title: MicroRNA-101 regulates the viability and invasion of cervical cancer cells.
abstract: BACKGROUND
  Cervical cancer has the second highest morbidity and mortality rates of any malignancy in women worldwide, and it is one of the leading causes of death in Uygur women in Xinjiang China. MicroRNAs are involved in cancer development and progression. Previously, we found that miR-101 is significantly down-regulated in cervical cancer tissues from Uyghur women. The underlying pathophysiology and relevance to tumorigenesis of miR-101 is still largely unknown. The purpose of this study was to elucidate the molecular mechanisms of miR-101 regulation of cervical cancer cell viability and invasion.
  
  
  METHODS
  The expression of miR-101 in cervical cancer cell line (SiHa) was detected by real-time PCR. A miR-101 mimic was overexpressed in SiHa cells, and MTT assays were performed to determine the impact on cell proliferation. Cell would heal assays and flow cytometry were used to detect migratory ability and cellular apoptosis, respectively. Immunohistochemistry was performed to assess protein expression of the miR-101 target gene COX-2.
  
  
  RESULTS
  MiR-101 was endogenously expressed in SiHa cells, and alterations in its expression had profound effects on cellular migration and invasion efficiency. Overexpression of miR-101 decreased proliferation in the MTT assay (the mimics at 490 nm absorbance is lower 60% than normal, and decreased cellular motility in the cell would healing assay (transfected: 37 ± 2 m, pre-transfected 184 ± 2 m). Apoptosis rate was significantly higher with overexpression of miR-101 relative to control (transfected: 76.6%, pre-transfected: 3.5%) (P < 0.05). The expression of Cox-2 was decreased in transfected cells.
  
  
  CONCLUSIONS
  MiR-101 likely acts as a tumor suppressor in cervical cancer. Overexpression of miR-101 decreased expression of its target gene Cox-2 and inhibited proliferation and invasion, and promoted apoptosis to suppress tumorigenicity. MiR-101 is a promising new target for the development of therapeutic strategies for the clinical treatment of cervical cancer.
authors.affiliation: Department of Pathology, Basic Medical Sciences, Xinjiang Medical University Urumqi, Xinjiang, China.
authors.forename: Chen
authors.initials: C
authors.lastname: Lin
authors.affiliation: Department of Pathology, The Affiliated Tumor Hospital of Xinjiang Medical University Urumqi, Xinjiang, China.
authors.forename: Fei
authors.initials: F
authors.lastname: Huang
authors.affiliation: The Third Gynecologic, The Affiliated Tumor Hospital of Xinjiang Medical University Urumqi, Xinjiang, China.
authors.forename: Guqun
authors.initials: G
authors.lastname: Shen
authors.affiliation: Department of Anatomy, Basic Medical Sciences, Xinjiang Medical University Urumqi, Xinjiang, China.
authors.forename: Adilijiang
authors.initials: A
authors.lastname: Yiming
mesh_terms: D017209:Apoptosis / Q000235:genetics; D045744:Cell Line, Tumor; D002465:Cell Movement / Q000235:genetics*; D049109:Cell Proliferation / Q000235:genetics*; D002470:Cell Survival / Q000235:genetics*; D051546:Cyclooxygenase 2 / Q000235:genetics / Q000378:metabolism; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D035683:MicroRNAs / Q000235:genetics / Q000378:metabolism*; D009361:Neoplasm Invasiveness / Q000235:genetics* / Q000473:pathology; D014162:Transfection; D002583:Uterine Cervical Neoplasms / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D014945:Wound Healing / Q000235:genetics
chemical_list: C534072:MIRN101 microRNA, human; D035683:MicroRNAs; D051546:Cyclooxygenase 2
keywords: Cox-2; MiR-101; cervical cancer; invasion; proliferation