MiR-129-5p is required for histone deacetylase inhibitor-induced cell death in thyroid cancer cells

Patrick Brest, Sandra Lassalle, Veronique Hofman, Olivier Bordone, Virginie Gavric Tanga, Christelle Bonnetaud, Chimene Moreilhon, Geraldine Rios, Jose Santini, Pascal Barbry, Catharina Svanborg, Baharia Mograbi, Bernard Mari, Paul Hofman

Research output: Contribution to journalArticlepeer-review

75 Citations (SciVal)


The molecular mechanism responsible for the antitumor activity of histone deacetylase inhibitors (HDACi) remains elusive. As HDACi have been described to alter miRNA expression, the aim of this study was to characterize HDACi-induced miRNAs and to determine their functional importance in the induction of cell death alone or in combination with other cancer drugs. Two HDACi, trichostatin A and vorinostat, induced miR-129-5p overexpression, histone acetylation and cell death in BCPAP, TPC-1, 8505C, and CAL62 cell lines and in primary cultures of papillary thyroid cancer (PTC) cells. In addition, miR-129-5p alone was sufficient to induce cell death and knockdown experiments showed that expression of this miRNA was required for HDACi-induced cell death. Moreover, miR-129-5p accentuated the anti-proliferative effects of other cancer drugs such as etoposide or human a-lactalbumin made lethal for tumor cells (HAMLET). Taken together, our data show that miR-129-5p is involved in the antitumor activity of HDACi and highlight a miRNA-driven cell death mechanism. Endocrine-Related Cancer (2011) 18 711-719
Original languageEnglish
Pages (from-to)711-719
JournalEndocrine-Related Cancer
Issue number6
Publication statusPublished - 2011

Subject classification (UKÄ)

  • Microbiology in the medical area
  • Immunology in the medical area


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