miR‑1303 promotes the proliferation, migration and invasion of prostate cancer cells through regulating the Wnt/β‑catenin pathway by targeting DKK3
- Bo Liu
- Weidong Zhou
- Huiyang Jiang
- Zhendong Xiang
- Lei Wang
Affiliations: Department of Urology, Tongji Hospital, Tongji University of Medicine, Shanghai 200065, P.R. China
- Published online on: October 23, 2019 https://doi.org/10.3892/etm.2019.8120
Copyright: © Liu
et al. This is an open access article distributed under the
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Commons Attribution License.
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MicroRNA‑1303 (miR‑1303) is involved in the tumorigenesis and progression of several cancers, and yet the role of miR‑1303 in prostate cancer (PCa) and its underlying mechanism are unknown. To explore this issue, the present study aimed to use PCa tissues, cell lines and a PCa‑engrafted mouse model to determine the expression and roles of miR‑1303 in PCa. Furthermore, a series of experiments were conducted to explore the underlying mechanisms of action of miR‑1303 in PCa cells. miR‑1303 was demonstrated to be highly expressed in PCa tissues and cell lines. The level of miR‑1303 expression was closely associated with higher Gleason scores and a more developed tumor stage in patients with PCa, and patients with higher levels of miR‑1303 displayed a reduced overall survival rate. miR‑1303 overexpression promoted the proliferation, migration and invasion of PCa cells. In vivo experiments showed that miR‑1303 inhibition suppressed the growth of PCa tumors in mice. Additionally, dickkopf Wnt signaling pathway inhibitor 3 (DKK3) was identified as a target of miR‑1303. Knockdown of miR‑1303 suppressed the proliferation, migration and invasion of PCa cells, increased DKK3 expression, and inhibited the activity of the Wnt/β‑catenin pathway. In conclusion, miR‑1303 may promote proliferation, migration and invasion of PCa cells through activating the Wnt/β‑catenin pathway by regulating DKK3 expression. These results indicated that miR‑1303 may be considered as a potential biomarker for PCa treatment.