Journal
ENDOCRINE-RELATED CANCER
Volume 18, Issue 6, Pages 711-719Publisher
BIOSCIENTIFICA LTD
DOI: 10.1530/ERC-10-0257
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Funding
- Institut National du Cancer (INCa, France) [PL0079, 07/3D1616/Pdoc-110-32/NG-NC, R06080AA]
- French Medical Research (FRM, France)
- European Community (MICROENVIMET) [FP7-HEALTH-F2-2008-201279]
- CHUN-CNRS
- Gunnar Nilsson Cancer Foundation
- Sharon D Lund Foundation
- Swedish Cancer Society
- Swedish Research Council
- Medical Faculty, Lund University
- Soderberg, Pediatric Cancer
- Anna-Lisa and Sven-Erik Lundgren Foundation
- Knut and Alice Wallenberg Foundation
- Lund City Jubileumsfond
- John and Augusta Persson Foundation for Medical Research
- Maggie Stephens Foundation
- Inga-Britt and Arne Lundberg Foundation
- H J Forssman Foundation for Medical Research
- Royal Physiographic Society
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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
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