A groundbreaking study by researchers at Technische Universität Dresden, reported on January 5, 2026, reveals a previously hidden molecular switch that significantly helps cancer cells thrive. This discovery shows the protein MCL1, long known for preventing cell death, also actively controls tumor metabolism, linking two critical mechanisms for cancer growth.
Until now, scientists largely studied cancer’s ability to evade programmed cell death (apoptosis) and its metabolic reprogramming as separate processes. The Dresden team’s work, highlighted in ScienceDaily, unifies these understandings, demonstrating MCL1’s unexpected role as a central orchestrator of cancer’s survival and energy use.
This insight transforms our view of MCL1, moving it beyond a mere survival factor to an active controller of major signaling and metabolic pathways. Understanding this dual function offers new avenues for developing more effective and safer cancer therapies, particularly by addressing a significant challenge in previous drug trials.
Unraveling MCL1’s dual role
For years, MCL1 was primarily recognized as a member of the Bcl-2 protein family, crucial for preventing cancer cells from undergoing apoptosis. However, Dr. Mohamed Elgendy’s team discovered MCL1 directly influences mTOR, a powerful regulator of cellular metabolism and growth. This connection drives how cancer cells generate and manage energy.
“Our findings show that MCL1 is much more than just a survival factor for tumor cells,” states Dr. Elgendy. “The protein actively intervenes in key metabolic and growth signaling pathways, thereby linking two fundamental cancer mechanisms.” This direct functional link between MCL1 and the mTORC1 complex reshapes current understanding.
The researchers further confirmed that drugs designed to block MCL1, currently in clinical development, also reduce mTOR signaling. This overlap is clinically significant, given that mTOR-targeting medications are already widely used in cancer care, suggesting a common vulnerability that helps cancer cells thrive.
Overcoming cardiotoxicity for safer treatments
A major hurdle for MCL1 inhibitors has been severe heart damage observed in clinical trials, leading to their suspension. The Dresden team’s most impactful discovery pinpointed the molecular cause of this cardiotoxicity. This critical insight enabled them to develop a dietary strategy that significantly reduced heart damage in advanced models.
“This outstanding research work exemplifies how excellent basic research can create direct benefits for our cancer patients,” says Prof. Uwe Platzbecker, Chief Medical Officer of the University Hospital Dresden. “The solution to the cardiotoxicity problem of MCL1 inhibitors can now pave the way for safer therapies.”
This protective effect was validated using advanced humanized mouse models, underscoring its potential for clinical translation. The broader significance of this work was recognized when editors of Nature Communications selected the paper for their “Editors’ Highlights,” showcasing notable cancer studies.
The identification of MCL1 as a multifaceted controller, rather than merely a survival factor, offers a paradigm shift in understanding how cancer cells thrive. This research unravels the intricate link between cancer cell survival and metabolism.
Crucially, by addressing the cardiotoxicity challenge associated with MCL1 inhibitors, this work paves the way for a new generation of safer, targeted cancer therapies. Future studies will likely focus on refining these dietary strategies and integrating MCL1 inhibitors more safely into existing treatment protocols.
