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Pharmacological inhibition of BMK1 suppresses tumor growth through promyelocytic leukemia protein.

Cancer cell | Sep 14, 2010

http://www.ncbi.nlm.nih.gov/pubmed/20832753

BMK1 is activated by mitogens and oncogenic signals and, thus, is strongly implicated in tumorigenesis. We found that BMK1 interacted with promyelocytic leukemia protein (PML), and inhibited its tumor-suppressor function through phosphorylation. Furthermore, activated BMK1 notably inhibited PML-dependent activation of p21. To further investigate the BMK-mediated inhibition of the tumor suppressor activity of PML in tumor cells, we developed a small-molecule inhibitor of the kinase activity of BMK1, XMD8-92. Inhibition of BMK1 by XMD8-92 blocked tumor cell proliferation in vitro and significantly inhibited tumor growth in vivo by 95%, demonstrating the efficacy and tolerability of BMK1-targeted cancer treatment in animals.

Pubmed ID: 20832753 RIS Download

Mesh terms: Animals | Cell Growth Processes | Cell Nucleus | Cytosol | Genes, Tumor Suppressor | HeLa Cells | Humans | Mitogen-Activated Protein Kinase 7 | Neoplasms | Nuclear Proteins | Phosphorylation | Protein Kinase Inhibitors | Signal Transduction | Transcription Factors | Tumor Suppressor Proteins

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Associated grants

  • Agency: NCI NIH HHS, Id: CA079871
  • Agency: NCI NIH HHS, Id: CA114059
  • Agency: NCI NIH HHS, Id: R01 CA079871-08
  • Agency: NCI NIH HHS, Id: R01 CA079871-09
  • Agency: NCI NIH HHS, Id: R01 CA079871-10
  • Agency: NCI NIH HHS, Id: R01 CA114059-03
  • Agency: NCI NIH HHS, Id: R01 CA114059-04
  • Agency: NCI NIH HHS, Id: R01 CA114059-05

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