title: Survivin silencing enhances radiosensitivity in oral squamous cell carcinoma cell.
abstract: OBJECTIVE
  Survivin is a member of the inhibitor of apoptosis protein (IAP) family. It is overexpressed in most cancer tissues and induces resistance to radiation therapy. In this study, we investigated whether knockdown of survivin by siRNA could induce apoptosis and enhance radiosensitivity in oral squamous cell carcinoma cells (OSCC).
  
  
  METHODS
  Oral squamous cell carcinoma cell lines KB was subjected to radiotherapy, small interfering RNA (siRNA) targeting survivin was transfected into KB cells in vitro, then subjected to radiotherapy. After irradiation or/and siRNA transfection, viable and dead cells were counted to determine radiation sensitivity by MTT assay, proliferation by colony-forming ability and apoptosis was analyzed by flow cytometry. Tumor-bearing mice were irradiated with 6 Gy of 60 Co-γ radiator.
  
  
  RESULTS
  The results showed knockdown of survivin in KB cells showed reduced cell proliferation and increased number of radiation-induced apoptosis. Apoptosis was increased by survivin silencing alone and increased further in combination with irradiation. Colony formation was significantly reduced by survivin silencing in combination with irradiation.
  
  
  CONCLUSIONS
  Survivin silencing sensitizes KB cells toward irradiation. Survivin silencing in combination with radiation inhibits cell proliferation and colony formation significantly and increases apoptosis more than each single treatment alone. In addition, survivin silencing significantly enhanced inhibition of tumor growth and potentiated cell apoptosis by irradiation in KB xenografts. In conclusion, survivin silencing could enhance sensitivity of human KB cells to radiotherapy in vitro and in vivo.
authors.affiliation: Department of Stomatology, the Affiliated Hospital of Qingdao University, Qingdao, Shandong, China. sunhuibinqd@126.com.
authors.forename: H-B
authors.initials: HB
authors.lastname: Sun
authors.forename: H-Y
authors.initials: HY
authors.lastname: Zheng
authors.forename: X
authors.initials: X
authors.lastname: Yan
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology; D002294:Carcinoma, Squamous Cell / Q000235:genetics / Q000378:metabolism* / Q000532:radiotherapy*; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000502:physiology; D020868:Gene Silencing / Q000502:physiology*; D006801:Humans; D051034:Inhibitor of Apoptosis Proteins / Q000172:deficiency* / Q000235:genetics; D051379:Mice; D008819:Mice, Nude; D009062:Mouth Neoplasms / Q000235:genetics / Q000378:metabolism* / Q000532:radiotherapy*; D034741:RNA, Small Interfering / Q000235:genetics; D011836:Radiation Tolerance / Q000502:physiology*; D000077022:Survivin; D023041:Xenograft Model Antitumor Assays / Q000379:methods
chemical_list: C107489:BIRC5 protein, human; D051034:Inhibitor of Apoptosis Proteins; D034741:RNA, Small Interfering; D000077022:Survivin