title: miR-101 inhibits the G1-to-S phase transition of cervical cancer cells by targeting Fos.
abstract: OBJECTIVE
  The chief objective of this study was to identify the miRNAs targeting Fos, a well-recognized proto-oncogene that is commonly overexpressed in cervical cancer, and its biological significance on the cellular behaviors of HeLa, a cervical cancer cell.
  
  
  METHODS
  We initially analyzed the 3'untranslated region (3'UTR) of Fos and screened the potential miRNAs targeting Fos using 3 bioinformatical Web sites. Luciferase reporter assay, real-time polymerase chain reaction, and Western blotting were used to validate the binding of chosen miRNA (miR-101) on the 3'UTR of Fos and the downstream regulation on its mRNA and protein levels. Furthermore, flow cytometry along with the Fos rescue strategy was applied to analyze the modulation of cell cycle of HeLa cells by miR-101.
  
  
  RESULTS
  Among these predicted candidate miRNAs, miR-101 was the miRNAs preferred by all the 3 used Web sites. The results of luciferase reporter assay, real-time polymerase chain reaction, and Western blotting demonstrated that miR-101 directly targeted on the 3'UTR of Fos and down-regulated the expression of Fos at mRNA and protein levels. Furthermore, cell cycle analysis showed that miR-101 arrests G1-to-S phase transition of HeLa cells, at least partially by targeting Fos.
  
  
  CONCLUSIONS
  We concluded that by targeting the proto-oncogene Fos, miR-101 is involved in G1-to-S phase transition in cervical cancer cells in vitro and might provide a new approach for the pharmacological interference node in cervical cancer treatment.
authors.affiliation: *Department of Obstetrics and Gynecology, The Second Affiliated Hospital of Chongqing Medical University; †Institute of Life Sciences; and ‡The M.O.E. Key Laboratory of Laboratory Medical Diagnostics, College of Laboratory Medicine, Chongqing Medical University, Chongqing, People's Republic of China.
authors.forename: Xiaolong
authors.initials: X
authors.lastname: Liang
authors.forename: Yi
authors.initials: Y
authors.lastname: Liu
authors.forename: Liqiong
authors.initials: L
authors.lastname: Zeng
authors.forename: Chao
authors.initials: C
authors.lastname: Yu
authors.forename: Zhongwen
authors.initials: Z
authors.lastname: Hu
authors.forename: Qin
authors.initials: Q
authors.lastname: Zhou
authors.forename: Zhu
authors.initials: Z
authors.lastname: Yang
mesh_terms: D001483:Base Sequence; D015536:Down-Regulation; D005260:Female; D016193:G1 Phase / Q000235:genetics; D059585:G1 Phase Cell Cycle Checkpoints / Q000235:genetics*; D015972:Gene Expression Regulation, Neoplastic; D016762:Genes, fos; D057809:HEK293 Cells; D006367:HeLa Cells; D006801:Humans; D035683:MicroRNAs / Q000502:physiology*; D008969:Molecular Sequence Data; D000090063:Proto-Oncogene Mas; D016196:S Phase / Q000235:genetics; D012689:Sequence Homology, Nucleic Acid; D002583:Uterine Cervical Neoplasms / Q000235:genetics*
chemical_list: C000715470:MAS1 protein, human; C534072:MIRN101 microRNA, human; D035683:MicroRNAs; D000090063:Proto-Oncogene Mas