癌症两大特征背后藏着同一调控机制

Core Insights - The research led by the Technical University of Dresden reveals a common molecular regulatory mechanism behind two classic cancer features: evasion of apoptosis and metabolic dysregulation [1] - The protein MCL1, previously considered solely an "anti-apoptotic factor," is shown to not only help cancer cells survive but also directly regulate their energy and growth signals [1] Group 1: Cancer Mechanisms - Apoptosis is a crucial process for eliminating abnormal or damaged cells, serving as a key defense against tumor development [1] - Tumor cells often achieve sustained growth by inhibiting apoptosis, with MCL1 being highly expressed in various tumors [1] - The understanding of MCL1's role in tumors has been limited to its function in preventing programmed cell death, underestimating its true impact [1] Group 2: Molecular Interactions - MCL1 is found to directly influence the mTOR signaling pathway, which is essential for integrating nutrient, energy, and growth signals in cells [1] - The direct functional link between MCL1 and the mTORC1 complex affects the energy supply and metabolic state of cancer cells [1] - This discovery connects two previously independent cancer mechanisms, highlighting MCL1's broader role in tumor biology [1] Group 3: Clinical Implications - The research addresses a long-standing clinical issue where multiple MCL1 inhibitor trials were halted due to severe cardiac toxicity [2] - The study elucidates the molecular mechanism behind this toxicity and proposes dietary intervention strategies to significantly reduce the risk of cardiac damage [2] - This advancement in understanding MCL1 inhibitors' cardiac toxicity is crucial for facilitating the re-entry of related therapies into clinical settings [2]