Journal
METALLOMICS
Volume 13, Issue 6, Pages -Publisher
OXFORD UNIV PRESS
DOI: 10.1093/mtomcs/mfab029
Keywords
G-quadruplex; platinum complexes; telomere dysfunction; DNA damage; ChIP seq; TRF2
Categories
Funding
- Centre National de Recherche Scientifique (CNRS)
- Institut National de la Sante et de la Recherche Medicale (INSERM)
- Institut Curie, Paris-Saclay University
- Association pour la Recherche contre le Cancer (ARC )
- Institut National du Cancer INCA [(2010-1-PLBIO)04UP5-14 835]
- European Union [666 003]
- Institut Curie
- Agence National de la Recherche (ANR) [(ANR)-10-EQPX-03]
- Agence Nationale de la Recherche (`Investissements d'Avenir' program) [ANR-10-INBS-09-08]
- Instituts Thematiques Multiorganismes (ITMO)-Cancer Aviesan (Plan Cancer III)
- SiRIC-Curie program [INCa-DGOS-465, INCa-DGOS-Inserm12554]
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Pt-ttpy shows dual targeting efficiency on DNA by inducing telomere dysfunction and genomic DNA damage at specific loci, while not particularly accumulating in potential G4 forming sequences.
Pt-ttpy (tolyl terpyridin-Pt complex) covalently binds to G-quadruplex (G4) structures in vitro and to telomeres in cellulo via its Pt moiety. Here, we identified its targets in the human genome, in comparison to Pt-tpy, its derivative without G4 affinity, and cisplatin. Pt-ttpy, but not Pt-tpy, induces the release of the shelterin protein TRF2 from telomeres concomitantly to the formation of DNA damage foci at telomeres but also at other chromosomal locations. gamma-H2AX chromatin immunoprecipitation (ChIP-seq) after treatment with Pt-ttpy or cisplatin revealed accumulation in G- and A-rich tandemly repeated sequences, but not particularly in potential G4 forming sequences. Collectively, Pt-ttpy presents dual targeting efficiency on DNA, by inducing telomere dysfunction and genomic DNA damage at specific loci.
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