
miR‐15b‐5p facilitates the tumorigenicity by targeting RECK and predicts tumour recurrence in prostate cancer
Author(s) -
Chen Ran,
Sheng Lu,
Zhang HaoJie,
Ji Ming,
Qian WeiQing
Publication year - 2018
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.13469
Subject(s) - gene knockdown , cancer research , ectopic expression , microrna , prostate cancer , cell growth , cell , cancer , luciferase , chemistry , biology , medicine , cell culture , transfection , gene , genetics
Micro RNA s (mi RNA s) have been reported to participate in many biological behaviours of multiple malignancies. Recent studies have shown that miR‐15b‐5p (miR‐15b) exhibits dual roles by accelerating or blocking tumour progression. However, the molecular mechanisms by which miR‐15b contributes to prostate cancer ( PC a) are still elusive. Here, miR‐15b expression was found significantly up‐regulated in PC a in comparison with the normal samples and was positively correlated with age and Gleason score in patients with PC a. Notably, PC a patients with miR‐15b high expression displayed a higher recurrence rate than those with miR‐15b low expression ( P = 0.0058). Knockdown of miR‐15b suppressed cell growth and invasiveness in 22 RV 1 and PC 3 cells, while overexpression of miR‐15b reversed these effects. Then, we validated that RECK acted as a direct target of miR‐15b by dual‐luciferase assay and revealed the negative correlation of RECK with miR‐15b expression in PC a tissues. Ectopic expression of RECK reduced cell proliferation and invasive potential and partially abrogated the tumour‐promoting effects caused by miR‐15b overexpression. Additionally, miR‐15b knockdown inhibited tumour growth activity in a mouse PC a xenograft model. Taken together, our findings indicate that miR‐15b promotes the progression of PC a cells by targeting RECK and represents a potential marker for patients with PC a.