title: MiR-124 suppresses cell motility and adhesion by targeting talin 1 in prostate cancer cells.
abstract: BACKGROUND
  MicroRNA is a type of endogenous non-coding RNA implicated in various cellular processes, and has been intensely investigated in the field of cancer research for many years. Here, we investigated the functions and mechanisms of miR-124 in prostate cancer, which is a putative tumor suppressor reported in many carcinomas.
  
  
  METHODS
  Using bioinformatics, talin 1 was indicated as a potential target of miR-124. We examined the expression levels of miR-124 and talin 1 in tissue specimens and cell lines. To explore the relationship between miR-124 and talin 1, miR-124 mimics, miR-124 inhibitors, and talin 1 small interfering RNA (siRNA) were transiently transfected into cancer cell lines, followed by analysis using luciferase reporter assays. Next, to investigate the functions of miR-124 in prostate cancer, we performed cell attachment, migration, and invasion assays. A rescue experiment was also conducted to demonstrate whether miR-124 suppressed cell adhesion and motility by targeting talin 1. Finally, we examined the related signaling pathways of miR-124 and talin 1.
  
  
  RESULTS
  MiR-124 was down-regulated in prostate cancer specimens and cell lines, while talin 1 was over-expressed in prostate cancer specimens and cell lines. These results showed an inverse correlation of miR-124 and talin 1 expression. Similar to talin 1 siRNA, overexpression of miR-124 by transient transfection of mimics led to a significant decrease in talin 1 levels. Luciferase report assays showed that the seed sequence of the talin 1 3'-untranslated region was a target of miR-124. Functional investigations revealed anti-attachment, anti-migration, and invasion-promoting effects of miR-124 in prostate cancer cells. The rescue experiment confirmed that miR-124 exerted its biological functions by targeting talin 1. Finally, we found that miR-124 and talin 1 impaired cellular adhesion and motility through integrins and the focal adhesion kinase/Akt pathway.
  
  
  CONCLUSIONS
  Our study demonstrated biological roles and the related mechanism of miR-124 in prostate cancer. The results indicate that talin 1 is very likely a novel player in the anti-metastatic signaling network of miR-124. By down-regulation of talin 1, miR-124 impairs the adhesion, migration, and invasion of prostate cancer cells.
authors.affiliation: Department of Urology, Zhejiang Cancer Hospital, 38 Guangji Road, Hangzhou, Zhejiang 310000 China.
authors.forename: Wei
authors.initials: W
authors.lastname: Zhang
authors.affiliation: Department of Urology, The First Affiliated Hospital of Zhejiang University, 79 Qinchun Road, Hangzhou, Zhejiang 310003 China.
authors.forename: Ye-Qing
authors.initials: YQ
authors.lastname: Mao
authors.affiliation: Department of Urology, Zhejiang Cancer Hospital, 38 Guangji Road, Hangzhou, Zhejiang 310000 China.
authors.forename: Hua
authors.initials: H
authors.lastname: Wang
authors.affiliation: Department of Pathology, Zhejiang Cancer Hospital, 38 Guangji Road, Hangzhou, Zhejiang 310000 China.
authors.forename: Wen-Juan
authors.initials: WJ
authors.lastname: Yin
authors.affiliation: Department of Urology, Zhejiang Cancer Hospital, 38 Guangji Road, Hangzhou, Zhejiang 310000 China.
authors.forename: Shao-Xing
authors.initials: SX
authors.lastname: Zhu
authors.affiliation: Medical equipment research institute of Zhejiang, 23 Huacheng Road, Hangzhou, Zhejiang 310000 China.
authors.forename: Wei-Cheng
authors.initials: WC
authors.lastname: Wang
keywords: Adhesion; Integrins; Invasion; MiR-124; Migration; Prostate cancer; Talin 1