mTORC1 shutdown unleashes TFEB to drive triple-negative breast cancer invasion.
作者信息
Gounis Michalis, Hamidi Hellyeh, Ivaska Johanna
机构信息
Turku Bioscience Centre, University of Turku and Åbo Akademi University, 20520 Turku, Finland.
Turku Bioscience Centre, University of Turku and Åbo Akademi University, 20520 Turku, Finland; Department of Life Technologies, University of Turku, 20520 Turku, Finland; InFLAMES Research Flagship, University of Turku, 20014 Turku, Finland; Western Finnish Cancer Center (FICAN West), University of Turku, 20520 Turku, Finland; Foundation for the Finnish Cancer Institute, Tukholmankatu 8, 00014 Helsinki, Finland.
出版信息
Dev Cell. 2025 Apr 7;60(7):979-981. doi: 10.1016/j.devcel.2025.03.006.
The PI3K/AKT/mTOR pathway is considered a key therapeutic target in triple-negative breast cancer (TNBC). In this issue of Developmental Cell, Remy et al. challenge this idea by demonstrating that mTORC1 inhibition activates TFEB, promoting MT1-MMP exocytosis, ECM degradation, and increased cell invasion, especially when combined with chemotherapy.
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