Treatment of nasopharyngeal carcinoma cells with the histone-deacetylase inhibitor abexinostat: cooperative effects with cis-platin and radiotherapy on patient-derived xenografts

PLoS One. 2014 Mar 11;9(3):e91325. doi: 10.1371/journal.pone.0091325. eCollection 2014.

Abstract

EBV-related nasopharyngeal carcinomas (NPCs) still raise serious therapeutic problems. The therapeutic potential of the histone-deacetylase (HDAC) inhibitor Abexinostat was investigated using 5 preclinical NPC models including 2 patient-derived xenografts (C15 and C17). The cytotoxicity of Abexinostat used either alone or in combination with cis-platin or irradiation was assessed in vitro by MTT and clonogenic assays using 2 EBV-negative (CNE1 and HONE1) and 3 EBV-positive NPC models (C15, C17 and C666-1). Subsequently, the 3 EBV-positive models were used under the form of xenografts to assess the impact of systemic treatments by Abexinostat or combinations of Abexinostat with cis-platin or irradiation. Several cell proteins known to be affected by HDAC inhibitors and the small viral non-coding RNA EBER1 were investigated in the treated tumors. Synergistic cytotoxic effects of Abexinostat combined with cis-platin or irradiation were demonstrated in vitro for each NPC model. When using xenografts, Abexinostat by itself (12.5 mg/kg, BID, 4 days a week for 3 weeks) had significant anti-tumor effects against C17. Cooperative effects with cis-platin (2 mg/kg, IP, at days 3, 10 and 17) and irradiation (1 Gy) were observed for the C15 and C17 xenografts. Simultaneously two types of biological alterations were induced in the tumor tissue, especially in the C17 model: a depletion of the DNA-repair protein RAD51 and a stronger in situ detection of the small viral RNA EBER1. Overall, these results support implementation of phase I/II clinical trials of Abexinostat for the treatment of NPC. A depletion of RAD51 is likely to contribute to the cooperation of Abexinostat with DNA damaging agents. Reduction of RAD51 combined to enhanced detection of EBER 1 might be helpful for early assessment of tumor response.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adult
  • Animals
  • Antineoplastic Agents / pharmacology
  • Benzofurans / pharmacology*
  • Benzofurans / toxicity
  • Carcinoma
  • Cell Line, Tumor
  • Cell Survival / drug effects
  • Cell Survival / radiation effects
  • Cisplatin / pharmacology
  • Disease Models, Animal
  • Drug Synergism
  • Female
  • Herpesvirus 4, Human / genetics
  • Histone Deacetylase Inhibitors / pharmacology*
  • Histone Deacetylase Inhibitors / toxicity
  • Humans
  • Hydroxamic Acids / pharmacology*
  • Hydroxamic Acids / toxicity
  • Inhibitory Concentration 50
  • Male
  • Mice
  • Nasopharyngeal Carcinoma
  • Nasopharyngeal Neoplasms / metabolism
  • Nasopharyngeal Neoplasms / pathology*
  • Nasopharyngeal Neoplasms / virology
  • RNA, Viral / genetics
  • RNA, Viral / metabolism
  • Rad51 Recombinase / genetics
  • Rad51 Recombinase / metabolism
  • Tumor Burden / drug effects
  • Tumor Burden / radiation effects
  • Tumor Stem Cell Assay
  • Xenograft Model Antitumor Assays

Substances

  • Antineoplastic Agents
  • Benzofurans
  • Epstein-Barr virus encoded RNA 1
  • Histone Deacetylase Inhibitors
  • Hydroxamic Acids
  • RNA, Viral
  • Rad51 Recombinase
  • abexinostat
  • Cisplatin

Grants and funding

Research carried by Pierre Busson's group has been supported by a contract linking Servier, a company developing Abexinostat, and Institut Gustave Roussy. Benjamin Verillaud was the recipient of a fellowship from the Institut National du Cancer (FOR – 2010-INCa_3113) and from the APHP-CNRS (RAFCNR11). Hélène Lelièvre, Anne Jacquet-Bescond, Laurence Kraus-Berthier, and Stéphane Depil are employed by Servier, and had a role in study design, data analysis, decision to publish, and preparation of the manuscript.