title: MicroRNA-92a functions as an oncogene in colorectal cancer by targeting PTEN.
abstract: BACKGROUND
  Our previous studies show that microRNA-92a (miR-92a) is overexpressed in colorectal cancer (CRC) and is thought to be correlated with the development of the cancer. However, its biological role in CRC remains poorly understood.
  
  
  OBJECTIVE
  The aim of the study was to determine the role of miR-92a and to elucidate its regulatory mechanism in CRC.
  
  
  METHODS
  The expression levels of miR-92a and phosphatase and tensin homologue (PTEN) were detected by qRT-PCR and western blot. MTT, migration and invasion assays were used to examine the proliferation, migration and invasion of pre-miR-92a transfected SW480 cells, and a mouse model was used to investigate tumorigenesis. In addition, the regulation of PTEN by miR-92a was evaluated by qRT-PCR, western blot and luciferase reporter assays.
  
  
  RESULTS
  The expression of miR-92a was significantly up-regulated in the tissues of CRC patients with lymph node metastasis. The ectopic expression of miR-92a enhanced CRC cell proliferation, migration and invasion. Similar results were found in xenograft assay performed in nude mice. Up-regulation of miR-92a induced EMT in CRC cells. There was an inverse correlation between the levels of miR-92a and PTEN in CRC tissues. The overexpression of miR-92a in CRC cells decreased PTEN expression at the translational level, and decreased PTEN-driven luciferase-reporter activity.
  
  
  CONCLUSIONS
  Our results demonstrated that miR-92a induced EMT and regulated cell growth, migration and invasion in the SW480 cells, at least partially, via suppression of PTEN expression. MiR-92a may serve as a novel therapeutic target in colorectal cancer.
authors.affiliation: First Department of General Surgery, Institute of Hepatobiliary, Pancreatic and Intestinal Disease, The Affiliated Hospital of North Sichuan Medical College, 63 Wenhua Road, Nanchong, 637000, People's Republic of China, zhanggj1977@126.com.
authors.forename: Guangjun
authors.initials: G
authors.lastname: Zhang
authors.forename: He
authors.initials: H
authors.lastname: Zhou
authors.forename: Huaxu
authors.initials: H
authors.lastname: Xiao
authors.forename: Zuoliang
authors.initials: Z
authors.lastname: Liu
authors.forename: Hongpeng
authors.initials: H
authors.lastname: Tian
authors.forename: Tong
authors.initials: T
authors.lastname: Zhou
mesh_terms: D002277:Carcinoma / Q000209:etiology / Q000378:metabolism*; D002465:Cell Movement / Q000235:genetics; D049109:Cell Proliferation; D002471:Cell Transformation, Neoplastic; D015179:Colorectal Neoplasms / Q000209:etiology / Q000378:metabolism*; D058750:Epithelial-Mesenchymal Transition; D045325:HCT116 Cells; D019073:HT29 Cells; D006801:Humans; D035683:MicroRNAs / Q000378:metabolism*; D009361:Neoplasm Invasiveness; D009857:Oncogenes; D051059:PTEN Phosphohydrolase / Q000037:antagonists & inhibitors* / Q000378:metabolism*; D057170:Translational Research, Biomedical
chemical_list: C541874:MIRN92 microRNA, human; D035683:MicroRNAs; D051059:PTEN Phosphohydrolase; C494929:PTEN protein, human
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