Decoding and unlocking the BCL-2 dependency of cancer cells.
review · Level V
Where this comes from
- Record sourced from PubMed, PMID 23783119.
- Also identified by DOI 10.1038/nrc3538.
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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.
Medical subject headings
- Antineoplastic Agents
- Neoplasms
- Proto-Oncogene Proteins c-bcl-2