title: The Tumor Suppressive Role of MiRNA-509-5p by Targeting FOXM1 in Non-Small Cell Lung Cancer.
abstract: OBJECTIVE
  Deregulation of microRNAs (miRNAs) expression is a frequent event in cancer development and progression. Recent studies have implied that abnormal expression of miRNAs is frequently observed in non-small cell lung cancer (NSCLC). Here, we examined the levels and biological functions of miR-509-5p in NSCLC.
  
  
  METHODS
  The levels of miR-509-5p were measured by real-time quantitative PCR (RT-PCR) in NSCLC cell lines and NSCLC tissues along with adjacent normal tissues. Cell viability was analyzed by MTT and colony formation assay. Cell migration and invasion were evaluated by transwell and wound healing assay. In addition, we predicted the putative targets of miR-509-5p by bioinformatics analyses. Moreover, by luciferase-reporter assay, we analyzed the relationship between miR-509-5p and the target in NSCLC cells.
  
  
  RESULTS
  miR-509-5p expression was significantly reduced in NSCLC tissues compared with adjacent normal tissues. In addition, miR-509-5p decreased cell proliferation, migration and invasive capability of NSCLC cells. Moreover, we found that FOXM1 was a putative target of miR-509-5p. Enforced miR-509-5p expression in NSCLC cells reduced both mRNA and protein levels of FOXM1. Furthermore, dual-luciferase reporter assay showed miR-509-5p could bind to the 3' untranslational regions of FOXM1 mRNA. Furthermore, overexpression of FOXM1 reversed cell viability, migration, invasion and vimentin levels suppressed by miR-509-5p mimics in H1299 cells.
  
  
  CONCLUSIONS
  miR-509-5p exerts tumor-suppressive effects by attenuating FOXM1 in NSCLC. Collectively, these findings provide further evidence that miR-509-5p may be considered as a novel and potential target for the diagnosis, prognosis and treatment of NSCLC.
authors.forename: Ning
authors.initials: N
authors.lastname: Ma
authors.forename: Weihua
authors.initials: W
authors.lastname: Zhang
authors.forename: Chenhui
authors.initials: C
authors.lastname: Qiao
authors.forename: Hong
authors.initials: H
authors.lastname: Luo
authors.forename: Xin
authors.initials: X
authors.lastname: Zhang
authors.forename: Donghai
authors.initials: D
authors.lastname: Liu
authors.forename: Suhua
authors.initials: S
authors.lastname: Zang
authors.forename: Liang
authors.initials: L
authors.lastname: Zhang
authors.forename: Jingyun
authors.initials: J
authors.lastname: Bai
mesh_terms: D020413:3' Untranslated Regions; D000072283:A549 Cells; D000070416:Antagomirs / Q000378:metabolism; D001483:Base Sequence; D015153:Blotting, Western; D015820:Cadherins / Q000378:metabolism; D002289:Carcinoma, Non-Small-Cell Lung / Q000235:genetics / Q000473:pathology; D045744:Cell Line, Tumor; D002465:Cell Movement; D002470:Cell Survival / Q000235:genetics; D000072278:Forkhead Box Protein M1 / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D017930:Genes, Reporter; D006801:Humans; D008175:Lung Neoplasms / Q000235:genetics / Q000473:pathology; D035683:MicroRNAs / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D060888:Real-Time Polymerase Chain Reaction; D016415:Sequence Alignment; D014746:Vimentin / Q000378:metabolism
chemical_list: D020413:3' Untranslated Regions; D000070416:Antagomirs; D015820:Cadherins; C107585:FOXM1 protein, human; D000072278:Forkhead Box Protein M1; D035683:MicroRNAs; D014746:Vimentin