Decoding and unlocking the BCL-2 dependency of cancer cells
- PMID: 23783119
- DOI: 10.1038/nrc3538
Decoding and unlocking the BCL-2 dependency of cancer cells
Abstract
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.
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