Ghost mitochondria drive metastasis through adaptive GCN2/Akt therapeutic vulnerability

Cancer metabolism, including in mitochondria, is a disease hallmark and therapeutic target, but its regulation is poorly understood. Here, we show that many human tumors have heterogeneous and often reduced levels of Mic60, or Mitofilin, an essential scaffold of mitochondrial structure. Despite a ca...

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Veröffentlicht in:	Proceedings of the National Academy of Sciences - PNAS 2022-02, Vol.119 (8), p.1-9
Hauptverfasser:	Ghosh, Jagadish C., Perego, Michela, Agarwal, Ekta, Bertolini, Irene, Wang, Yuan, Goldman, Aaron R., Tang, Hsin-Yao, Kossenkov, Andrew V., Libby, Catherine J., Languino, Lucia R., Plow, Edward F., Morotti, Annamaria, Ottobrini, Luisa, Locatelli, Marco, Speicher, David W., Caino, M. Cecilia, Cassel, Joel, Salvino, Joseph M., Robert, Marie E., Vaira, Valentina, Altieri, Dario C.
Format:	Artikel
Sprache:	eng
Schlagworte:	AKT protein Bioenergetics Biological Sciences Cancer Catastrophic collapse Cell Death Cell Line, Tumor Cell Movement - genetics Cell Proliferation Chemokines Cytokines Damage Depletion Drug screening Epithelial-Mesenchymal Transition Gene expression Humans Innate immunity Mesenchyme Metastases Metastasis Mitochondria Mitochondria - metabolism Mitochondria - physiology Mitochondrial Dynamics - physiology Mitochondrial Proteins - metabolism Muscle Proteins - metabolism Neoplasm Invasiveness - genetics Neoplasm Metastasis - physiopathology Neoplasms - genetics Neoplasms - metabolism Neoplasms - physiopathology Neoplastic Processes Protein Serine-Threonine Kinases - metabolism Proto-Oncogene Proteins c-akt - metabolism Reactive Oxygen Species Signal Transduction Signaling Stress response Therapeutic applications Therapeutic targets Tumors
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