title: MiR-205 promotes proliferation, migration and invasion of nasopharyngeal carcinoma cells by activation of AKT signalling.
abstract: OBJECTIVE
  To examine the role of microRNA (miR)-205 in proliferation, migration and invasion of nasopharyngeal carcinoma (NPC).
  
  
  METHODS
  The human NPC cell line CNE2 was transfected with miR-205 mimic, anti-miR-205 inhibitor or scrambled oligonucleotide (control). Cell proliferation was assessed via MTT assay. Cell migration and invasion were evaluated by transwell migration and Matrigel® invasion assay, respectively. Radiation induced apoptosis was quantified via Caspase-Glo3/7 assay. Apoptotic proteins and epithelial-mesenchymal transition (EMT) proteins were semiquantified by Western blot analysis.
  
  
  RESULTS
  Overexpression of miR-205 increased the proliferation, migration and invasion of CNE2 cells, and decreased radiation-induced apoptosis compared with control cells. MiR-205 overexpression downregulated E-cadherin and upregulated Snail expression via downregulation of PTEN and upregulation of AKT.
  
  
  CONCLUSIONS
  MiR-205 plays vital roles in tumourigenesis and tumour progression in NPC, and may be a potential treatment target.
authors.affiliation: Department of Radiation Oncology, Hangzhou Cancer Hospital, Hangzhou First People's Hospital, Hangzhou, China.
authors.forename: Yanjiao
authors.initials: Y
authors.lastname: Mao
authors.affiliation: Department of Radiation Oncology, Hangzhou Cancer Hospital, Hangzhou First People's Hospital, Hangzhou, China.
authors.forename: Shixiu
authors.initials: S
authors.lastname: Wu
authors.affiliation: Department of Radiation Oncology, Hangzhou Cancer Hospital, Hangzhou First People's Hospital, Hangzhou, China.
authors.forename: Ruping
authors.initials: R
authors.lastname: Zhao
authors.affiliation: Department of Radiation Oncology, Hangzhou Cancer Hospital, Hangzhou First People's Hospital, Hangzhou, China yanjiaomao@gmail.com.
authors.forename: Qinghua
authors.initials: Q
authors.lastname: Deng
mesh_terms: D000070416:Antagomirs / Q000235:genetics / Q000378:metabolism; D017209:Apoptosis / Q000528:radiation effects; D015820:Cadherins / Q000235:genetics / Q000378:metabolism; D045744:Cell Line, Tumor; D002465:Cell Movement; D049109:Cell Proliferation; D004847:Epithelial Cells / Q000378:metabolism* / Q000473:pathology / Q000528:radiation effects; D005720:Gamma Rays; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D035683:MicroRNAs / Q000037:antagonists & inhibitors / Q000235:genetics* / Q000378:metabolism; D009305:Nasopharynx / Q000378:metabolism / Q000473:pathology / Q000528:radiation effects; D009361:Neoplasm Invasiveness; D051059:PTEN Phosphohydrolase / Q000037:antagonists & inhibitors / Q000235:genetics* / Q000378:metabolism; D051057:Proto-Oncogene Proteins c-akt / Q000819:agonists / Q000235:genetics* / Q000378:metabolism; D015398:Signal Transduction / Q000235:genetics*; D000071250:Snail Family Transcription Factors / Q000235:genetics / Q000378:metabolism
chemical_list: D000070416:Antagomirs; D015820:Cadherins; D035683:MicroRNAs; D051059:PTEN Phosphohydrolase; D051057:Proto-Oncogene Proteins c-akt; D000071250:Snail Family Transcription Factors; C534425:MIR205, human; C000604407:SNAI1 protein, human; C494929:PTEN protein, human
keywords: AKT; EMT; NPC; PTEN; apoptosis; metastasis; miRNA; miRNA-205