Open AccessTumor‐suppressive micro RNA ‐145 induces growth arrest by targeting SENP 1 in human prostate cancer cells
Author(s) -
Wang Chunyang,
Tao Weiyang,
Ni Shaobin,
Chen Qiyin,
Zhao Zhongshan,
Ma Li,
Fu Yiming,
Jiao Zhixing
Publication year - 2015
Publication title -
cancer science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 1347-9032
DOI - 10.1111/cas.12626
Subject(s) - prostate cancer , microrna , carcinogenesis , downregulation and upregulation , cancer research , cell growth , cell cycle , biology , cancer , transfection , gene silencing , prostate , cell culture , untranslated region , messenger rna , biochemistry , genetics , gene
Prostate cancer ( PC a) prevails as the most commonly diagnosed malignancy in men and the third leading cause of cancer‐related deaths in developed countries. One of the distinct characteristics of prostate cancer is overexpression of the small ubiquitin‐like modifier ( SUMO )‐specific protease 1 ( SENP 1), and the upregulation of SENP 1 contributes to the malignant progression and cell proliferation of PC a. Previous studies have shown that the expression of micro RNA ‐145 (mi RNA ‐145) was extensively deregulated in PC a cell lines and primary clinical prostate cancer samples. Independent target prediction methods have indicated that the 3′‐untranslated region of SENP 1 mRNA is a potential target of miR‐145. Here we found that low expression of miR‐145 was correlated with high expression of SENP 1 in PC a cell line PC ‐3. The transient introduction of miR‐145 caused cell cycle arrest in PC ‐3 cells, and the opposite effect was observed when miR‐145 inhibitor was transfected. Further studies revealed that the SENP 1 3′‐untranslated region was a regulative target of miR‐145 in vitro . Micro RNA ‐145 also suppressed tumor formation in vivo in nude mice. Taken together, miR‐145 plays an important role in tumorigenesis of PC a through interfering SENP 1.