Dresden study reveals new role of MCL1 in cancer cells
Researchers from the Mildred Scheel Junior Research Group at the Technical University of Dresden have shown for the first time that the protein MCL1 not only inhibits apoptosis, but also controls tumor metabolism. The work, led by Mohamed Elgendy and published in Nature Communications, combines two cancer characteristics – avoidance of cell death and metabolic disorders – via a common mechanism.
MCL1 is overexpressed in many tumors and interacts directly with the regulator mTOR – thereby influencing the bioenergetics of cancer cells. This discovery expands the understanding of MCL1 as an active factor in signaling and metabolic pathways. In models, a functional connection between MCL1 and mTORC1 was confirmed.
Clinically relevant: MCL1 inhibitors, in development as cancer therapeutics, also block mTOR signaling, similar to established mTOR inhibitors. The study also clarifies the cardiotoxicity of such inhibitors that discontinued studies and proposes a dietary approach to reduction, validated in a humanized mouse model.
The interdisciplinary cooperation included partners from the Czech Republic, Austria and Italy. The results could lead to safer therapies and were awarded as a highlight in Nature Communications.
Elgendy has been leading a group on cancer metabolism since 2019, funded by ERC and ERA-NET. The Mildred Scheel Young Investigator Center, supported by German Cancer Aid, promotes such innovations at five locations.
Original Paper:
MCL1 modulates mTORC1 signaling to promote bioenergetics and tumorigenesis | Nature Communications
Editor: X-Press Journalistenbüro GbR
Gender Notice. The personal designations used in this text always refer equally to female, male and diverse persons. Double/triple naming and gendered designations are used for better readability. ected.
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