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Tumor suppression and sensitization to tumor necrosis factor alpha-induced apoptosis by an interferon-inducible protein, p202, in breast cancer cells.

p202, an IFN-inducible protein, interacts with several important regulatory proteins, leading to growth arrest or differentiation. In this report, we demonstrate that, in addition to inhibiting in vitro cell growth, p202 can also suppress the tumorigenicity of breast cancer cells in vivo. Furthermore, we found that p202 expression could sensitize breast cancer cells to apoptosis induced by tumor necrosis factor alpha treatment. One possible mechanism contributing to this sensitization is the inactivation of nuclear factor-kappaB by its interaction with p202. These results provide a scientific basis for a novel therapeutic strategy that combines p202 and tumor necrosis factor alpha treatment against breast cancer.

Pubmed ID: 10646849


  • Wen Y
  • Yan DH
  • Spohn B
  • Deng J
  • Lin SY
  • Hung MC


Cancer research

Publication Data

January 1, 2000

Associated Grants

  • Agency: NCI NIH HHS, Id: CA 77858
  • Agency: NCI NIH HHS, Id: R0-1 CA 58880

Mesh Terms

  • Apoptosis
  • Breast Neoplasms
  • Carrier Proteins
  • Female
  • Humans
  • Intracellular Signaling Peptides and Proteins
  • NF-kappa B
  • Neoplasm Proteins
  • Phenotype
  • Phosphoproteins
  • Transfection
  • Tumor Cells, Cultured
  • Tumor Necrosis Factor-alpha