Journal
FEBS JOURNAL
Volume 289, Issue 20, Pages 6209-6234Publisher
WILEY
DOI: 10.1111/febs.16136
Keywords
apoptosis; BCL2 family; cell cycle; MCL1; MCL1 inhibitor
Categories
Funding
- Spanish Ministry of Economy and Competitiveness [PID2020-115048RB-I00, SAF2017-84689-R]
- Generalitat Valenciana [PROMETEO/2019/065]
- Spanish Cancer Association (AECC) [PRDVA21475LEIV]
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MCL1, as an antiapoptotic member of the BCL2 family, has a key regulatory role in cell death, cell cycle progression, and mitochondrial homeostasis. Overexpression of MCL1 in cancer contributes to cell survival and chemoresistance, posing challenges to the clinical application of MCL1 inhibitors. Understanding the complexity of MCL1 regulation and function is crucial for the development of successful cancer treatments.
Myeloid cell leukemia-1 (MCL1), an antiapoptotic member of the BCL2 family characterized by a short half-life, functions as a rapid sensor that regulates cell death and other relevant processes that include cell cycle progression and mitochondrial homeostasis. In cancer, MCL1 overexpression contributes to cell survival and resistance to diverse chemotherapeutic agents; for this reason, several MCL1 inhibitors are currently under preclinical and clinical development for cancer treatment. However, the nonapoptotic functions of MCL1 may influence their therapeutic potential. Overall, the complexity of MCL1 regulation and function represent challenges to the clinical application of MCL1 inhibitors. We now summarize the current knowledge regarding MCL1 structure, regulation, and function that could impact the clinical success of MCL1 inhibitors.
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