ArticleJournal of cancer research and clinical oncology2003
A small inhibitor of the interaction between Bax and Bcl-X(L) can synergize with methylprednisolone to induce apoptosis in Bcl-X(L)-overexpressing breast-cancer cells.
Article in Journal of cancer research and clinical oncology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed, 15 citations in OpenAlex.
- The regulation of the mitochondrial apoptotic pathway by glucocorticoid receptor in collaboration with Bcl-2 family proteins in developing T cells.Apoptosis : an international journal on programmed cell death · 2017Article
- Expanding the chemical diversity of CK2 inhibitors.Molecular and cellular biochemistry · 2008Article
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeTo identify inhibitors of the interaction between Bax and Bcl-X(L).
methodsUsing an assay based on biosensor technology, we screened a chemical library of 10,000 compounds for inhibitors of the interaction between Bax and Bcl-X(L). Using cell-culture systems we tested active compounds for their ability to induce apoptosis in Bcl-X(L)-overexpressing MCF7 cells and increase the sensitivities of the cells to apoptosis-inducing drugs [vincristine sulphate, dexamethasone, cycloheximide and 6alpha-methylprednisolone (MP)].
resultsA single compound, 2',4',5',7'-tetrabromofluorescein (A5), from the library was found to inhibit this interaction efficiently. Several structural analogues of A5 were tested and two of these [4',5'-dibromofluorescein (A9) and 3,4,5,6-tetrabromofluorescein (A11)] were found to be active, and their activities were confirmed by an independent in vitro pull-down assay. These active compounds were observed to induce apoptosis in Bcl-X(L)-overexpressing MCF7 cells. Moreover, two of the compounds (A5 and A11) appeared to increase the sensitivities of the cells to MP. A more rigorous test using the isobologram technique showed that there is a synergistic cytotoxic effect between A11 and MP.
conclusionsWe have identified a small inhibitor of the interaction between Bax and Bcl-X(L) that can synergize with methylprednisolone to induce apoptosis in Bcl-X(L)-overexpressing breast-cancer cells.
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