Regulation of Bcl-xL: a little bit of this and a little bit of STAT

Curr Opin Oncol. 2000 Nov;12(6):543-9. doi: 10.1097/00001622-200011000-00006.


The Bcl-2 family of proteins are key regulators of apoptosis. Bcl-xL, is an anti-apoptotic protein with a high degree of homology to Bcl-2; however, the signals that regulate Bcl-xL and Bcl-2 appear to be different. Levels of Bcl-xL, but not Bcl-2, are increased in response to various survival signals. Furthermore, an inverse correlation between the levels of Bcl-2 and Bcl-xL has been reported for a number of cancers. Although the precise molecules that control Bcl-xL activity are unclear, the STAT, Rel/NF-kappaB, and Ets transcription factor families have recently been reported to directly regulate the bcl-x gene. Activated Ras, integrin, vitronectin, and hepatocyte growth factor signaling cascades have also been linked to changes in Bcl-xL expression. Bcl-xL can also be affected by post-translational mechanisms. Here we review recent advances in identifying the signaling pathways and factors involved in regulation of the bcl-x gene.

Publication types

  • Review

MeSH terms

  • Animals
  • DNA-Binding Proteins / metabolism
  • Extracellular Matrix / metabolism
  • Gene Expression Regulation, Neoplastic*
  • Humans
  • Milk Proteins*
  • Models, Biological
  • NF-kappa B / metabolism
  • Proto-Oncogene Proteins / metabolism
  • Proto-Oncogene Proteins c-bcl-2 / metabolism*
  • Proto-Oncogene Proteins c-ets
  • STAT3 Transcription Factor
  • STAT5 Transcription Factor
  • Trans-Activators / metabolism
  • Transcription Factors / metabolism
  • bcl-X Protein


  • BCL2L1 protein, human
  • DNA-Binding Proteins
  • Milk Proteins
  • NF-kappa B
  • Proto-Oncogene Proteins
  • Proto-Oncogene Proteins c-bcl-2
  • Proto-Oncogene Proteins c-ets
  • STAT3 Transcription Factor
  • STAT3 protein, human
  • STAT5 Transcription Factor
  • Trans-Activators
  • Transcription Factors
  • bcl-X Protein