MicroRNA-155 promotes bladder cancer growth by repressing the tumor suppressor DMTF1
Metrics: PDF 1664 views | HTML 2373 views | ?
Yang Peng1,*, Wen Dong1,3,*, Tian-xin Lin1,3,*, Guang-zheng Zhong1, Bei Liao2, Bo Wang1,3, Peng Gu1, Li Huang1, Yun Xie1, Fu-ding Lu1, Xu Chen1, Wei-bin Xie1, Wang He1, Shao-xu Wu1, Jian Huang1
1Department of Urology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, People’s Republic of China
2Department of Medical Examination Center, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, People’s Republic of China
3Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, SunYat-Sen Memorial Hospital, SunYat-Sen University, Guangzhou, People’s Republic of China
*These authors have contributed equally to this work
Wen Dong, e-mail: firstname.lastname@example.org
Jian Huang, e-mail: email@example.com
Keywords: microRNA-155, bladder cancer, DMTF1, Arf, cell proliferation
Received: November 24, 2014 Accepted: April 6, 2015 Published: April 18, 2015
MicroRNA-155 (miR-155) is dysregulated in human cancers. In this study, we reported that miR-155 was over-expressed in bladder cancer tissues. We found that miR-155 promoted cell proliferation in vitro and tumorigenesis in vivo. MiR-155 directly reduced the expression of the tumor suppressor DMTF1. The expression of DMTF1 was decreased in bladder cancer tissues. Similar to the restoring miR-155 expression, knockdown of DMTF1 promoted cell growth and cell cycle progression, whereas DMTF1 over-expression rescued the effect of miR-155. Moreover, we investigated DMTF1-Arf-p53 pathway and found that DMTF1 worked in both p53-dependent and p53-independent manners. Taken together, our findings suggested that miR-155 functions as a tumor promoter in bladder cancer, which is partially through repressing DMTF1 expression. The identification of miR-155 and its novel target DMTF1 will be valuable in developing diagnostic markers and therapeutic applications for bladder cancer.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.