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HdmX overexpression inhibits oncogene induced cellular senescence

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Pages 3396-3402 | Published online: 15 Aug 2010

References

  • Ventura A, Kirsch DG, McLaughlin ME, Tuveson DA, Grimm J, Lintault L, et al. Restoration of p53 function leads to tumour regression in vivo. Nature 2007; 445:661 - 665
  • Xue W, Zender L, Miething C, Dickins RA, Hernando E, Krizhanovsky V, et al. Senescence and tumour clearance is triggered by p53 restoration in murine liver carcinomas. Nature 2007; 445:656 - 660
  • Korotchkina LG, Demidenko ZN, Gudkov AV, Blagosklonny MV. Cellular quiescence caused by the Mdm2 inhibitor nutlin-3A. Cell Cycle 2009; 8:3777 - 3781
  • Huang B, Deo D, Xia M, Vassilev LT. Pharmacologic p53 activation blocks cell cycle progression but fails to induce senescence in epithelial cancer cells. Mol Cancer Res 2009; 7:1497 - 1509
  • Heminger K, Markey M, Mpagi M, Berberich SJ. Alterations in gene expression and sensitivity to genotoxic stress following HdmX or Hdm2 knockdown in human tumor cells harboring wild-type p53. Aging 2009; 1:89 - 108
  • Campisi J. Senescent cells, tumor suppression and organismal aging: Good citizens, bad neighbors. Cell 2005; 120:513 - 522
  • Roninson IB. Tumor cell senescence in cancer treatment. Cancer Res 2003; 63:2705 - 2715
  • Ferbeyre G, de Stanchina E, Lin AW, Querido E, McCurrach ME, Hannon GJ, et al. Oncogenic ras and p53 cooperate to induce cellular senescence. Mol Cell Biol 2002; 22:3497 - 3508
  • Danovi D, Meulmeester E, Pasini D, Migliorini D, Capra M, Frenk R, et al. Amplification of Mdmx (or Mdm4) directly contributes to tumor formation by inhibiting p53 tumor suppressor activity. Mol Cell Biol 2004; 24:5835 - 5843
  • Brown JP, Wei W, Sedivy JM. Bypass of senescence after disruption of p21CIP1/WAF1 gene in normal diploid human fibroblasts. Science 1997; 277:831 - 834
  • Pantoja C, Serrano M. Murine fibroblasts lacking p21 undergo senescence and are resistant to transformation by oncogenic Ras. Oncogene 1999; 18:4974 - 4982
  • Wade M, Wahl GM. Targeting Mdm2 and Mdmx in cancer therapy: Better living through medicinal chemistry?. Mol Cancer Res 2009; 7:1 - 11
  • Kortlever RM, Higgins PJ, Bernards R. Plasminogen activator inhibitor-1 is a critical downstream target of p53 in the induction of replicative senescence. Nat Cell Biol 2006; 8:877 - 884
  • Carnero A, Beach DH. Absence of p21WAF1 cooperates with c-myc in bypassing Ras-induced senescence and enhances oncogenic cooperation. Oncogene 2004; 23:6006 - 6011
  • Li C, Chen L, Chen J. DNA damage induces MDMX nuclear translocation by p53-dependent and -independent mechanisms. Mol Cell Biol 2002; 22:7562 - 7571
  • Sharp DA, Kratowicz SA, Sank MJ, George DL. Stabilization of the MDM2 oncoprotein by interaction with the structurally related MDMX protein. J Biol Chem 1999; 274:38189 - 38196
  • Reed D, Shen Y, Shelat AA, Arnold LA, Ferreira AM, Zhu F, et al. Identification and characterization of the first small molecule inhibitor of MDMX. J Biol Chem 2010; 285:10786 - 10796
  • Kawai H, Lopez-Pajares V, Kim MM, Wiederschain D, Yuan ZM. RING domain-mediated interaction is a requirement for MDM2's E3 ligase activity. Cancer Res 2007; 67:6026 - 6030
  • Stad R, Ramos YF, Little NA, Grivell S, Attema J, van De Eb AJ, et al. Hdmx stabilizes Mdm2 and p53. J Biol Chem 2000; 275:28039 - 28044
  • Demidenko ZN, Korotchkina LG, Gudkov AV, Blagosklonny MV. Paradoxical suppression of cellular senescence by p53. Proc Natl Acad Sci USA 2010; 107:9660 - 9664
  • Gilkes DM, Chen L, Chen J. MDMX regulation of p53 response to ribosomal stress. EMBO J 2006; 25:5614 - 5625
  • Hu B, Gilkes DM, Chen J. Efficient p53 activation and apoptosis by simultaneous disruption of binding to MDM2 and MDMX. Cancer Res 2007; 67:8810 - 8817
  • Markey M, Berberich SJ. Full-length hdmX transcripts decrease following genotoxic stress. Oncogene 2008; 27:6657 - 6666

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