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Direct Activation of BAX by BTSA1 Overcomes Apoptosis Resistance in Acute Myeloid Leukemia
Open accessAbstract
SUMMARY The BCL-2 family protein BAX is a central mediator of apoptosis. Overexpression of anti-apoptotic BCL-2 proteins contributes to tumor development and resistance to therapy by suppressing BAX and its activators. We report the discovery of BTSA1, a pharmacologically optimized BAX activator that binds with high affinity and specificity to the N-terminal activation site and induces conformational changes to BAX leading to BAX-mediated apoptosis. BTSA1-induced BAX activation effectively promotes apoptosis in leukemia cell lines and patient samples while sparing healthy cells. BAX expression levels and cytosolic conformation regulate sensitivity to BTSA1. BTSA1 potently suppressed human acute myeloid leukemia (AML) xenografts and increased host survival without toxicity. This study provides proof-of-concept for direct BAX activation as a treatment strategy in AML.
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Metadata
- Authors
- Reyna, D. E., Garner, T. P., Lopez, A., Kopp, F., Choudhary, G. S., Sridharan, A., Narayanagari, S.-R., Mitchell, K., Dong, B., Bartholdy, B. A., Walensky, L. D., Verma, A., Steidl, U., & Gavathiotis, E.
- Venue
- Cancer Cell
- Publisher
- Elsevier BV
- Published
- 2017-10
- Volume
- 32
- Issue
- 4
- Pages
- 490-505.e10
- ISSN
- 1535-6108 (ISSN-L)
- OpenAlex
- W2761494335
- Cited by
- 163
- References
- 14
- FWCI
- 5.14
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Reyna, D. E., Garner, T. P., Lopez, A., Kopp, F., Choudhary, G. S., Sridharan, A., Narayanagari, S.-R., Mitchell, K., Dong, B., Bartholdy, B. A., Walensky, L. D., Verma, A., Steidl, U., & Gavathiotis, E. (2017). Direct Activation of BAX by BTSA1 Overcomes Apoptosis Resistance in Acute Myeloid Leukemia. Cancer Cell. https://doi.org/10.1016/j.ccell.2017.09.001
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
