Cell Cycle. 2017 Oct 18;16(20):1954-1964. doi: 10.1080/15384101.2017.1367071. Epub 2017 Sep 12.
题目：
MiR-26b reverses temozolomide resistance via targeting Wee1 in glioma cells.
作者：
Wang L1, Su J1, Zhao Z1, Hou Y1, Yin X1, Zheng N1, Zhou X1, Yan J2, Xia J3, Wang Z1,3,4.
单位：
1a The Cyrus Tang Hematology Center and Collaborative Innovation Center of Hematology , Soochow University , Suzhou , China.
2b Department of Abdominal Oncosurgery , Jilin Province Cancer Hospital , Changchun , Jilin , China.
3c Department of Biochemistry and Molecular Biology , Bengbu Medical College , Anhui , China.
4d Department of Pathology , Beth Israel Deaconess Medical Center, Harvard Medical School , MA , USA.
摘要：
Emerging evidence has demonstrated that microRNAs (miRNA) play a critical role in chemotherapy-induced epithelial-mesenchymal transition (EMT) in glioma. However, the underlying mechanism of chemotherapy-triggered EMT has not been fully understood. In the current study, we determined the role of miR-26b in regulation of EMT in stable temozolomide (TMZ)-resistant (TR) glioma cells, which have displayed mesenchymal features. Our results illustrated that miR-26b was significantly downregulated in TR cells. Moreover, ectopic expression of miR-26b by its mimics reversed the phenotype of EMT in TR cells. Furthermore, we found that miR-26b governed TR-mediate EMT partly due to governing its target Wee1. Notably, overexpression of miR-26b sensitized TR cells to TMZ. These findings suggest that upregulation of miR-26b or targeting Wee1 could serve as novel approaches to reverse chemotherapy resistance in glioma.