regulate Foxp3 to promote autophagy and enhance the efficacy of cisplatin in thyroid cancer. miR-125 may be of therapeutic significance in thyroid cancer.Entities:
Keywords: Foxp3; autophagy; chemotherapy; miR-125b; thyroid cancer
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Year: 2018 PMID: 30005868 PMCID: PMC6127503 DOI: 10.1016/j.ymthe.2018.06.015
Source DB: PubMed Journal: Mol Ther ISSN: 1525-0016 Impact factor: 11.454