TY - JOUR
T1 - MiR-129-5p is required for histone deacetylase inhibitor-induced cell death in thyroid cancer cells
AU - Brest, Patrick
AU - Lassalle, Sandra
AU - Hofman, Veronique
AU - Bordone, Olivier
AU - Tanga, Virginie Gavric
AU - Bonnetaud, Christelle
AU - Moreilhon, Chimene
AU - Rios, Geraldine
AU - Santini, Jose
AU - Barbry, Pascal
AU - Svanborg, Catharina
AU - Mograbi, Baharia
AU - Mari, Bernard
AU - Hofman, Paul
PY - 2011
Y1 - 2011
N2 - 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
AB - 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
U2 - 10.1530/ERC-10-0257
DO - 10.1530/ERC-10-0257
M3 - Article
C2 - 21946411
SN - 1479-6821
VL - 18
SP - 711
EP - 719
JO - Endocrine-Related Cancer
JF - Endocrine-Related Cancer
IS - 6
ER -
