International Journal of Radiation Oncology * Biology * Physics
Volume 76, Issue 1 , Pages 5-8 , January 2010

Lin28-let7 Modulates Radiosensitivity of Human Cancer Cells With Activation of K-Ras

  • Jee-Sun Oh, M.S.

      Affiliations

    • Medical Science Research Institute, Seoul National University Bundang Hospital, Seongnamsi, Korea
  • ,
  • Jae-Jin Kim, B.S.

      Affiliations

    • Medical Science Research Institute, Seoul National University Bundang Hospital, Seongnamsi, Korea
  • ,
  • Ju-Yeon Byun, M.S.

      Affiliations

    • Medical Science Research Institute, Seoul National University Bundang Hospital, Seongnamsi, Korea
  • ,
  • In-Ah Kim, M.D., Ph.D.

      Affiliations

    • Department of Radiation Oncology, Cancer Research Institute, Seoul National University, Seoul, Korea
    • Corresponding Author InformationReprint requests to: In-Ah Kim, Department of Radiation Oncology, Seoul National University Bundang Hospital, 300 Gumidong Seongnamsi, Kyeonggido, Korea, 463-707. Tel: (+82) 31-787-7651

Received 5 February 2009 ,Revised 24 June 2009 ,Accepted 10 August 2009.

References 

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  2. Esquela-Kerscher A, Slack FJ. Oncomir-microRNAs with a role in cancer. Nat Rev. 2006;6:259–269
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  7. Heo I, Joo C, Cho J, et al. Lin28 mediates the terminal uridylation of let-7 precursor microRNA. Mol Cell. 2008;32:276–284
  8. Kim IA, Shin JH, Kim IH, et al. Histone deacetylase inhibitor-mediated radiosensitization of human cancer cells: Class differences and the potential influence of p53. Clin Cancer Res. 2006;12:940–949
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  10. Dergham ST, Dugan MC, Kucway R, et al. Prevalence and clinical significance of combined K-ras mutation and p53 aberration in pancreatic adenocarcinoma. Int J Pancreatol. 1997;21:127–143
  11. Takamizawa J, Konishi H, Yanagisawa K, et al. Reduced expression of the let-7 microRNAs in human lung cancers in association with shortened postoperative survival. Cancer Res. 2004;64:3753–3375
  12. Weidhaas JB, Babar I, Nallur S, et al. MicroRNAs as potential agents to alter resistance to cytotoxic anticancer therapy. Cancer Res. 2007;67:11111–11116

 J.-S. Oh, J.-J. Kim, and J.-Y. B. contributed equally to this study.

 Supported by grants from the Korean Ministry of Education, Science & Technology (BAERI #M20708630001-07B0863-00110 & KRF#E00381).

 Conflict of interest: none.

PII: S0360-3016(09)02969-1

doi: 10.1016/j.ijrobp.2009.08.028

International Journal of Radiation Oncology * Biology * Physics
Volume 76, Issue 1 , Pages 5-8 , January 2010