title: MiR-27a modulates radiosensitivity of triple-negative breast cancer (TNBC) cells by targeting CDC27.
abstract: BACKGROUND
  MiR-27a is significantly overexpressed in triple-negative breast cancer (TNBC). However, the exact biological function of MiR-27a in TNBC is not fully understood. In this study, we verified miR-27a expression in TNBC cells and explored how its overexpression modulates radiosensitivity of the cells.
  
  
  METHODS
  qRT-PCR analysis was performed to study miR-27a expression in TNBC lines MDA-MB-435 and MDA-MB-231 and in normal human breast epithelial cell line MCF10A. Dual luciferase assay was performed to verify a putative downstream target of miR-27a, CDC27. CCK-8 assay was used to assess the influence of miR-27a-CDC27 axis on cell proliferation under irradiation (IR) treatment.
  
  
  RESULTS
  We confirmed significantly higher miR-27a expression in 2 TNBC cell lines--MDA-MB-435 and MDA-MB-231--than in human breast epithelial cell line MCF10A. miR-27a could modulate proliferation and radiosensitivity of TNBC cells. CDC-27 is a direct target of miR-27a and its downregulation conferred increased radioresistance of the cells.
  
  
  CONCLUSIONS
  The miR-27a-CDC27 axis might play an important role in modulating response to radiotherapy in TNBC cells. Testing miR-27a expression might be a useful way to identify a subgroup of patients who will benefit from an IR-based therapeutic approach.
authors.affiliation: Clinical Laboratory, The Central Hospital of Yishui, Linyi, Shandong, China (mainland).
authors.forename: Yong-qiang
authors.initials: YQ
authors.lastname: Ren
authors.affiliation: Dpartment of Radiology, People's Hospital of Binzhou, Binzhou, Shandong, China (mainland).
authors.forename: Fengkui
authors.initials: F
authors.lastname: Fu
authors.affiliation: Department of Breast Surgery, Affiliated Hospital of Hebei University of Engineering, Handan, Hebei, China (mainland).
authors.forename: Jianjun
authors.initials: J
authors.lastname: Han
mesh_terms: D064191:Apc3 Subunit, Anaphase-Promoting Complex-Cyclosome / Q000037:antagonists & inhibitors* / Q000096:biosynthesis / Q000235:genetics / Q000502:physiology; D001665:Binding Sites; D001940:Breast / Q000166:cytology; D045744:Cell Line, Tumor / Q000528:radiation effects; D002478:Cells, Cultured; D017124:Conserved Sequence; D015536:Down-Regulation; D004847:Epithelial Cells / Q000378:metabolism; D005260:Female; D015972:Gene Expression Regulation, Neoplastic / Q000187:drug effects; D057809:HEK293 Cells; D006801:Humans; D035683:MicroRNAs / Q000502:physiology*; D058990:Molecular Targeted Therapy; D009363:Neoplasm Proteins / Q000037:antagonists & inhibitors* / Q000096:biosynthesis / Q000235:genetics / Q000502:physiology; D009841:Oligonucleotides / Q000494:pharmacology; D034622:RNA Interference; D034741:RNA, Small Interfering / Q000494:pharmacology; D011836:Radiation Tolerance / Q000235:genetics; D011993:Recombinant Fusion Proteins / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction; D064726:Triple Negative Breast Neoplasms / Q000235:genetics / Q000473:pathology / Q000532:radiotherapy*; D014410:Tumor Stem Cell Assay
chemical_list: D064191:Apc3 Subunit, Anaphase-Promoting Complex-Cyclosome; C577366:CDC27 protein, human; C531388:MIRN27 microRNA, human; D035683:MicroRNAs; D009363:Neoplasm Proteins; D009841:Oligonucleotides; D034741:RNA, Small Interfering; D011993:Recombinant Fusion Proteins