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1. Anticancer chemotherapy and radiotherapy trigger both non-cell-autonomous and cell-autonomous death.

Author

Martins I, Raza SQ, Voisin L, Dakhli H, Allouch A, Law F, Sabino D, De Jong D, Thoreau M, Mintet E, Dugué D, Piacentini M, Gougeon ML, Jaulin F, Bertrand P, Brenner C, Ojcius DM, Kroemer G, Modjtahedi N, Deutsch E, and Perfettini JL

Subjects
Animals, Antineoplastic Agents therapeutic use, Cell Death drug effects, Cell Death radiation effects, Cell Line, Tumor, Cisplatin pharmacology, HCT116 Cells, Humans, Jurkat Cells, MCF-7 Cells, Mice, Neoplasms drug therapy, Neoplasms pathology, Neoplasms radiotherapy, Oxaliplatin pharmacology, Paclitaxel pharmacology, Radiotherapy, Antineoplastic Agents pharmacology, Apoptosis drug effects, Apoptosis radiation effects, Bystander Effect drug effects, Bystander Effect radiation effects, Gamma Rays therapeutic use
Abstract

Even though cell death modalities elicited by anticancer chemotherapy and radiotherapy have been extensively studied, the ability of anticancer treatments to induce non-cell-autonomous death has never been investigated. By means of multispectral imaging flow-cytometry-based technology, we analyzed the lethal fate of cancer cells that were treated with conventional anticancer agents and co-cultured with untreated cells, observing that anticancer agents can simultaneously trigger cell-autonomous and non-cell-autonomous death in treated and untreated cells. After ionizing radiation, oxaliplatin, or cisplatin treatment, fractions of treated cancer cell populations were eliminated through cell-autonomous death mechanisms, while other fractions of the treated cancer cells engulfed and killed neighboring cells through non-cell-autonomous processes, including cellular cannibalism. Under conditions of treatment with paclitaxel, non-cell-autonomous and cell-autonomous death were both detected in the treated cell population, while untreated neighboring cells exhibited features of apoptotic demise. The transcriptional activity of p53 tumor-suppressor protein contributed to the execution of cell-autonomous death, yet failed to affect the non-cell-autonomous death by cannibalism for the majority of tested anticancer agents, indicating that the induction of non-cell-autonomous death can occur under conditions in which cell-autonomous death was impaired. Altogether, these results reveal that chemotherapy and radiotherapy can induce both non-cell-autonomous and cell-autonomous death of cancer cells, highlighting the heterogeneity of cell death responses to anticancer treatments and the unsuspected potential contribution of non-cell-autonomous death to the global effects of anticancer treatment.

Published
2018
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2. Anticancer chemotherapy and radiotherapy trigger both non-cell-autonomous and cell-autonomous death

