Decoding and unlocking the BCL-2 dependency of cancer cells

Nat Rev Cancer. 2013 Jul;13(7):455-65. doi: 10.1038/nrc3538. Epub 2013 Jun 20.


Cancer cells are subject to many apoptotic stimuli that would kill them were it not for compensatory prosurvival alterations. BCL-2-like (BCL-2L) proteins contribute to such aberrant behaviour by engaging a network of interactions that is potent at promoting survival but that is also fragile: inhibition of a restricted number of interactions may suffice to trigger cancer cell death. Currently available and novel compounds that inhibit these interactions could be efficient therapeutic agents if this phenotype of BCL-2L dependence was better understood at a molecular, cellular and systems level and if it could be diagnosed by relevant biomarkers.

Publication types

  • Review

MeSH terms

  • Antineoplastic Agents / pharmacology
  • Antineoplastic Agents / therapeutic use*
  • Humans
  • Molecular Targeted Therapy
  • Neoplasms / etiology*
  • Neoplasms / metabolism
  • Neoplasms / prevention & control*
  • Proto-Oncogene Proteins c-bcl-2 / antagonists & inhibitors*
  • Proto-Oncogene Proteins c-bcl-2 / physiology*


  • Antineoplastic Agents
  • Proto-Oncogene Proteins c-bcl-2