Dexamethasone inhibits TRAIL-induced apoptosis of thyroid cancer cells via Bcl-xL induction

Antonello Petrella, Simona Francesca Ercolino, Michela Festa, Antonio Gentilella, Alessandra Tosco, Suzanne D. Conzen, Luca Parente

Research output: Contribution to journalArticlepeer-review

42 Scopus citations


We have investigated the effect of dexamethasone (DEX) on the apoptosis induced by TRAIL (tumour necrosis factor-related apoptosis inducing ligand) in follicular undifferentiated thyroid (FRO) cancer cells. Apoptosis was measured by percent hypodiploid nuclei, caspase-3 and -8 activation, and mitochondrial membrane depolarisation. DEX nearly abolished TRAIL-induced apoptosis. The DEX protective effect was reverted by the steroid receptor antagonist RU486 suggesting that the DEX action is mediated by glucocorticoid receptor (GR) activation. The role of Bcl proteins in the DEX effect was then investigated. In FRO cells DEX stimulated in a time-dependent fashion the expression of Bcl-xL, but not that of Bcl-2, Bax and Bad. In addition, Bcl-xL mRNA was significantly increased in the presence of DEX, suggesting a transcriptional regulation by the steroid. Transfection of the cells with siRNAs against Bcl-xL inhibited both basal and DEX-stimulated Bcl-xL expression and restored apoptosis in TRAIL-stimulated cells treated with DEX. These results demonstrate that dexamethasone protects thyroid cancer cells from apoptosis induced by TRAIL. DEX acts via GR activation and up-regulation of the expression of the anti-apoptotic protein Bcl-xL.

Original languageEnglish (US)
Pages (from-to)3287-3293
Number of pages7
JournalEuropean Journal of Cancer
Issue number18
StatePublished - Dec 2006
Externally publishedYes


  • Apoptosis
  • Bcl-2 proteins
  • Dexamethasone
  • Thyroid cancer

ASJC Scopus subject areas

  • Oncology
  • Cancer Research


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