title: miR-152 controls migration and invasive potential by targeting TGFα in prostate cancer cell lines.
abstract: BACKGROUND
  MicroRNAs (miRNAs) are a class of short non-coding RNAs that function in diverse biological processes. Aberrant miR-152 expression has been frequently reported in various malignant tumors. However, the mechanism of miR-152 in prostate cancer (PCa) remains unclear. This study aims to determine the function of miR-152 in PCa cells and identify the novel molecular targets regulated by miR-152.
  
  
  METHODS
  The expression levels of transforming growth factor-alpha (TGFα) were determined in three samples of PCa and adjacent non-tumorous tissues by Western blot analysis. miR-152 levels in 48 primary PCa and 15 non-malignant tissue samples were measured by qRT-PCR. The effects of forced miR-152 expression or TGFα knockdown on PCa cells were evaluated by cell migration and invasion assays, as well as Western blot analysis. Dual-luciferase reporter assay was used to identify binding sites between miR-152 and TGFα 3'-UTR.
  
  
  RESULTS
  TGFα was upregulated in PCa tissue samples compared with that in adjacent normal ones. miR-152 expression was significantly decreased in primary PCa samples compared with that in non-malignant samples. Patients with Gleason scores >7 exhibited lower miR-152 levels than those with lower scores. Moreover, low miR-152 expression is correlated with advanced pathological T-stages. Forced miR-152 expression or TGFα knockdown significantly reduced the migratory and invasive capabilities of PCa cells in vitro. TGFα is a direct target gene of miR-152.
  
  
  CONCLUSIONS
  Our findings suggest that miR-152 can act as a tumor suppressor that targets TGFα. miR-152 is a promising molecular target that inhibits PCa cell migration and invasion.
authors: State Key Laboratory of Reproductive Medicine, Department of Urology, First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
authors: Chen
authors: C
authors: Zhu
authors: Jie
authors: J
authors: Li
authors: Qi
authors: Q
authors: Ding
authors: Gong
authors: G
authors: Cheng
authors: Hai
authors: H
authors: Zhou
authors: Liangjun
authors: L
authors: Tao
authors: Hongzhou
authors: H
authors: Cai
authors: Pu
authors: P
authors: Li
authors: Qiang
authors: Q
authors: Cao
authors: Xiaobing
authors: X
authors: Ju
authors: Xiaoxin
authors: X
authors: Meng
authors: Chao
authors: C
authors: Qin
authors: Lixin
authors: L
authors: Hua
authors: Pengfei
authors: P
authors: Shao
authors: Changjun
authors: C
authors: Yin
mesh_terms: D045744:Cell Line, Tumor; D002465:Cell Movement / Q000235:genetics*; D049109:Cell Proliferation; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D008297:Male; D035683:MicroRNAs / Q000235:genetics / Q000378:metabolism*; D009361:Neoplasm Invasiveness / Q000235:genetics*; D011471:Prostatic Neoplasms / Q000235:genetics / Q000378:metabolism*; D016211:Transforming Growth Factor alpha / Q000235:genetics / Q000378:metabolism*; D015854:Up-Regulation / Q000235:genetics
chemical_list: C550856:MIRN152 microRNA, human; D035683:MicroRNAs; D016211:Transforming Growth Factor alpha