Myeloid cell leukemia-1 as a therapeutic target

Abstract

Apoptosis, or programmed cell death, is essential for normal development and homeostasis. Insufficient apoptosis may contribute to the pathogenesis of malignancy and acute and chronic inflammation. Apoptosis may be induced by the death receptor or the mitochondrial pathways. Myeloid cell leukemia (Mcl)-1 is a member of the Bcl-2 family that contributes to the control of mitochondrial integrity, which is critical for maintaining cell viability. Mcl-1 has been shown to be essential for the development and survival of a variety of cell types. This review characterizes the role of Mcl-1 in the regulation of apoptosis and the promotion of disease, and defines novel strategies that have been identified to target this molecule.

Keywords::

• apoptosis
• inflammation
• malignancy
• Mcl-1

Acknowledgements

Support for this work provided in part by grants from the National Institutes of Health (AR049217 and AR048269). RM Pope has received a research contract from Gemin X Biotechnologies, Inc.