Ends end it via mitochondria: A telomere-dependent tumor suppressive mechanism acts during replicative crisis
Author: Venus Marie Gaela1, Liuh-Yow Chen2
Affiliation:
1 Institute of Molecular Biology, Academia Sinica, Taipei, Taiwan; Molecular and Cell Biology, Taiwan International Graduate Program, Academia Sinica and Graduate Institute of Life Science, National Defense Medical Center, Taipei, Taiwan.
2 Institute of Molecular Biology, Academia Sinica, Taipei, Taiwan. Electronic address: lyowchen@gate.sinica.edu.tw.
Conference/Journal: Mol Cell
Date published: 2023 Apr 6
Other:
Volume ID: 83 , Issue ID: 7 , Pages: 1027-1029 , Special Notes: doi: 10.1016/j.molcel.2023.03.012. , Word Count: 48
Nassour et al.1 report that telomere dysfunction communicates with mitochondria via the ZBP1-TERRA-MAVS axis. This pathway activates a detrimental innate immune response that may promote the elimination of cells prone to oncogenic transformation during replicative crisis, thus serving as a telomere-dependent tumor-suppressive mechanism.
PMID: 37028414 DOI: 10.1016/j.molcel.2023.03.012
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