title: Upregulation of mir-221 and mir-222 in atypical teratoid/rhabdoid tumors: potential therapeutic targets.
abstract: OBJECTIVE
  The aim of this study is to search for new therapeutic targets for atypical teratoid-rhabdoid tumors (ATRT).
  
  
  METHODS
  To achieve this, we compared the expression of 365 microRNAs among ATRT, medulloblastomas, and normal brain.
  
  
  RESULTS
  MiR-221 and miR-222 were within the top differentially expressed microRNAs. The deregulated expression of miR221/222 was demonstrated to inhibit the expression of the tumor suppressor and inhibitor of cell cycle p27(Kip1). Here, we demonstrated the negative regulation of p27(Kip1) by miR-221/222 in ATRT using microarray, real-time reverse transcriptase polymerase chain reaction, and immunohistochemistry.
  
  
  CONCLUSIONS
  As anti-miR therapy was recently proposed as an alternative treatment for cancer, these findings suggest that anti-miR-221/222 therapy might have therapeutic potential in ATRT.
authors.affiliation: Cancer Biology and Epigenomics Program, Children's Memorial Research Center, Department of Pediatrics, Feinberg School of Medicine, Children's Memorial Hospital, 2300 Children's Plaza, Chicago, IL 60614, USA. ssredni@childrensmemorial.org
authors.forename: Simone Treiger
authors.initials: ST
authors.lastname: Sredni
authors.forename: Maria de Fátima
authors.initials: Mde F
authors.lastname: Bonaldo
authors.forename: Fabrício Falconi
authors.initials: FF
authors.lastname: Costa
authors.forename: Chiang-Ching
authors.initials: CC
authors.lastname: Huang
authors.forename: Christopher Allan
authors.initials: CA
authors.lastname: Hamm
authors.forename: Veena
authors.initials: V
authors.lastname: Rajaram
authors.forename: Tadanori
authors.initials: T
authors.lastname: Tomita
authors.forename: Stewart
authors.initials: S
authors.lastname: Goldman
authors.forename: Jared Marshall
authors.initials: JM
authors.lastname: Bischof
authors.forename: Marcelo Bento
authors.initials: MB
authors.lastname: Soares
mesh_terms: D001921:Brain / Q000378:metabolism*; D001932:Brain Neoplasms / Q000188:drug therapy / Q000378:metabolism*; D002868:Chromosomal Proteins, Non-Histone / Q000378:metabolism; D050760:Cyclin-Dependent Kinase Inhibitor p27 / Q000378:metabolism; D004268:DNA-Binding Proteins / Q000378:metabolism; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D007223:Infant; D007231:Infant, Newborn; D008297:Male; D035683:MicroRNAs / Q000378:metabolism*; D020411:Oligonucleotide Array Sequence Analysis; D012333:RNA, Messenger / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D018335:Rhabdoid Tumor / Q000188:drug therapy / Q000378:metabolism*; D000071796:SMARCB1 Protein; D013724:Teratoma / Q000188:drug therapy / Q000378:metabolism*; D014157:Transcription Factors / Q000378:metabolism
chemical_list: D002868:Chromosomal Proteins, Non-Histone; D050760:Cyclin-Dependent Kinase Inhibitor p27; D004268:DNA-Binding Proteins; D035683:MicroRNAs; D012333:RNA, Messenger; D000071796:SMARCB1 Protein; D014157:Transcription Factors; C525709:MIR221, human; C525710:MIR222, human; C513266:SMARCB1 protein, human