The multiple mechanisms of MCL1 in the regulation of cell fate.
Hayley WiddenWilliam J PlaczekPublished in: Communications biology (2021)
MCL1 (myeloid cell leukemia-1) is a widely recognized pro-survival member of the Bcl-2 (B-cell lymphoma protein 2) family and a promising target for cancer therapy. While the role MCL1 plays in apoptosis is well defined, its participation in emerging non-apoptotic signaling pathways is only beginning to be appreciated. Here, we synthesize studies characterizing MCL1s influence on cell proliferation, DNA damage response, autophagy, calcium handling, and mitochondrial quality control to highlight the broader scope that MCL1 plays in cellular homeostasis regulation. Throughout this review, we discuss which pathways are likely to be impacted by emerging MCL1 inhibitors, as well as highlight non-cancerous disease states that could deploy Bcl-2 homology 3 (BH3)-mimetics in the future.
Keyphrases
- dna damage response
- cell death
- oxidative stress
- cell proliferation
- quality control
- cancer therapy
- cell fate
- acute myeloid leukemia
- endoplasmic reticulum stress
- bone marrow
- physical activity
- anti inflammatory
- diffuse large b cell lymphoma
- stem cells
- cell cycle
- dendritic cells
- cell therapy
- induced apoptosis
- free survival
- epithelial mesenchymal transition