Ends end it via mitochondria: A telomere-dependent tumor suppressive mechanism acts during replicative crisis

Venus Marie Gaela; Liuh-Yow Chen

doi:10.1016/j.molcel.2023.03.012

Ends end it via mitochondria: A telomere-dependent tumor suppressive mechanism acts during replicative crisis

Mol Cell. 2023 Apr 6;83(7):1027-1029. doi: 10.1016/j.molcel.2023.03.012.

Authors

Venus Marie Gaela¹, Liuh-Yow Chen²

Affiliations

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.

PMID: 37028414
DOI: 10.1016/j.molcel.2023.03.012

Abstract

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.

Publication types

Research Support, Non-U.S. Gov't
Comment

MeSH terms

DNA Replication
Humans
Mitochondria / metabolism
Neoplasms* / metabolism
RNA, Long Noncoding*
Telomere / metabolism

Substances

RNA, Long Noncoding