The DOI matches its Crossref record; 4 of the 4 references it cites were found in a registry or an index.
Acquired resistance to ABT-737 in lymphoma cells that up-regulate MCL-1 and BFL-1
Open accessAbstract
ABT-737 is a small-molecule antagonist of BCL-2 currently under evaluation in clinical trials in the oral form of ABT-263. We anticipate that acquired resistance to this promising drug will inevitably arise. To study potential mechanisms of resistance to ABT-737, we derived resistant lines from initially sensitive OCI-Ly1 and SU-DHL-4 lymphoma cell lines via long-term exposure. Resistance was based in the mitochondria and not due to an inability of the drug to bind BCL-2. Resistant cells had increased levels of BFL-1 and/or MCL-1 proteins, which are not targeted by ABT-737. Proapoptotic BIM was displaced from BCL-2 by ABT-737 in both parental and resistant cells, but in resistant cells, BIM was sequestered by the additional BFL-1 and/or MCL-1. Decreasing MCL-1 levels with flavopiridol, PHA 767491, or shRNA restored sensitivity to ABT-737 resistant cells. MCL-1 was up-regulated not by protein stabilization but rather by increased transcript levels. Surprisingly, in addition to stable increases in MCL-1 transcript and protein in resistant cells, there was a dynamic increase within hours after ABT-737 treatment. BFL-1 protein and transcript levels in resistant cells were similarly dynamically up-regulated. This dynamic increase suggests a novel mechanism whereby modulation of antiapoptotic protein function communicates with nuclear transcriptional machinery.
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Metadata
- Authors
- Yecies, D., Carlson, N. E., Deng, J., & Letai, A.
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2010-04-22
- Volume
- 115
- Issue
- 16
- Pages
- 3304-3313
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- OpenAlex
- W2017333581
- Cited by
- 360
- References
- 4
- FWCI
- 13.35
- Type
- journal article
- Language
- en
- Open access
- green
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