J Cancer 2017; 8(13):2501-2510. doi:10.7150/jca.17407 This issue Cite
Research Paper
1. Department of Radiation Oncology, Affiliated Cancer Hospital & Institute of Guangzhou Medical University, Guangzhou 510095, China;
2. Department of Pathology, Integrated Hospital of Traditional Chinese Medicine, Southern Medical University, Guangzhou 510315, China;
3. Guangdong Provincial Key Laboratory of Molecular Oncologic Pathology, Southern Medical University, Guangzhou 510515, China;
4. Department of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, China;
5. Department of Pathology, Affiliated Chenzhou Hospital, Southern Medical University (The First People's Hospital of Chenzhou), Chenzhou 423000, China;
6. Department of Urology, Nanfang Hospital, Southern Medical University/The First School of Clinical Medicine, Southern Medical University, Guangzhou 510515, China.
* These authors contributed equally to this work.
miRNAs play critical role in the development and progression of prostate cancer. Here we studied the role of miR-618 in prostate cancer migration and invasion. miR-618 was downregulated in metastatic androgen-independent prostate cancer (AIPC), patients with low miR-618 had poor outcome. Overexpression of miR-618 inhibited migration and invasion and induced mesenchymal to epithelial transition (MET). Conversely, knockdown of miR-618 promoted migration and invasion and induced epithelial to mesenchymal transition (EMT). FOXP2 was the direct target of miR-618, and promoted TGF-β expression, inhibition of TGF-β reversed the effect of miR-618 knockdown. We further analyzed the correlation between miR-618 expression and FOXP2 in human prostate cancer tissues, and found there was a negative correlation between miR-618 expression and FOXP2 levels. In conclusion, we found miR-618 inhibited prostate cancer migration and invasion by targeting FOXP2 and inhibiting TGF-β.
Keywords: prostate cancer, miR-618, FOXP2, migration, TGF-β.