Author

Martins, Isabelle, Raza, Syed Qasim, Voisin, Laurent, Dakhli, Haithem, Allouch, Awatef, Law, Frédéric, Sabino, Dora, De Jong, Dorine, Thoreau, Maxime, Mintet, Elodie, Dugué, Delphine, Piacentini, Mauro, Gougeon, Marie-Lise, Jaulin, Fanny, Bertrand, Pascale, Brenner, Catherine, Ojcius, David M, Kroemer, Guido, Modjtahedi, Nazanine, Deutsch, Eric, Perfettini, Jean-Luc, Radiothérapie moléculaire (UMR 1030), Université Paris-Sud - Paris 11 (UP11)-Institut Gustave Roussy (IGR)-Institut National de la Santé et de la Recherche Médicale (INSERM), Université Paris-Saclay, University of Veterinary and Animal Sciences [Lahore, Pakistan] (UVAS), Biomarqueurs prédictifs et nouvelles stratégies moléculaires en thérapeutique anticancéreuse (U981), National Institute for Infectious Diseases 'Lazzaro Spallanzani', Università degli Studi di Roma Tor Vergata [Roma], Immunité Anti-virale, Biothérapie et Vaccins (IABV), Institut Pasteur [Paris] (IP), Laboratoire Réparation Et Vieillissement (LREV), Université Paris-Sud - Paris 11 (UP11)-Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut de Biologie François JACOB (JACOB), Direction de Recherche Fondamentale (CEA) (DRF (CEA)), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Direction de Recherche Fondamentale (CEA) (DRF (CEA)), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA), Signalisation et physiopathologie cardiaque, Université Paris-Sud - Paris 11 (UP11)-IFR141-Institut National de la Santé et de la Recherche Médicale (INSERM), University of the Pacific [San Francisco], University of the Pacific, Apoptose, cancer et immunité (Equipe labellisée Ligue contre le cancer - CRC - Inserm U1138), Institut Gustave Roussy (IGR)-Centre de Recherche des Cordeliers (CRC (UMR_S_1138 / U1138)), École Pratique des Hautes Études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-École Pratique des Hautes Études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU), Karolinska University Hospital [Stockholm], Pôle de biologie, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Européen Georges Pompidou [APHP] (HEGP), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO), Plateforme de métabolomique, Direction de la recherche [Gustave Roussy], Institut Gustave Roussy (IGR)-Institut Gustave Roussy (IGR), This work was supported by funds from La Ligue contre le Cancer Comité du Val-de-Marne, Agence Nationale de la Recherche (ANR), Institut National du Cancer (INCA-2015-1-PLBIO-07-IGR-1), Laboratory of Excellence (LabEx) LERMIT, the SIRIC Stratified Oncology Cell DNA Repair and Tumor Immune Elimination (SOCRATE), NATIXIS, Electricité de France and Fondation Gustave Roussy (to J-L.P.), and from the Ligue contre le Cancer Comité de Charente-Maritime (équipe labelisée), Agence National de la Recherche (ANR) – Projets blancs, ANR under the frame of E-Rare-2, the ERA-Net for Research on Rare Diseases, Association pour la Recherche sur le Cancer (ARC), Cancéropôle Ile-de-France, Chancelerie des universités de Paris (Legs Poix), Fondation pour la Recherche Médicale (FRM), a donation by Elior, the European Commission (ArtForce), the European Research Council (ERC), Fondation Carrefour, Institut National du Cancer (INCa), Inserm (HTE), Institut Universitaire de France, LeDucq Foundation, the LabEx Immuno-Oncology, the RHU Torino Lumière, the Searave Foundation, the SIRIC Stratified Oncology Cell DNA Repair and Tumor Immune Elimination (SOCRATE), the SIRIC Cancer Research and Personalized Medicine (CARPEM), and the Paris Alliance of Cancer Research Institutes (PACRI) (to G.K.). I.M. is supported by the SIRIC Stratified Oncology Cell DNA Repair and Tumor Immune Elimination (SOCRATE) and INCA (INCA-DGOS-INSERM 6043). S.Q.R is funded by Higher Education Commission (Pakistan) and by the Laboratory of Excellence LERMIT with a grant from ANR (ANR-10-LABX-33) under the program 'Investissements d’Avenir' ANR-11-IDEX-0003-01. E.M. and M.T. are also supported by the Laboratory of Excellence LERMIT with a grant from ANR (ANR-10-LABX-33) under the program 'Investissements d’Avenir' ANR-11-IDEX-0003-01. L.V. is funded by a grant from INCA (INCA-2015-1-PLBIO-07-IGR-1). H.D and D.D are, respectively, recipients of PhD fellowships from LabEx LERMIT and Fondation Philantropia. Q.W. is supported by China Scholarship Council., The authors would like to thank C. Leteur, Y. Lecluse, P. Rameau, and S. Salome-Desnoulez for their technical supports., Institut Pasteur [Paris], École pratique des hautes études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-École pratique des hautes études (EPHE), Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut Gustave Roussy (IGR)-Université Paris-Sud - Paris 11 (UP11), and Université Paris Diderot - Paris 7 (UPD7)-Université Paris-Sud - Paris 11 (UP11)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut de Biologie François JACOB (JACOB)

Subjects
Settore BIO/06, Paclitaxel, Oncology and Carcinogenesis, Antineoplastic Agents, Apoptosis, [SDV.CAN]Life Sciences [q-bio]/Cancer, [SDV.BC]Life Sciences [q-bio]/Cellular Biology, Cell Line, Jurkat Cells, Mice, Cell Line, Tumor, Neoplasms, Breast Cancer, Animals, Humans, lcsh:QH573-671, Cancer, Tumor, Radiotherapy, Cell Death, lcsh:Cytology, Bystander Effect, HCT116 Cells, Oxaliplatin, Gamma Rays, MCF-7 Cells, Biochemistry and Cell Biology, Cisplatin
Abstract

International audience; Even though cell death modalities elicited by anticancer chemotherapy and radiotherapy have been extensively studied, the ability of anticancer treatments to induce non-cell-autonomous death has never been investigated. By means of multispectral imaging flow-cytometry-based technology, we analyzed the lethal fate of cancer cells that were treated with conventional anticancer agents and co-cultured with untreated cells, observing that anticancer agents can simultaneously trigger cell-autonomous and non-cell-autonomous death in treated and untreated cells. After ionizing radiation, oxaliplatin, or cisplatin treatment, fractions of treated cancer cell populations were eliminated through cell-autonomous death mechanisms, while other fractions of the treated cancer cells engulfed and killed neighboring cells through non-cell-autonomous processes, including cellular cannibalism. Under conditions of treatment with paclitaxel, non-cell-autonomous and cell-autonomous death were both detected in the treated cell population, while untreated neighboring cells exhibited features of apoptotic demise. The transcriptional activity of p53 tumor-suppressor protein contributed to the execution of cell-autonomous death, yet failed to affect the non-cell-autonomous death by cannibalism for the majority of tested anticancer agents, indicating that the induction of non-cell-autonomous death can occur under conditions in which cell-autonomous death was impaired. Altogether, these results reveal that chemotherapy and radiotherapy can induce both non-cell-autonomous and cell-autonomous death of cancer cells, highlighting the heterogeneity of cell death responses to anticancer treatments and the unsuspected potential contribution of non-cell-autonomous death to the global effects of anticancer treatment.

Published
2018
Full Text
View/download PDF

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