Cited by 176PARP inhibition in cancer therapyCell death mechanisms and regulationDNA Repair Mechanisms

Cisplatin Resistance Associated with PARP Hyperactivation

Michels, Judith, Vitale, Ilio, Galluzzi, Lorenzo, Adam, Julien, Olaussen, Ken André, Kepp, Oliver, Senovilla, Laura, Talhaoui, Ibtissam +18 more·2013·Cancer Research

Published version of a preprint

Abstract

Non–small cell lung carcinoma patients are frequently treated with cisplatin (CDDP), most often yielding temporary clinical responses. Here, we show that PARP1 is highly expressed and constitutively hyperactivated in a majority of human CDDP-resistant cancer cells of distinct histologic origin. Cells manifesting elevated intracellular levels of poly(ADP-ribosyl)ated proteins (PARhigh) responded to pharmacologic PARP inhibitors as well as to PARP1-targeting siRNAs by initiating a DNA damage response that translated into cell death following the activation of the intrinsic pathway of apoptosis. Moreover, PARP1-overexpressing tumor cells and xenografts displayed elevated levels of PAR, which predicted the response to PARP inhibitors in vitro and in vivo more accurately than PARP1 expression itself. Thus, a majority of CDDP-resistant cancer cells appear to develop a dependency to PARP1, becoming susceptible to PARP inhibitor–induced apoptosis. Cancer Res; 73(7); 2271–80. ©2013 AACR.

Integrity signals

Registry

Crossref · 10.1158/0008-5472.can-12-3000

Cites

47 of 47 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Mitotic catastrophe is a major mechanism of action of anticancer chemotherapeutics, reflecting increased resistance of neoplastic cells to intrinsic apoptosis.

    “However, mitotic catastrophe appears to constitute a major mechanism of action of anticancer chemotherapeutics, mostly reflecting the increased resistance of neoplastic cells to the induction of intrinsic apoptosis [1004–1009].”

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Michels, J., Vitale, I., Galluzzi, L., Adam, J., Olaussen, K. A., Kepp, O., Senovilla, L., Talhaoui, I., Guegan, J., Enot, D. P., Talbot, M., Robin, A., Girard, P., Oréar, C., Lissa, D., Sukkurwala, A. Q., Garcia, P., Behnam-Motlagh, P., Kohno, K., Wu, G. S., Brenner, C., Dessen, P., Saparbaev, M., Soria, J.-C., Castedo, M., & Kroemer, G.
Affiliations
  • Université Paris-Sud (FR)
  • Authors' Affiliations: 1U848, 2U981, 3U985, INSERM; 4Institut Gustave Roussy; 5Université Paris Sud; 6UMR8200, CNRS; Plateformes de 7Bioinformatique, 8Génomique, and 9Metabolomique, Institut Gustave Roussy; Villejuif; 10Université Paris Descartes; 11Department of Thoracic Oncology, Institut Mutualiste Montsouris; 12Equipe 11 labellisée par la Ligue Nationale contre le Cancer, Centre de Recherche des Cordeliers; 13Pôle de Biologie, Hôpital Européen Georges Pompidou AP-HP, Paris; 14U769, INSERM-LabEx LERMIT, Université Paris-Sud, Châtenay Malabry, France; 15Department of Medical Biosciences, Clinical Chemistry, Umeå University, Umeå, Sweden; 16Department of Molecular Biology, School of Medicine, University of Occupational and Environmental Health, Kitakyushu/Fukuoka, Japan; and 17Molecular Therapeutics Program, Karmanos Cancer Institute, Department of Oncology and Pathology, Wayne State University School of Medicine, Detroit, Michigan
Venue
Cancer Research
Published
2013-04-01
Volume
73
Issue
7
Pages
2271-2280
ISSN
  • 0008-5472 (ISSN-L)
  • 1538-7445
OpenAlex
W2060534647
Cited by
176
References
47
Citations by year
2026: 4 · 2025: 10 · 2024: 10 · 2023: 10 · 2022: 11 · 2021: 15 · 2020: 14 · 2019: 12 · 2018: 13 · 2017: 15 · 2016: 17 · 2015: 19 · 2014: 18 · 2013: 8
FWCI
11.25
Type
journal article
Language
en
Open access
closed
Locations
  • Cancer Research (publishedVersion)
  • PubMed (publishedVersion)
  • HAL (submittedVersion)
Funders
U.S. Food and Drug Administration
Topics
  • Health Sciences › Medicine › Oncology › PARP inhibition in cancer therapy
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
Keywords
cisplatin resistance, PARP1, PARP inhibitors, non-small cell lung cancer, DNA damage response, mitochondrial apoptosis, poly(ADP-ribosyl)ation, siRNA knockdown, xenografts, chemoresistance
MeSH terms
Poly(ADP-ribose) Polymerase Inhibitors, Poly (ADP-Ribose) Polymerase-1, Animals, Antineoplastic Agents, Carcinoma, Non-Small-Cell Lung, Cisplatin, Female, Humans, Lung Neoplasms, Mice, Nude, Phenanthrenes, Poly(ADP-ribose) Polymerases, RNA, Messenger, Tumor Cells, Cultured, Blotting, Western, Apoptosis, Drug Resistance, Neoplasm, Reverse Transcriptase Polymerase Chain Reaction, Xenograft Model Antitumor Assays, Cell Proliferation, Mice, Real-Time Polymerase Chain Reaction

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review