Cytokine overexpression and constitutive NFκB in cancer

Tao Lu, George R. Stark

Research output: Contribution to journalReview article

51 Scopus citations

Abstract

The NFκB family of transcription factors, central mediators of immune responses, are also involved in oncogenesis. Loss of regulation of the normally latent NFκB contributes importantly to the deregulated growth, resistance to apoptosis and propensity to metastasize observed in many cancers. Thus, pathways for activation of NFκB are promising targets for new agents that may help to prevent or treat cancer. We find that the abnormal secretion of multiple cytokines that activate NFκB by binding to cell-surface receptors is one of the major causes of constitutive NFκB activity in cancer. A novel finding is that the latent form of TGFβ, secreted by some of these cells, can activate NFκB. To understand the basis of this abnormal cytokine secretion, we are using forward genetic methods to identify specific causative mutations in cancer cells.

Original languageEnglish (US)
Pages (from-to)1114-1117
Number of pages4
JournalCell Cycle
Volume3
Issue number9
StatePublished - Sep 2004

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Keywords

  • Apoptosis
  • Autocrine loops
  • Forward genetics
  • Latent TGF β
  • PC3 cells
  • TGF β
  • mRNA overexpression

ASJC Scopus subject areas

  • Molecular Biology
  • Developmental Biology
  • Cell Biology

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